Ignet

Gene Pair Information

Gene Pair: AGTR1, AGT

Related Sentences

#	PMID	Sentence
1	9176840	Mouse glomerular epithelial cells in culture with features of podocytes in vivo express aminopeptidase A and angiotensinogen but not other components of the renin-angiotensin system.
2	9176840	By indirect immunofluorescence, the cells were positive for cytokeratin, vimentin, desmin, and the ZO-1 protein, a component of the tight junction complex.
3	9176840	The mRNA expression of several components of the renin-angiotensin system was also examined, and some factors indirectly coupled to the renin-angiotensin system component angiotensin II in this podocytic culture by RT-PCR analysis. mRNA Expression for the angiotensin II degrading hydrolase aminopeptidase A and angiotensinogen was found, but this was not found for any other component of this system, such as renin, angiotensin-converting enzyme, or the angiotensin II receptors AT1a, AT1b, and AT2.
4	9176840	In addition, expression of the growth factors transforming growth factor-beta and interleukin-7, and the extracellular matrix components fibronectin, laminin B2, perlecan, and collagen IV alpha 1, was observed.
5	9249605	Immunohistochemical localization of ANG II AT1 receptor in adult rat kidney using a monoclonal antibody.
6	9291188	During glomerular injury, inhibition of the renin-angiotensin system by angiotensin-converting-enzyme inhibitors reduces proteinuria and retards the progression to end-stage renal insufficiency.
7	9291188	The AT1 receptor antagonist losartan inhibited Ang II-mediated [Ca2+]i increase with an IC50 of about 0.3 nmol/liter (N = 35).
8	9291188	The effect of Ang II is mediated via an AT1 receptor.
9	9736279	The Ang subtype 1 (AT1) receptor antagonist losartan inhibited both Ang II-mediated depolarization and [Ca2+]i increase in podocytes (N = 5 to 35).
10	9736279	Our results support the concept that Ang II might influence podocyte function directly via an AT1 receptor.
11	11174028	Renal and vascular injury induced by exogenous angiotensin II is AT1 receptor-dependent.
12	11174028	We also examined the role of the local renin-angiotensin system (RAS) by examining the expression of angiotensin-converting enzyme (ACE) and the effect of treatment with the ACE inhibitor, ramipril.
13	11174028	Renal injury was manifested by proteinuria, glomerular phenotypic changes (mesangial expression of alpha-actin and podocyte expression of desmin), and tubulointerstitial injury with the tubular upregulation of the macrophage-adhesive protein, osteopontin, the interstitial accumulation of macrophages and myofibroblasts, and the deposition of collagen types III and IV.
14	11174028	Ang II infusion decreased AT1 receptor number in the renal interstitium but not in glomeruli.
15	11174028	Ang II infusion was also associated with an increase in ACE protein in both the proximal tubular brush border as well as at interstitial sites of injury, but despite evidence for activation of the local RAS, treatment with ramipril was without effect.
16	11174028	These studies demonstrate that the renal and vascular injury induced by Ang II infusion is mediated by the AT1 receptor despite downregulation of the receptor in the interstitium.