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1دورية أكاديمية
المؤلفون: Julie Warin, Nicolas Vedrenne, Vivian Tam, Mengxia Zhu, Danqing Yin, Xinyi Lin, Bluwen Guidoux-D’halluin, Antoine Humeau, Luce Roseiro, Lily Paillat, Claire Chédeville, Caroline Chariau, Frank Riemers, Markus Templin, Jérôme Guicheux, Marianna A. Tryfonidou, Joshua W.K. Ho, Laurent David, Danny Chan, Anne Camus
المصدر: iScience, Vol 27, Iss 2, Pp 109018- (2024)
مصطلحات موضوعية: Biological sciences, Biology of human development, Developmental biology, Natural sciences, Omics, Transcriptomics, Science
الوصف: Summary: Understanding the emergence of human notochordal cells (NC) is essential for the development of regenerative approaches. We present a comprehensive investigation into the specification and generation of bona fide NC using a straightforward pluripotent stem cell (PSC)-based system benchmarked with human fetal notochord. By integrating in vitro and in vivo transcriptomic data at single-cell resolution, we establish an extended molecular signature and overcome the limitations associated with studying human notochordal lineage at early developmental stages. We show that TGF-β inhibition enhances the yield and homogeneity of notochordal lineage commitment in vitro. Furthermore, this study characterizes regulators of cell-fate decision and matrisome enriched in the notochordal niche. Importantly, we identify specific cell-surface markers opening avenues for differentiation refinement, NC purification, and functional studies. Altogether, this study provides a human notochord transcriptomic reference that will serve as a resource for notochord identification in human systems, diseased-tissues modeling, and facilitating future biomedical research.
وصف الملف: electronic resource
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2دورية أكاديمية
المؤلفون: Rebecca J. Williams, Lisanne T. Laagland, Frances C. Bach, Lizzy Ward, Wilson Chan, Vivian Tam, Adel Medzikovic, Shaghayegh Basatvat, Lily Paillat, Nicolas Vedrenne, Joseph W. Snuggs, Deepani W. Poramba‐Liyanage, Judith A. Hoyland, Danny Chan, Anne Camus, Stephen M. Richardson, Marianna A. Tryfonidou, Christine L. Le Maitre
المصدر: JOR Spine, Vol 6, Iss 3, Pp n/a-n/a (2023)
مصطلحات موضوعية: culture systems, development, intervertebral disc, notochordal cells, nucleus pulposus, tissue‐specific progenitor cells, Orthopedic surgery, RD701-811
الوصف: Abstract Background Lineage‐tracing experiments have established that the central region of the mature intervertebral disc, the nucleus pulposus (NP), develops from the embryonic structure called “the notochord”. However, changes in the cells derived from the notochord which form the NP (i.e., notochordal cells [NCs]), in terms of their phenotype and functional identity from early developmental stages to skeletal maturation are less understood. These key issues require further investigation to better comprehend the role of NCs in homeostasis and degeneration as well as their potential for regeneration. Progress in utilizing NCs is currently hampered due to poor consistency and lack of consensus methodology for in vitro NC extraction, manipulation, and characterization. Methods Here, an international group has come together to provide key recommendations and methodologies for NC isolation within key species, numeration, in vitro manipulation and culture, and characterization. Results Recommeded protocols are provided for isolation and culture of NCs. Experimental testing provided recommended methodology for numeration of NCs. The issues of cryopreservation are demonstrated, and a pannel of immunohistochemical markers are provided to inform NC characterization. Conclusions Together we hope this article provides a road map for in vitro studies of NCs to support advances in research into NC physiology and their potential in regenerative therapies.
وصف الملف: electronic resource
Relation: https://doaj.org/toc/2572-1143
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المؤلفون: Lily Paillat, Laurent Loufrani, Abdallah Dib, Tamas Aranyi, Ábel Fóthi, Françoise Schmitt, Abigaëlle Guillot, Céline Fassot, Cyrielle Payen, Daniel Henrion, Mathilde Munier, Jennifer Bourreau
المصدر: International Journal of Obesity. 45:1074-1085
مصطلحات موضوعية: Fetus, medicine.medical_specialty, Nutrition and Dietetics, Offspring, business.industry, Endocrinology, Diabetes and Metabolism, Insulin, medicine.medical_treatment, Medicine (miscellaneous), Adipose tissue, 030209 endocrinology & metabolism, Vasodilation, 03 medical and health sciences, 0302 clinical medicine, Endocrinology, medicine.anatomical_structure, In utero, Internal medicine, medicine, 030212 general & internal medicine, Epigenetics, business, Mesenteric arteries
الوصف: Background/objectives Maternal obesity impacts vascular functions linked to metabolic disorders in offspring, leading to cardiovascular diseases during adulthood. Even if the relation between prenatal conditioning of cardiovascular diseases by maternal obesity and vascular function begins to be documented, little is known about resistance arteries. They are of particular interest because of their specific role in the regulation of local blood flow. Then our study aims to determine if maternal obesity can directly program fetal vascular dysfunction of resistance arteries, independently of metabolic disorders. Methods With a model of rats exposed in utero to mild maternal diet-induced obesity (OMO), we investigated third-order mesenteric arteries of 4-month old rats in absence of metabolic disorders. The methylation profile of these vessels was determined by reduced representation bisulfite sequencing (RRBS). Vascular structure and reactivity were investigated using histomorphometry analysis and wire-myography. The metabolic function was evaluated by insulin and glucose tolerance tests, plasma lipid profile, and adipose tissue analysis. Results At 4 months of age, small mesenteric arteries of OMO presented specific epigenetic modulations of matrix metalloproteinases (MMPs), collagens, and potassium channels genes in association with an outward remodeling and perturbations in the endothelium-dependent vasodilation pathways (greater contribution of EDHFs pathway in OMO males compared to control rats, and greater implication of PGI2 in OMO females compared to control rats). These vascular modifications were detected in absence of metabolic disorders. Conclusions Our study reports a specific methylation profile of resistance arteries associated with vascular remodeling and vasodilation balance perturbations in offspring exposed in utero to maternal obesity, in absence of metabolic dysfunctions.
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المؤلفون: Cyrielle Payen, Abigaëlle Guillot, Lily Paillat, Abel Fothi, Abdallah Dib, Jennifer Bourreau, Françoise Schmitt, Laurent Loufrani, Tamas Aranyi, Daniel Henrion, Mathilde Munier, Céline Fassot
المساهمون: Physiopathologie Cardiovasculaire et Mitochondriale (MITOVASC), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université d'Angers (UA), Institute of Enzymology [Budapest], Research Centre for Natural Sciences, Hungarian Academy of Sciences (MTA)-Hungarian Academy of Sciences (MTA), Hémodynamique, Interaction Fibrose et Invasivité tumorales Hépatiques (HIFIH), Université d'Angers (UA), Centre Hospitalier Universitaire d'Angers (CHU Angers), PRES Université Nantes Angers Le Mans (UNAM), Semmelweis University [Budapest], Cardiovascular Functions In Vitro (CARFI), Reference Center for rare Disease of Thyroid and Hormone Receptors, PRES Université Nantes Angers Le Mans (UNAM)-PRES Université Nantes Angers Le Mans (UNAM), Fondation de France, grant N° 00075806 'Influence of maternal obesity on fetal programming of cardiovascular abnormalities'
المصدر: HAL
International Journal of Obesity
International Journal of Obesity, Nature Publishing Group, 2021مصطلحات موضوعية: Male, Potassium Channels, DNA Methylation, Diet, High-Fat, Matrix Metalloproteinases, vascular function, Epigenesis, Genetic, Rats, maternal obesity, Obesity, Maternal, Rats, Sprague-Dawley, fetal programming, Sex Factors, Pregnancy, sexual dimorphism, Prenatal Exposure Delayed Effects, Animals, Female, Vascular Resistance, Collagen, Endothelium, Vascular, [SDV.AEN]Life Sciences [q-bio]/Food and Nutrition
الوصف: International audience; Backgroung/ Objectives: maternal obesity impacts vascular functions linked to metabolic disorders in offspring, leading to cardiovascular diseases during adulthood. Even if the relation between prenatal conditioning of cardiovascular diseases by maternal obesity and the vascular function begins to be documented, little is known about resistance arteries. They are of particular interest because of their specific role in the regulation of local blood flow. Then our study aims to determine if maternal obesity can directly program fetal vascular dysfunction of resistance arteries, independently of metabolic disorders.Methods: with a model of rats exposed in utero to mild maternal diet-induced obesity (OMO), we investigated third-order mesenteric arteries of 4-month old rats in absence of metabolic disorders. The methylation profile of these vessels was determined by Reduced Representation Bisulfite Sequencing (RRBS). Vascular structure and reactivity were investigated using histomorphometry analysis and wire-myography. Metabolic function was evaluated by insulin and glucose tolerance tests, plasma lipid profile and adipose tissue analysis.Results: at 4 months of age, small mesenteric arteries of OMO presented specific epigenetic modulations of matrix metalloproteinases (MMPs), collagens, and potassium channels genes in association with an outward remodeling and perturbations in the endothelium-dependent vasodilation pathways (greater contribution of EDHFs pathway in OMO males compared to control rats, and greater implication of PGI2 in OMO females compared to control rats). These vascular modifications were detected in absence of metabolic disorders.Conclusion: our study reports a specific methylation profile of resistance arteries associated to vascular remodeling and vasodilation balance perturbations in offspring exposed in utero to maternal obesity, in absence of metabolic dysfunctions.
URL الوصول: https://explore.openaire.eu/search/publication?articleId=pmid_dedup__::ee9f80f51da4f1d9a571c5bef0051942
https://hal.archives-ouvertes.fr/hal-03164923