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@article{ISI:000653627900006,

title = {Nuclear translocation of MRTFA in MCF7 breast cancer cells shifts ER 

 alpha nuclear/genomic to extra-nuclear/non genomic actions},

author = {Charly Jehanno and Frederic Percevault and Noureddine Boujrad and Pascale Le Goff and Coralie Fontaine and Jean-Francois Arnal and Michael Primig and Farzad Pakdel and Denis Michel and Raphael Metivier and Gilles Flouriot},

doi = {10.1016/j.mce.2021.111282},

issn = {0303-7207},

year  = {2021},

date = {2021-06-01},

journal = {MOLECULAR AND CELLULAR ENDOCRINOLOGY},

volume = {530},

abstract = {The Myocardin-related transcription factor A [MRTFA, also known as 

 Megakaryoblastic Leukemia 1 (MKL1))] is a major actor in the epithelial 

 to mesenchymal transition (EMT). We have previously shown that 

 activation and nuclear accumulation of MRTFA mediate endocrine 

 resistance of estrogen receptor alpha (ER alpha) positive breast cancers 

 by initiating a partial transition from luminal to basal-like phenotype 

 and impairing ER alpha cistrome and transcriptome. In the present study, 

 we deepen our understanding of the mechanism by monitoring functional 

 changes in the receptor's activity. We demonstrate that MRTFA nuclear 

 accumulation down-regulates the expression of the unliganded (Apo-)ER 

 alpha and causes a redistribution of the protein localization from its 

 normal nuclear place to the entire cell volume. This phenomenon is 

 accompanied by a shift in Apo-ER alpha monomer/dimer ratio towards the 

 monomeric state, leading to significant functional consequences on ER 

 alpha activities. In particular, the association of Apo-ER alpha with 

 chromatin is drastically decreased, and the remaining ER alpha binding 

 sites are substantially less enriched in ERE motifs than in control 

 conditions. Monitored by proximity Ligation Assay, ER alpha interactions 

 with P160 family coactivators are partly impacted when MRTFA accumulates 

 in the nucleus, and those with SMRT and NCOR1 corepressors are 

 abolished. Finally, ER alpha interactions with kinases such as c-src and 

 PI3K are increased, thereby enhancing MAP Kinase and AKT activities. In 

 conclusion, the activation and nuclear accumulation of MRTFA in ER alpha 

 positive breast cancer cells remodels both ER alpha location and 

 functions by shifting its activity from nuclear genome regulation to 

 extra-nuclear non-genomic signaling.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{ISI:000650003400022,

title = {Validation of a Score for the Detection of Subjects with High Risk for 

 Severe High-Altitude Illness},

author = {Jean-Paul Richalet and Fabien Pillard and David Le Moal and Daniel Riviere and Philippe Oriol and Mathias Poussel and Bruno Chenuel and Stephane Doutreleau and Samuel Verges and Sophie Demanez and Michel Vergnion and Jean-Michel Boulet and Herve Douard and Maryse Dupre and Olivier Mesland and Romain Remetter and Evelyne Lonsdorfer-Wolf and Alain Frey and Louis Vilcoq and Anne Nedelec Jaffuel and David Debeaumont and Guy Duperrex and Francois Lecoq and Christophe Hedon and Maurice Hayot and Guido Giardini and Francois J Lhuissier},

doi = {10.1249/MSS.0000000000002586},

issn = {0195-9131},

year  = {2021},

date = {2021-06-01},

journal = {MEDICINE AND SCIENCE IN SPORTS AND EXERCISE},

volume = {53},

number = {6},

pages = {1294-1302},

abstract = {Purpose 

 A decision tree based on a clinicophysiological score (severe 

 high-altitude illness (SHAI) score) has been developed to detect 

 subjects susceptible to SHAI. We aimed to validate this decision tree, 

 to rationalize the prescription of acetazolamide (ACZ), and to specify 

 the rule for a progressive acclimatization. Methods 

 Data were obtained from 641 subjects in 15 European medical centers 

 before and during a sojourn at high altitude. Depending on the value of 

 the SHAI score, advice was given and ACZ was eventually prescribed. The 

 outcome was the occurrence of SHAI at high altitude as a function of the 

 SHAI score, ACZ prescription, and use and fulfillment of the 

 acclimatization rule. Results 

 The occurrence of SHAI was 22.6%, similar to what was observed 18 yr 

 before (23.7%), whereas life-threatening forms of SHAI (high-altitude pulmonary and cerebral edema) were less frequent (2.6%-0.8%},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{ISI:000641611600001,

title = {PI3KC2 beta inactivation stabilizes VE-cadherin junctions and preserves 

 vascular integrity},

author = {Typhaine Anquetil and Romain Solinhac and Aude Jaffre and Gaetan Chicanne and Julien Viaud and Jean Darcourt and Cyrille Orset and Eva Geuss and Christoph Kleinschnitz and Bart Vanhaesebroeck and Denis Vivien and Karim Hnia and Vincent Larrue and Bernard Payrastre and Marie-Pierre Gratacap},

doi = {10.15252/embr.202051299, Early Access Date = APR 2021},

issn = {1469-221X},

year  = {2021},

date = {2021-06-01},

journal = {EMBO REPORTS},

volume = {22},

number = {6},

abstract = {Endothelium protection is critical, because of the impact of vascular 

 leakage and edema on pathological conditions such as brain ischemia. 

 Whereas deficiency of class II phosphoinositide 3-kinase alpha (PI3KC2 

 alpha) results in an increase in vascular permeability, we uncover a 

 crucial role of the beta isoform (PI3KC2 beta) in the loss of 

 endothelial barrier integrity following injury. Here, we studied the 

 role of PI3KC2 beta in endothelial permeability and endosomal 

 trafficking in vitro and in vivo in ischemic stroke. Mice with inactive 

 PI3KC2 beta showed protection against vascular permeability, edema, 

 cerebral infarction, and deleterious inflammatory response. Loss of 

 PI3KC2 beta in human cerebral microvascular endothelial cells stabilized 

 homotypic cell-cell junctions by increasing Rab11-dependent VE-cadherin 

 recycling. These results identify PI3KC2 beta as a potential new 

 therapeutic target to prevent aggravating lesions following ischemic 

 stroke.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{ISI:000654668500001,

title = {Estetrol Combined to Progestogen for Menopause or Contraception 

 Indication Is Neutral on Breast Cancer},

author = {Anne Gallez and Silvia Blacher and Erik Maquoi and Erika Konradowski and Marc Joiret and Irina Primac and Celine Gerard and Melanie Taziaux and Rene Houtman and Liesbet Geris and Francoise Lenfant and Elisabetta Marangoni and Nor Eddine Sounni and Jean-Michel Foidart and Agnes Noel and Christel Pequeux},

doi = {10.3390/cancers13102486},

year  = {2021},

date = {2021-05-01},

journal = {CANCERS},

volume = {13},

number = {10},

abstract = {Simple Summary 

 Hormonal treatments, especially those used to treat menopause symptoms 

 are known to increase breast cancer risk. It is thus necessary to 

 identify new formulations with a better benefit/risk profile. The aim of 

 this translational study was to evaluate the breast cancer risk 

 associated with a combination of a natural estrogen named estetrol, with 

 progestogens such as natural progesterone and drospirenone. Since the 

 assessment of breast cancer risk in patients during drug development is 

 not possible given the requirement of long-term studies in large 

 populations, this study provides new evidence that a therapeutic dose of 

 estetrol for menopause treatment or contraception, combined with 

 progesterone or drospirenone, may provide a better benefit/risk profile 

 toward breast cancer risk compared to the hormonal treatments currently 

 available for patients. 

 Given the unequivocal benefits of menopause hormone therapies (MHT) and 

 combined oral contraceptives (COC), there is a clinical need for new 

 formulations devoid of any risk of breast cancer promotion. Accumulating 

 data from preclinical and clinical studies support that estetrol (E4) is 

 a promising natural estrogen for MHT and COC. Nevertheless, we report 

 here that E4 remains active on the endometrium, even under a dose that 

 is neutral on breast cancer growth and lung metastasis dissemination. 

 This implies that a progestogen should be combined with E4 to protect 

 the endometrium of non-hysterectomized women from hyperplasia and 

 cancer. Through in vivo observations and transcriptomic analyses, our 

 work provides evidence that combining a progestogen to E4 is neutral on 

 breast cancer growth and dissemination, with very limited 

 transcriptional impact. The assessment of breast cancer risk in patients 

 during the development of new MHT or COC is not possible given the 

 requirement of long-term studies in large populations. This 

 translational preclinical research provides new evidence that a 

 therapeutic dose of E4 for MHT or COC, combined with progesterone or 

 drospirenone, may provide a better benefit/risk profile towards breast 

 cancer risk compared to hormonal treatments currently available for 

 patients.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{ISI:000653091300001,

title = {Postmenopausal women management: CNGOF and GEMVi clinical practice 

 guidelines (Short version)},

author = {F Tremollieres and N Chabbert-Buffet and G Plu-Bureau and C Rousset-Jablonski and J-M Lecerf and M Duclos and J-M Pouilles and A Gosset and G Boutet and C Hocke and E Maris and J Hugon-Rodin and L Maitrot-Mantelet and G Robin and G Andre and N Hamdaoui and C Mathelin and P Lopes and O Graesslin and X Fritel},

doi = {10.1016/j.gofs.2021.03.010},

issn = {2468-7197},

year  = {2021},

date = {2021-05-01},

journal = {GYNECOLOGIE OBSTETRIQUE FERTILITE & SENOLOGIE},

volume = {49},

number = {5},

pages = {305-317},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{ISI:000653091300006,

title = {Menopause hormone treatment. Postmenopausal women management : CNGOF and 

 GEMVi clinical practice guidelines},

author = {A Gosset and G Robin and B Letombe and J-M Pouilles and F Tremollieres},

doi = {10.1016/j.gofs.2021.03.019},

issn = {2468-7197},

year  = {2021},

date = {2021-05-01},

journal = {GYNECOLOGIE OBSTETRIQUE FERTILITE & SENOLOGIE},

volume = {49},

number = {5},

pages = {358-372},

abstract = {Menopause Hormonal Treatment (MHT) was initially developed to correct 

 the climacteric symptoms induced by postmenopausal estrogen deficiency. 

 In non-hysterectomized women, MHT combines estrogens and a progestogen, 

 the latter opposing the negative impact of estrogen on endometrial 

 proliferation. In France, and contrary to the USA and Northern European 

 countries, MHT mainly combines 1713-estradiol, which is the 

 physiological estrogen produced by the ovary, and progesterone or its 

 derivative, dihydrogesterone. France has been a pioneer in the 

 development of cutaneous administration routes (gel or transdermal 

 patch) for estradiol, allowing better metabolic tolerance and a 

 reduction of the risk of venous thromboembolism compared to the oral 

 route. The choice of the doses as well as the treatment regimen is 

 underpinned by tolerance as well as acceptance and compliance. The risk 

 of breast cancer, which is one of the main risks of MHT, is higher with 

 estro-progestogen combinations than with estrogens alone ; the 

 preferential use of progesterone or dihydrogesterone being likely to 

 limit the excess risk of breast cancer associated with MHT at least for 

 duration of treatment of less than 5 to 7 years. The question of the 

 optimal duration of MHT remains an issue and must take into account the 

 initial indication of treatment as well as the benefit-risk balance, 

 which is specific to each woman. Continuation of MHT is conditioned by 

 the benefit-risk balance, which must be evaluated regularly, but also by 

 the evolution of symptoms when MHT is stopped as well as 

 menopause-related health risks or induced by MHT. After stopping MHT, it 

 is necessary to maintain a medical follow-up to be adapted to the 

 clinical situation of each woman and in particular, her cardiovascular 

 and gynecological risk factors. (C) 2021 Elsevier Masson SAS. All rights 

 reserved.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{ISI:000653091300010,

title = {Menopause, menopause hormone therapy and osteoporosis. Postmenopausal 

 women management : CNGOF and GEMVi clinical practice guidelines},

author = {J-M Pouilles and A Gosset and F Tremollieres},

doi = {10.1016/j.gofs.2021.03.015},

issn = {2468-7197},

year  = {2021},

date = {2021-05-01},

journal = {GYNECOLOGIE OBSTETRIQUE FERTILITE & SENOLOGIE},

volume = {49},

number = {5},

pages = {420-437},

abstract = {Postmenopausal osteoporosis is a frequent clinical condition, which 

 affects nearly 1 in 3 women. Estrogen deficiency leads to rapid bone 

 loss, which is maximal within the first years after the menopause 

 transition and can be prevented by menopause hormone therapy (MHT). 

 Assessment of the individual risk of osteoporosis is primarily based on 

 the measurement of bone mineral density (BMD) at the spine and femur by 

 DXA. Clinical risk factors (CRFs) for fractures taken either alone or in 

 combination in the FRAX score were shown not to reliably predict 

 fractures and/or osteoporosis (as defined by a T-score <-2.5) in early 

 postmenopausal women. If DXA measurement is indicated in all women with 

 CRFs for fractures, it can be proposed on a case-by-case basis, when 

 knowledge of BMD is likely to condition the management of women at the 

 beginning of menopause, particularly the benefit-risk balance of MHT. 

 MHT prevents both bone loss and degradation of the bone 

 microarchitecture in early menopause. It significantly reduces the risk 

 of fracture at all bone sites by 20 to 40% regardless of basal level of 

 risk with an estrogen-dependent dose-effect. Given the inter-individual 

 variability in bone response, individual monitoring of the bone effect 

 of MHT is warranted when prescribed for the prevention of osteoporosis. 

 This monitoring is based on repeated measurement of lumbar and femoral 

 BMD (on the same DXA measurement system) after 2 years of MHT, the 

 response criterion being no significant bone loss. Discontinuation of 

 treatment is associated with a resumption of transient bone loss 

 although there is a large variability in the rate of bone loss among 

 women. Basically, there is a return to the level of fracture risk 

 comparable to that of in untreated woman of the same age within 2 to 5 

 years. Therefore, when MHT is prescribed for the prevention of 

 osteoporosis in women with an increased risk at the beginning of 

 menopause, measurement of BMD is recommended when MHT is stopped in 

 order to consider further management of the risk of fracture whenever 

 necessary (with possibly another antiosteoporotic treatment). (C) 2021 

 Elsevier Masson SAS. All rights reserved.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{ISI:000647314900009,

title = {Neutral Sphingomyelinase 2 Heightens Anti-Melanoma Immune Responses and 

 Anti-PD-1 Therapy Efficacy},

author = {Anne Montfort and Florie Bertrand and Julia Rochotte and Julia Gilhodes and Thomas Filleron and Jean Milhes and Carine Dufau and Caroline Imbert and Joelle Riond and Marie Tosolini and Christopher J Clarke and Florent Dufour and Andrei A Constantinescu and Nilton De Franca Junior and Virginie Garcia and Michel Record and Pierre Cordelier and Pierre Brousset and Philippe Rochaix and Sandrine Silvente-Poirot and Nicole Therville and Nathalie Andrieu-Abadie and Thierry Levade and Yusuf A Hannun and Herve Benoist and Nicolas Meyer and Olivier Micheau and Celine Colacios and Bruno Segui},

doi = {10.1158/2326-6066.CIR-20-0342},

issn = {2326-6066},

year  = {2021},

date = {2021-05-01},

journal = {CANCER IMMUNOLOGY RESEARCH},

volume = {9},

number = {5},

pages = {568-582},

abstract = {Dysregulation of lipid metabolism affects the behavior of cancer cells, 

 but how this happens is not completely understood. Neutral 

 sphingomyelinase 2 (nSMase2), encoded by SMPD3, catalyzes the breakdown 

 of sphingomyelin to produce the anti-oncometabolite ceramide. We found 

 that this enzyme was often downregulated in human metastatic melanoma, 

 likely contributing to immune escape. Overexpression of nSMase2 in mouse 

 melanoma reduced tumor growth in syngeneic wild-type but not 

 CD8-deficient mice. In wild-type mice, nSMase2-overexpressing tumors 

 showed accumulation of both ceramide and CD8(+) tumor-infiltrating 

 lymphocytes, and this was associated with increased level of transcripts 

 encoding IFN gamma and CXCL9. Overexpressing the catalytically inactive 

 nSMase2 failed to alter tumor growth, indicating that the deleterious 

 effect nSMase2 has on melanoma growth depends on its enzymatic activity. 

 In vitro, small extracellular vesicles from melanoma cells 

 overexpressing wild-type nSMase2 augmented the expression of IL12, 

 CXCL9, and CCL19 by bone marrow-derived dendritic cells, suggesting that 

 melanoma nSMase2 triggers T helper 1 (Th1) polarization in the earliest 

 stages of the immune response. Most importantly, overexpression of 

 wild-type nSMase2 increased anti-PD-1 efficacy in murine models of 

 melanoma and breast cancer, and this was associated with an enhanced Th1 

 response. Therefore, increasing SMPD3 expression in melanoma may serve 

 as an original therapeutic strategy to potentiate Th1 polarization and 

 CD8(+) T-cell-dependent immune responses and overcome resistance to 

 anti-PD-1.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{ISI:000621105900003,

title = {Role of oxidative stress in the dysfunction of the placental endothelial 

 nitric oxide synthase in preeclampsia},

author = {Paul Guerby and Oriane Tasta and Audrey Swiader and Frederic Pont and Emmanuel Bujold and Olivier Parant and Christophe Vayssiere and Robert Salvayre and Anne Negre-Salvayre},

doi = {10.1016/j.redox.2021.101861},

issn = {2213-2317},

year  = {2021},

date = {2021-04-01},

journal = {REDOX BIOLOGY},

volume = {40},

abstract = {Preeclampsia (PE) is a multifactorial pregnancy disease, characterized 

 by new-onset gestational hypertension with (or without) proteinuria or 

 end-organ failure, exclusively observed in humans. It is a leading cause 

 of maternal morbidity affecting 3-7% of pregnant women worldwide. PE 

 pathophysiology could result from abnormal placentation due to a 

 defective trophoblastic invasion and an impaired remodeling of uterine 

 spiral arteries, leading to a poor adaptation of utero-placental 

 circulation. This would be associated with hypoxia/reoxygenation 

 phenomena, oxygen gradient fluctuations, altered antioxidant capacity, 

 oxidative stress, and reduced nitric oxide (NO) bioavailability. This 

 results in part from the reaction of NO with the radical anion 

 superoxide (O-2(center dot-)), which produces peroxynitrite ONOO-, a 

 powerful pro-oxidant and inflammatory agent. Another mechanism is the 

 progressive inhibition of the placental endothelial nitric oxide 

 synthase (eNOS) by oxidative stress, which results in eNOS uncoupling 

 via several events such as a depletion of the eNOS substrate Larginine 

 due to increased arginase activity, an oxidation of the eNOS cofactor 

 tetrahydrobiopterin (BH4), or eNOS post-translational modifications (for 

 instance by S-glutathionylation). The uncoupling of eNOS triggers a 

 switch of its activity from a NO-producing enzyme to a NADPH 

 oxidase-like system generating O-2(center dot-), thereby potentiating 

 ROS production and oxidative stress. Moreover, in PE placentas, eNOS 

 could be post-translationally modified by lipid peroxidation-derived 

 aldehydes such as 4-oxononenal (ONE) a highly bioreactive agent, able to 

 inhibit eNOS activity and NO production. This review summarizes the 

 dysfunction of placental eNOS evoked by oxidative stress and lipid 

 peroxidation products, and the potential consequences on PE 

 pathogenesis.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{ISI:000621104800004,

title = {Galanin promotes autophagy and alleviates apoptosis in the hypertrophied 

 heart through FoxO1 pathway},

author = {Ilenia Martinelli and Andrei Timotin and Paula Moreno-Corchado and Dimitri Marsal and Solomiia Kramar and Halina Loy and Carine Joffre and Frederic Boal and Helene Tronchere and Oksana Kunduzova},

doi = {10.1016/j.redox.2021.101866},

issn = {2213-2317},

year  = {2021},

date = {2021-04-01},

journal = {REDOX BIOLOGY},

volume = {40},

abstract = {Autophagy and apoptosis are powerful regulators of multiple facets of 

 cellular metabolism and homeostasis. Here, we uncover that galanin, a 

 pleiotropic peptide, regulates cardiac autophagy and deactivates 

 apoptotic cell death through the Forkhead box protein O1 (FoxO1) 

 pathway. In hypertrophied heart, galanin promotes autophagy and 

 metabolic shift from fatty acid (FA) to glucose oxidation and preserves 

 mitochondrial integrity. In cardiomyoblasts, galanin triggers 

 autophagosome formation and alleviates hypertrophy, apoptotic cell 

 death, and mitochondrial stress. Mechanistically, galanin dictates cell 

 autophagic and anti-apoptotic phenotypes through FoxO1 pathway. 

 Together, these findings uncover a previously unknown role for galanin 

 in the regulation of cardiac autophagy and provide new insights into the 

 molecular mechanisms supporting cell survival in the hypertrophic 

 reprogramming of the heart.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{ISI:000623262300050,

title = {AnaConDa Device: Solution to Perform Cardiac Surgery Without Intravenous 

 Anesthetic During the Corona Virus Disease 2019 Pandemic},

author = {Francois Labaste and Valentin Rey and Helene Gonzalez and Bertrand Marcheix and Olivier Fourcade and Vincent Minville},

doi = {10.1053/j.jvca.2020.09.121},

issn = {1053-0770},

year  = {2021},

date = {2021-04-01},

journal = {JOURNAL OF CARDIOTHORACIC AND VASCULAR ANESTHESIA},

volume = {35},

number = {4},

pages = {1267-1268},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{ISI:000632688100008,

title = {Elafibranor improves diet-induced nonalcoholic steatohepatitis 

 associated with heart failure with preserved ejection fraction in Golden 

 Syrian hamsters},

author = {Francois Briand and Julie Maupoint and Emmanuel Brousseau and Natalia Breyner and Melanie Bouchet and Clement Costard and Thierry Leste-Lasserre and Mathieu Petitjean and Li Chen and Audrey Chabrat and Virgile Richard and Remy Burcelin and Caroline Dubroca and Thierry Sulpice},

doi = {10.1016/j.metabol.2021.154707},

issn = {0026-0495},

year  = {2021},

date = {2021-04-01},

journal = {METABOLISM-CLINICAL AND EXPERIMENTAL},

volume = {117},

abstract = {Background: Cardiovascular disease is the leading cause of deaths in 

 nonalcoholic steatohepatitis (NASH) patients. Mouse models, while widely 

 used for drug development, do not fully replicate human NASH nor 

 integrate the associated cardiac dysfunction, i.e. heart failure with 

 preserved ejection fraction (HFpEF). To overcome these limitations, we 

 established a nutritional hamster model developing both NASH and HFpEF. 

 We then evaluated the effects of the dual peroxisome proliferator 

 activated receptor alpha/delta agonist elafibranor developed for the 

 treatment of NASH patients. 

 Methods: Male Golden Syrian hamsters were fed for 10 to 20 weeks with a 

 free choice diet, which presents hamsters with a choice between control 

 chow diet with normal drinking water or a high fat/high cholesterol diet 

 with 10% fructose enriched drinking water. Biochemistry, histology and 

 echocardiography analysis were performed to characterize NASH and HFpEF. 

 Once the model was validated, elafibranor was evaluated at 15 mg/kg/day 

 orally QD for 5 weeks. 

 Results: Hamsters fed a free choice diet for up to 20 weeks developed 

 NASH, including hepatocyte ballooning (as confirmed with cytokeratin-18 

 immunostaining), bridging fibrosis, and a severe diastolic dysfunction 

 with restrictive profile, but preserved ejection fraction. Elafibranor 

 resolved NASH, with significant reduction in ballooning and fibrosis 

 scores, and improved diastolic dysfunction with significant reduction in 

 E/A and E/E ` ratios. Conclusion: Our data demonstrate that the free 

 choice diet induced NASH hamster model replicates the human phenotype 

 and will be useful for validating novel drug candidates for the 

 treatment of NASH and associated HFpEF. 

 (c) 2021 The Authors. Published by Elsevier Inc. This is an open access 

 article under the CC BY-NC-ND license (http:// 

 creativecommons.org/licenses/by-nc-nd/4.0/).},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{ISI:000639315900007,

title = {Data Sharing Under the General Data Protection Regulation Time to 

 Harmonize Law and Research Ethics?},

author = {Antonia Vlahou and Dara Hallinan and Rolf Apweiler and Angel Argiles and Joachim Beige and Ariela Benigni and Rainer Bischoff and Peter C Black and Franziska Boehm and Jocelyn Ceraline and George P Chrousos and Christian Delles and Pieter Evenepoel and Ivo Fridolin and Griet Glorieux and Alain J van Gool and Isabel Heidegger and John P A Ioannidis and Joachim Jankowski and Vera Jankowski and Carmen Jeronimo and Ashish M Kamat and Rosalinde Masereeuw and Gert Mayer and Harald Mischak and Alberto Ortiz and Giuseppe Remuzzi and Peter Rossing and Joost P Schanstra and Bernd J Schmitz-Draeger and Goce Spasovski and Jan A Staessen and Dimitrios Stamatialis and Peter Stenvinkel and Christoph Wanner and Stephen B Williams and Faiez Zannad and Carmine Zoccali and Raymond Vanholder},

doi = {10.1161/HYPERTENSIONAHA.120.16340},

issn = {0194-911X},

year  = {2021},

date = {2021-04-01},

journal = {HYPERTENSION},

volume = {77},

number = {4},

pages = {1029-1035},

abstract = {The General Data Protection Regulation (GDPR) became binding law in the 

 European Union Member States in 2018, as a step toward harmonizing 

 personal data protection legislation in the European Union. The 

 Regulation governs almost all types of personal data processing, hence, 

 also, those pertaining to biomedical research. The purpose of this 

 article is to highlight the main practical issues related to data and 

 biological sample sharing that biomedical researchers face regularly, 

 and to specify how these are addressed in the context of GDPR, after 

 consulting with ethics/legal experts. We identify areas in which 

 clarifications of the GDPR are needed, particularly those related to 

 consent requirements by study participants. Amendments should target the 

 following: (1) restricting exceptions based on national laws and 

 increasing harmonization, (2) confirming the concept of broad consent, 

 and (3) defining a roadmap for secondary use of data. These changes will 

 be achieved by acknowledged learned societies in the field taking the 

 lead in preparing a document giving guidance for the optimal 

 interpretation of the GDPR, which will be finalized following a period 

 of commenting by a broad multistakeholder audience. In parallel, 

 promoting engagement and education of the public in the relevant issues 

 (such as different consent types or residual risk for 

 re-identification), on both local/national and international levels, is 

 considered critical for advancement. We hope that this article will open 

 this broad discussion involving all major stakeholders, toward 

 optimizing the GDPR and allowing a harmonized transnational research 

 approach.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{ISI:000637074600007,

title = {Antibody-based delivery of interleukin-9 to neovascular structures: 

 Therapeutic evaluation in cancer and arthritis},

author = {Baptiste Gouyou and Tiziano Ongaro and Samuele Cazzamalli and Roberto De Luca and Anne Kerschenmeyer and Philippe Valet and Alessandra Villa and Dario Neri and Mattia Matasci},

doi = {10.1177/1535370220981578},

issn = {1535-3702},

year  = {2021},

date = {2021-04-01},

journal = {EXPERIMENTAL BIOLOGY AND MEDICINE},

volume = {246},

number = {8},

pages = {940-951},

abstract = {Interleukin-9 is a cytokine with multiple functions, including the 

 ability to activate group 2 innate lymphoid cells, which has been 

 postulated to be therapeutically active in mouse models of arthritis. 

 Similarly, interleukin-9 has been suggested to play an important role in 

 tumor immunity. Here, we describe the cloning, expression, and 

 characterization of three fusion proteins based on murine interleukin-9 

 and the F8 antibody, specific to the alternatively spliced EDA domain of 

 fibronectin. EDA is strongly expressed in cancer and in various 

 arthritic conditions, while being undetectable in the majority of 

 healthy organs. Interleukin-9-based fusion proteins with an irrelevant 

 antibody specific to hen egg lysozyme served as negative control in our 

 study. The fusion proteins were characterized by quantitative 

 biodistribution analysis in tumor-bearing mice using radioiodinated 

 protein preparations. The highest tumor uptake and best tumor:organ 

 ratios were observed for a format, in which the interleukin-9 moiety was 

 flanked by two units of the F8 antibody in single-chain Fv format. 

 Biological activity of interleukin-9 was retained when the payload was 

 fused to antibodies. However, the targeted delivery of interleukin-9 to 

 the disease site resulted in a modest anti-tumor activity in three 

 different murine models of cancer (K1735M2, CT26, and F9), while no 

 therapeutic benefit was observed in a collagen induced model of 

 arthritis. Collectively, these results confirm the possibility to 

 deliver interleukin-9 to the site of disease but cast doubts about the 

 alleged therapeutic activity of this cytokine in cancer and arthritis, 

 which has been postulated in previous publications.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{ISI:000639562600017,

title = {Role of C5 inhibition in Idiopathic Inflammatory Myopathies and 

 Scleroderma Renal Crisis-Induced Thrombotic Microangiopathies},

author = {Anna Gouin and David Ribes and Magali Colombat and Dominique Chauveau and Gregoire Prevot and Olivier Lairez and Gregory Pugnet and Veronique Fremeaux-Bacchi and Antoine Huart and Julie Belliere and Stanislas Faguer},

doi = {10.1016/j.ekir.2021.01.021},

issn = {2468-0249},

year  = {2021},

date = {2021-04-01},

journal = {KIDNEY INTERNATIONAL REPORTS},

volume = {6},

number = {4},

pages = {1015-1021},

abstract = {Introduction: Connective tissue diseases, including systemic sclerosis 

 and idiopathic inflammatory myopathies (IIMs), are a very rare cause of 

 thrombotic microangiopathies (TMAs). Whether dysregulation of the 

 complement pathways underlies these secondary forms of TMA and may be 

 targeted by complement blocking agents remains elusive. 

 Methods: Kidney pathology and outcomes of 18 critically ill patients with TMA related to inflammatory myopathy flare-up (IIM},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{ISI:000639562600005,

title = {Rituximab in Membranous Nephropathy},

author = {Philipp Gauckler and Jae Il Shin and Federico Alberici and Vincent Audard and Annette Bruchfeld and Martin Busch and Chee Kay Cheung and Matija Crnogorac and Elisa Delbarba and Kathrin Eller and Stanislas Faguer and Kresimir Galesic and Sian Griffin and Martijn W F van den Hoogen and Zdenka Hruskova and Anushya Jeyabalan and Alexandre Karras and Catherine King and Harbir Singh Kohli and Gert Mayer and Rutger Maas and Masahiro Muto and Sergey Moiseev and Balazs Odler and Ruth J Pepper and Luis F Quintana and Jai Radhakrishnan and Raja Ramachandran and Alan D Salama and Ulf Schonermarck and Marten Segelmark and Lee Smith and Vladimir Tesar and Jack Wetzels and Lisa Willcocks and Martin Windpessl and Ladan Zand and Reza Zonozi and Andreas Kronbichler and RITERM Study Grp},

doi = {10.1016/j.ekir.2020.12.035},

issn = {2468-0249},

year  = {2021},

date = {2021-04-01},

journal = {KIDNEY INTERNATIONAL REPORTS},

volume = {6},

number = {4},

pages = {881-893},

abstract = {Membranous nephropathy (MN) is the most common cause of primary 

 nephrotic syndrome among adults. The identification of phospholipase A2 

 receptor (PLA2R) as target antigen in most patients changed the 

 management of MN dramatically, and provided a rationale for B-cell 

 depleting agents such as rituximab. The efficacy of rituximab in 

 inducing remission has been investigated in several studies, including 3 

 randomized controlled trials, in which complete and partial remission of 

 proteinuria was achieved in approximately two-thirds of treated 

 patients. Due to its favorable safety profile, rituximab is now 

 considered a first-line treatment option for MN, especially in patients 

 at moderate and high risk of deterioration in kidney function. However, 

 questions remain about how to best use rituximab, including the optimal 

 dosing regimen, a potential need for maintenance therapy, and assessment 

 of long-term safety and efficacy outcomes. In this review, we provide an 

 overview of the current literature and discuss both strengths and 

 limitations of ``the new standard.''},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{ISI:000642298600029,

title = {Complement C5 inhibition reverses bleomycin-induced thrombotic 

 microangiopathy},

author = {Sofiane Salhi and David Ribes and Stanislas Faguer},

doi = {10.1093/ckj/sfaa101},

issn = {2048-8505},

year  = {2021},

date = {2021-04-01},

journal = {CLINICAL KIDNEY JOURNAL},

volume = {14},

number = {4},

pages = {1275-1276},

abstract = {Whether C5 blocking may improve the outcomes of patients developing 

 chemotherapy-induced thrombotic microangiopathy (TMA) remains elusive. 

 Lung fibrosis is a well-known complication of bleomycin, whereas TMA5 

 are very rare (<20 cases described). Here, we report an exceptional case 

 of a male patient that developed acute respiratory distress syndrome and 

 TMA following administration of bleomycin, cisplatin and etoposide . 

 Refractoriness to plasma exchanges prompted us to use eculizumab as 

 salvage therapy. Eculizumab led to complete remission of the TMA before 

 Day 2. However, the patient progressed towards refractory respiratory 

 failure, suggesting that pathophysiological mechanisms of 

 bleomycin-induced lung fibrosis and TMA differ.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{ISI:000618022400010,

title = {Bone mineral density in women with deep infiltrating endometriosis who 

 have undergone early bilateral oophorectomy},

author = {Anna Gosset and Claire Escanes and Jean-Michel Pouilles and Fabien Vidal and Yann Tanguy Le Gac and Genevieve Plu-Bureau and Florence A Tremollieres},

doi = {10.1097/GME.0000000000001696},

issn = {1072-3714},

year  = {2021},

date = {2021-03-01},

journal = {MENOPAUSE-THE JOURNAL OF THE NORTH AMERICAN MENOPAUSE SOCIETY},

volume = {28},

number = {3},

pages = {300-306},

abstract = {Objective: To study bone mineral density (BMD) in women with and without 

 pelvic deep infiltrating endometriosis (DIE) who underwent early 

 bilateral oophorectomy (BO). Methods: A case-control study was performed 

 in 83 women who underwent early BO before the age of 45 years, 31 for 

 DIE and 52 for another clinical condition. All the women answered a 

 standardized computer-assisted questionnaire to record their clinical 

 and historical data and were medically examined. Lumbar spine and 

 femoral neck BMDs were measured by dual-energy X-ray absorptiometry 

 after early BO. Simultaneously, serum calcium, intact parathyroid, 

 25-hydroxyvitamin D, and cross-linked C-telopeptide were also measured. 

 Unadjusted and adjusted odds ratios (with 95% confidence intervals 

 [CI]) for endometriosis were calculated using logistic regression. 

 Results: The mean lumbar spine and femoral neck BMDs were significantly 

 higher in women who underwent early BO for DIE than in those who 

 underwent early BO for another clinical condition. After adjusting for 

 age at BMD measurement, years since menopause, age at menarche and body 

 mass index, odds ratio for endometriosis associated with a 1-SD increase 

 in lumbar spine and femoral neck BMD was 2.59 (95% CI: 1.45-4.62) and 

 2.16 (95% CI: 1.23-3.81), respectively. Conclusion: Higher lumbar spine 

 and femoral neck BMDs are associated with an increase in the likelihood 

 of pelvic DIE in women who underwent early BO. This might be expected to 

 the extent that endometriosis is itself associated with enhanced 

 estrogen status, although further studies are needed to confirm such a 

 hypothesis. These findings suggest that BMD measurement could contribute 

 to the hormonal management of surgical menopause in women with DIE.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{ISI:000613753600001,

title = {Role of oculocerebrorenal syndrome of Lowe (OCRL) protein in 

 megakaryocyte maturation, platelet production and functions: a study in 

 patients with Lowe syndrome},

author = {Marion Egot and Dominique Lasne and Sonia Poirault-Chassac and Tristan Mirault and Dominique Pidard and Elise Dreano and Caroline Elie and Sophie Gandrille and Aurore Marchelli and Dominique Baruch and John Rendu and Julien Faure and Claire Flaujac and Marie-Pierre Gratacap and Pierre Sie and Pascale Gaussem and Remi Salomon and Genevieve Baujat and Christilla Bachelot-Loza},

doi = {10.1111/bjh.17346, Early Access Date = FEB 2021},

issn = {0007-1048},

year  = {2021},

date = {2021-03-01},

journal = {BRITISH JOURNAL OF HAEMATOLOGY},

volume = {192},

number = {5},

pages = {909-921},

abstract = {Lowe syndrome (LS) is an oculocerebrorenal syndrome of Lowe (OCRL1) 

 genetic disorder resulting in a defect of the OCRL protein, a 

 phosphatidylinositol-4,5-bisphosphate 5-phosphatase containing various 

 domains including a Rho GTPase-activating protein (RhoGAP) homology 

 domain catalytically inactive. We previously reported surgery-associated 

 bleeding in patients with LS, suggestive of platelet dysfunction, 

 accompanied with a mild thrombocytopenia in several patients. To 

 decipher the role of OCRL in platelet functions and in megakaryocyte 

 (MK) maturation, we conducted a case-control study on 15 patients with 

 LS (NCT01314560). While all had a drastically reduced expression of 

 OCRL, this deficiency did not affect platelet aggregability, but 

 resulted in delayed thrombus formation on collagen under flow 

 conditions, defective platelet spreading on fibrinogen and impaired clot 

 retraction. We evidenced alterations of the myosin light chain 

 phosphorylation (P-MLC), with defective Rac1 activity and, inversely, 

 elevated active RhoA. Altered cytoskeleton dynamics was also observed in 

 cultured patient MKs showing deficient proplatelet extension with 

 increased P-MLC that was confirmed using control MKs transfected with 

 OCRL-specific small interfering(si)RNA (siOCRL). Patients with LS also 

 had an increased proportion of circulating barbell-shaped proplatelets. 

 Our present study establishes that a deficiency of the OCRL protein 

 results in a defective actomyosin cytoskeleton reorganisation in both 

 MKs and platelets, altering both thrombopoiesis and some platelet 

 responses to activation necessary to ensure haemostasis.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{ISI:000633337900001,

title = {4-Hydroxynonenal Contributes to Fibroblast Senescence in Skin Photoaging 

 Evoked by UV-A Radiation},

author = {Audrey Swiader and Caroline Camare and Paul Guerby and Robert Salvayre and Anne Negre-Salvayre},

doi = {10.3390/antiox10030365},

year  = {2021},

date = {2021-03-01},

journal = {ANTIOXIDANTS},

volume = {10},

number = {3},

abstract = {Solar ultraviolet A (UV-A) radiation promotes a huge variety of damages 

 on connective tissues and dermal fibroblasts, including cellular 

 senescence, a major contributor of skin photoaging. The mechanisms of 

 skin photoaging evoked by UV-A partly involve the generation of reactive 

 oxygen species and lipid peroxidation. We previously reported that 

 4-hydroxynonenal (HNE), a lipid peroxidation-derived aldehyde, forms 

 adducts on elastin in the skins of UV-A irradiated hairless mice, 

 possibly contributing to actinic elastosis. In the present study, we 

 investigated whether and how HNE promotes fibroblast senescence in skin 

 photoaging. Dermal fibroblasts of skins from UV-A-exposed hairless mice 

 exhibited an increased number of gamma H2AX foci characteristic of cell 

 senescence, together with an accumulation of HNE adducts partly 

 colocalizing with the cytoskeletal protein vimentin. Murine fibroblasts 

 exposed to UV-A radiation (two cycles of 15 J/cm(2)), or HNE (30 mu M, 4 

 h), exhibited senescence patterns characterized by an increased gamma 

 H2AX foci expression, an accumulation of acetylated proteins, and a 

 decreased expression of the sirtuin SIRT1. HNE adducts were detected on 

 vimentin in cultured fibroblasts irradiated by UV-A or incubated with 

 HNE. The HNE scavenger carnosine prevented both vimentin modification 

 and fibroblast senescence evoked by HNE in vitro and in the skins of 

 UV-A-exposed mice. Altogether, these data emphasize the role of HNE and 

 lipid peroxidation-derived aldehydes in fibroblast senescence, and 

 confirm the protective effect of carnosine in skin photoaging.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}