[Vasoactive peptides and the development of renal sclerosis: contribution of transgenes]

Détails

ID Serval
serval:BIB_CD9068367D54
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
[Vasoactive peptides and the development of renal sclerosis: contribution of transgenes]
Périodique
J Soc Biol
Auteur⸱e⸱s
Dussaule J. C., Boffa J. J., Tharaux P. L., Flamant M., Fakhouri F., Chatziantoniou C.
ISSN
1295-0661 (Print)
ISSN-L
1295-0661
Statut éditorial
Publié
Date de publication
2002
Volume
196
Numéro
4
Pages
275-80
Langue
français
Notes
Dussaule, Jean-Claude
Boffa, Jean-Jacques
Tharaux, Pierre-Louis
Flamant, Martin
Fakhouri, Fadi
Chatziantoniou, Christos
fre
English Abstract
Review
France
J Soc Biol. 2002;196(4):275-80.
Résumé
Vasoactive peptides are implied in the development of renal sclerosis as evidenced by the efficiency of their antagonists in preventing glomerulosclerosis of experimental and human nephropathies. Genetically engineered models provide a new approach to investigate the mechanisms of the renal profibrotic actions of angiotensin II and endothelin. Overexpression of the human angiotensinogen and renin genes in rats induces renal sclerosis independently of changes in systemic hemodynamics. The same results are observed when the endothelin-1 gene is overexpressed in mice. Transgenic mice harboring the luciferase gene under the control of the collagen I-alpha 2 chain promoter (procol alpha 2[1]) and made hypertensive by induction of nitric oxide (NO) deficiency were used to study the renal profibrotic actions of vasoactive peptides. In this strain of mice, luciferase activity is an early index of renal fibrosis. Luciferase activity was increased in preglomerular arterioles and glomeruli when mice were deficient in NO. The pharmacological blockade of angiotensin II and endothelin prevented the development of renal sclerosis without modifying blood pressure. Moreover, when the endothelin receptor antagonist was administered after the development of renal fibrosis, preformed glomerulosclerosis partially regressed. Acute administration of vasoactive peptides and TGF-beta in transgenic procol alpha 2[1] mice showed that the angiotensin II activation of collagen I gene requires participation and/or cooperation of endothelin and TGF-beta. Recent data suggest that the profibrotic actions of vasoactive peptides also need the activation of EGF receptor, ERK and rho kinase pathways in renal and vascular cells.
Mots-clé
Angiotensin II/antagonists & inhibitors, Animals, Collagen Type II/*genetics, Endothelin Receptor Antagonists, Endothelin-1/antagonists & inhibitors/*physiology, Enzyme Inhibitors/pharmacology/therapeutic use, Fibrosis, Genes, Reporter, Glomerulosclerosis, Focal Segmental/prevention & control, Humans, Kidney/*pathology, Luciferases/genetics, MAP Kinase Signaling System/physiology, Mice, NG-Nitroarginine Methyl Ester/pharmacology/therapeutic use, Nitric Oxide/deficiency/physiology, Nitric Oxide Synthase/antagonists & inhibitors, Renin-Angiotensin System/*physiology, Sclerosis, Transforming Growth Factor beta/physiology/toxicity, *Transgenes
Pubmed
Création de la notice
01/03/2022 10:18
Dernière modification de la notice
02/03/2022 6:36
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