Academic literature on the topic 'Cellules épithéliales pariétales glomérulaires'
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Journal articles on the topic "Cellules épithéliales pariétales glomérulaires":
Tharaux, P.-L., H. Lazareth, F. Garo, O. Lenoir, S. Boulkroun, A. Rocha, I. Giscos-Douriez, L. Guyonnet, C. Hénique-Gréciet, and M. C. Zennaro. "Le récepteur minéralocorticoïde participe à l’activation des cellules épithéliales pariétales et à la destruction glomérulaire au cours des glomérulonéphrites extracapillaires." Néphrologie & Thérapeutique 17, no. 5 (September 2021): 286. http://dx.doi.org/10.1016/j.nephro.2021.07.307.
Deschênes, G. "Nouvelle culture de cellules épithéliales glomérulaires: des podocytes plus accessibles." Archives de Pédiatrie 5, no. 4 (April 1998): 431. http://dx.doi.org/10.1016/s0929-693x(98)80251-0.
Birmelé, B., A. de Agostini, and E. Girardin. "Augmentation de la synthèse d'héparans sulfatespar des cellules épithéliales glomérulaires en présence de ciclosporine A." Archives de Pédiatrie 5, no. 7 (July 1998): 817–18. http://dx.doi.org/10.1016/s0929-693x(98)80083-3.
Birmelé, B., A. de Agostini, H. Nivet, and E. Girardin. "Le surnageant de cellules mononucléées sanguinesd'enfants ayant un syndrome néphrotique idiopathique diminue la synthèse de glycosaminoglycans par des cellules épithéliales glomérulaires." Archives de Pédiatrie 5, no. 7 (July 1998): 820. http://dx.doi.org/10.1016/s0929-693x(98)80091-2.
Lazareth, Hélène, Olivia Lenoir, Carole Hénique, Cédric Bouzigues, Claude Boucheix, and Pierre-Louis Tharaux. "Rôle pathogénique de l’expression anormale de la tétraspanine CD9 par les cellules épithéliales pariétales dans les glomérulopathies extracapillaires." médecine/sciences 36, no. 10 (October 2020): 852–55. http://dx.doi.org/10.1051/medsci/2020154.
Dissertations / Theses on the topic "Cellules épithéliales pariétales glomérulaires":
Lazareth, Hélène. "Implication des facteurs locaux (CD9, HB-EGF, PDGF-BB) au sein des cellules épithéliales pariétales glomérulaires au cours de la glomérulonéphrite extracapillaire et de la hyalinose segmentaire et focale : Études in vitro et in vivo." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLX100.
The mechanisms driving the development of extracapillary lesions in focal segmental glomerulosclerosis (FSGS) and crescentic glomerulonephritis (CGN) remain poorly understood. A key question is how parietal epithelial cells (PEC) invade glomerular capillaries, thereby promoting injury and kidney failure. Here we show that expression of the tetraspanin CD9 increases markedly in PEC in mouse models of CGN and FSGS, and in kidneys from individuals diagnosed with these diseases. Cd9 gene targeting in PEC prevents glomerular damage in CGN and FSGS mouse models.Mechanistically, CD9 deficiency prevents the oriented migration of PEC into the glomerular tuft and their acquisition of CD44 and β1 integrin expression. These findings highlight a critical role for de novo expression of CD9 as a common pathogenic switch driving the PEC phenotype in CGN and FSGS, while offering a potential therapeutic avenue to treat these conditions
Sakhi, Hamza. "Rôle de la Heat Shock Protein 27 au cours des glomérulonéphrites extracapillaires." Electronic Thesis or Diss., Paris 12, 2022. http://www.theses.fr/2022PA120079.
Crescentic glomerulonephritis (CG) is an aggressive glomerular disease associated with severe kidney outcome. While the main treatment consisting in immunosuppressive therapy is associated with major side-effects in frail patients, to date no drugs targeting the mechanisms directly involved in epithelial crescent formation are available. Indeed, recent studies identified parietal epithelial cells (PEC) as a major component of crescent formation.In this study, we showed that Heat shock protein 27 (HSP27/HSPB1), a stress-inducible protein involved in cancer cell proliferation and migration, is overexpressed in activated PEC of crescentic lesions both in in nephrotoxic nephritis mouse model and humans. Moreover, circulating HSP27 is associated with disease activity in humans with biopsy-proven CG. HSP27 inhibition through OGX-427, an antisens oligonucloeotide targeting HSPB1 mRNA, and Ivermectin (which inhibits HSP27 dimerization) reduce crescent formation in experimental CG model and PEC activation and migration in vitro. However, in NTN murine model, HSP27 inhibition with OGX-427 but no with Ivermectin was associated with a worsening of endothelial injury.Overall, these results identify HSP27 as a new pathogenic protein during crescent formation and a biomarker of disease activity in human CG. Optimal therapeutic option inhibiting HSP27 with the aim to reduce molecular processes leading to proliferative glomerulonephritis remains to be determined
Yerouchalmi-Desmottes, Rose-Marie. "Production par les cellules glomérulaires humaines et de rat d'une cytokine à activité interleukine-1." Paris 11, 1987. http://www.theses.fr/1987PA112320.