scholarly journals A Novel Phosphoinositide 3-Kinase-dependent Pathway for Angiotensin II/AT-1 Receptor-mediated Induction of Collagen Synthesis in MES-13 Mesangial Cells

2007 ◽  
Vol 282 (26) ◽  
pp. 18819-18830 ◽  
Author(s):  
Naohiro Yano ◽  
Daisuke Suzuki ◽  
Masayuki Endoh ◽  
Ting C. Zhao ◽  
James F. Padbury ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Collagen Synthesis ◽  
Mesangial Cells ◽  
Phosphoinositide 3 Kinase ◽  
Dependent Pathway

Molecular mechanism of ADP-ribosyl cyclase activation in angiotensin II signaling in murine mesangial cells

2008 ◽  
Vol 294 (4) ◽  
pp. F982-F989 ◽  
Author(s):  
Seon-Young Kim ◽  
Rukhsana Gul ◽  
So-Young Rah ◽  
Suhn Hee Kim ◽  
Sung Kwang Park ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Protein Tyrosine Kinase ◽  
Nuclear Translocation ◽  
Mesangial Cells ◽  
Dependent Manner ◽  
Ang Ii ◽  
Akt Phosphorylation ◽  
Cyclase Activation ◽  
Adp Ribosyl Cyclase ◽  
Phosphoinositide 3 Kinase

ADP-ribosyl cyclase (ADPR-cyclase) produces a Ca2+-mobilizing second messenger cyclic ADP-ribose (cADPR) from NAD+. In this study, we investigated the molecular basis of ADPR-cyclase activation and the following cellular events in angiotensin II (ANG II) signaling in mouse mesangial cells (MMCs). Treatment of MMCs with ANG II induced an increase in intracellular Ca2+ concentrations through a transient Ca2+ release via an inositol 1,4,5-trisphosphate receptor and a sustained Ca2+ influx via L-type Ca2+ channels. The sustained Ca2+ signal, but not the transient Ca2+ signal, was blocked by a cADPR antagonistic analog, 8-bromo-cADPR (8-Br-cADPR), and an ADPR-cyclase inhibitor, 4,4′-dihydroxyazobenzene (DHAB). In support of the results, ANG II stimulated cADPR production in a time-dependent manner, and DHAB inhibited ANG II-induced cADPR production. Application of pharmacological inhibitors revealed that activation of ADPR-cyclase by ANG II involved ANG II type 1 receptor, phosphoinositide 3-kinase, protein tyrosine kinase, and phospolipase C-γ1. Moreover, DHAB as well as 8-Br-cADPR abrogated ANG II-mediated Akt phosphorylation, nuclear translocation of nuclear factor of activated T cell, and uptake of [3H]thymidine and [3H]leucine in MMCs. These results demonstrate that ADPR-cyclase in MMCs plays a pivotal role in ANG II signaling for cell proliferation and protein synthesis.

Angiotensin II activates Akt/protein kinase B by an arachidonic acid/redox‐dependent pathway and independent of phosphoinositide 3‐kinase

2001 ◽  
Vol 15 (11) ◽  
pp. 1909-1920 ◽  
Author(s):  
Yves Gorin ◽  
Nam‐Ho Kim ◽  
Denis Feliers ◽  
Basant Bhandari ◽  
Goutam Ghosh Choudhury ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Angiotensin Ii ◽  
Protein Kinase ◽  
Protein Kinase B ◽  
Phosphoinositide 3 Kinase ◽  
Dependent Pathway

Luteolin Antagonizes Angiotensin II-Dependent Proliferation and Collagen Synthesis of Cultured rat Cardiac Fibroblasts

2015 ◽  
Vol 16 (5) ◽  
pp. 430-439 ◽  
Author(s):  
Tingting Wang ◽  
Defeng Pan ◽  
Yingying Zhang ◽  
Dongye Li ◽  
Yanbin Zhang ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Collagen Synthesis ◽  
Cardiac Fibroblasts

scholarly journals (Pro)renin receptor: another member of the system controlled by angiotensin II?

2011 ◽  
Vol 13 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Luciana G Pereira ◽  
Carine P Arnoni ◽  
Edgar Maquigussa ◽  
Priscila C Cristovam ◽  
Juliana Dreyfuss ◽  
...  
Keyword(s):  
Gene Expression ◽  
Angiotensin Ii ◽  
Mesangial Cells ◽  
At1 Receptor ◽  
Receptor Internalization ◽  
Prorenin Receptor ◽  
Receptor Blockers ◽  
And Function ◽  
At1 Receptor Blockers

The prorenin receptor [(P)RR] is upregulated in the diabetic kidney and has been implicated in the high glucose (HG)-induced overproduction of profibrotic molecules by mesangial cells (MCs), which is mediated by ERK1/2 phosphorylation. The regulation of (P)RR gene transcription and the mechanisms by which HG increases (P)RR gene expression are not fully understood. Because intracellular levels of angiotensin II (AngII) are increased in MCs stimulated with HG, we used this in vitro system to evaluate the possible role of AngII in (P)RR gene expression and function by comparing the effects of AT1 receptor blockers (losartan or candesartan) and (P)RR mRNA silencing (siRNA) in human MCs (HMCs) stimulated with HG. HG induced an increase in (P)RR and fibronectin expression and in ERK1/2 phosphorylation. These effects were completely reversed by (P)RR siRNA and losartan but not by candesartan (an angiotensin receptor blocker that, in contrast to losartan, blocks AT1 receptor internalization). These results suggest that (P)RR gene activity may be controlled by intracellular AngII and that HG-induced ERK1/2 phosphorylation and fibronectin overproduction are primarily induced by (P)RR activation. This relationship between AngII and (P)RR may constitute an additional pathway of MC dysfunction in response to HG stimulation.

scholarly journals Aldosterone does not require angiotensin II to activate NCC through a WNK4–SPAK–dependent pathway

2012 ◽  
Vol 463 (6) ◽  
pp. 853-863 ◽  
Author(s):  
Nils van der Lubbe ◽  
Christina H. Lim ◽  
Marcel E. Meima ◽  
Richard van Veghel ◽  
Lena Lindtoft Rosenbaek ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Dependent Pathway

P-450 Metabolites of Arachidonic Acid in the Control of Cardiovascular Function

2002 ◽  
Vol 82 (1) ◽  
pp. 131-185 ◽  
Author(s):  
Richard J. Roman
Keyword(s):  
Arachidonic Acid ◽  
Angiotensin Ii ◽  
Vascular Tone ◽  
Mesangial Cells ◽  
Cardiovascular Function ◽  
Tubuloglomerular Feedback ◽  
Peripheral Vasculature ◽  
Therapeutic Benefits

Recent studies have indicated that arachidonic acid is primarily metabolized by cytochrome P-450 (CYP) enzymes in the brain, lung, kidney, and peripheral vasculature to 20-hydroxyeicosatetraenoic acid (20-HETE) and epoxyeicosatrienoic acids (EETs) and that these compounds play critical roles in the regulation of renal, pulmonary, and cardiac function and vascular tone. EETs are endothelium-derived vasodilators that hyperpolarize vascular smooth muscle (VSM) cells by activating K+channels. 20-HETE is a vasoconstrictor produced in VSM cells that reduces the open-state probability of Ca2+-activated K+channels. Inhibitors of the formation of 20-HETE block the myogenic response of renal, cerebral, and skeletal muscle arterioles in vitro and autoregulation of renal and cerebral blood flow in vivo. They also block tubuloglomerular feedback responses in vivo and the vasoconstrictor response to elevations in tissue Po2both in vivo and in vitro. The formation of 20-HETE in VSM is stimulated by angiotensin II and endothelin and is inhibited by nitric oxide (NO) and carbon monoxide (CO). Blockade of the formation of 20-HETE attenuates the vascular responses to angiotensin II, endothelin, norepinephrine, NO, and CO. In the kidney, EETs and 20-HETE are produced in the proximal tubule and the thick ascending loop of Henle. They regulate Na+transport in these nephron segments. 20-HETE also contributes to the mitogenic effects of a variety of growth factors in VSM, renal epithelial, and mesangial cells. The production of EETs and 20-HETE is altered in experimental and genetic models of hypertension, diabetes, uremia, toxemia of pregnancy, and hepatorenal syndrome. Given the importance of this pathway in the control of cardiovascular function, it is likely that CYP metabolites of arachidonic acid contribute to the changes in renal function and vascular tone associated with some of these conditions and that drugs that modify the formation and/or actions of EETs and 20-HETE may have therapeutic benefits.

Angiotensin II stimulation of phospholipase D in rat renal mesangial cells is mediated by the AT1 receptor subtype

1992 ◽  
Vol 225 (1) ◽  
pp. 57-62 ◽  
Author(s):  
Josef Pfeilschifter ◽  
Andrea Huwiler ◽  
Claire Merriweather ◽  
Vreny A. Briner
Keyword(s):  
Angiotensin Ii ◽  
Phospholipase D ◽  
Mesangial Cells ◽  
At1 Receptor ◽  
Receptor Subtype ◽  
Stimulation Of

scholarly journals Overexpression of aminopeptidase A abolishes the growth promoting effects of angiotensin II in cultured mouse mesangial cells

1997 ◽  
Vol 52 (5) ◽  
pp. 1250-1260 ◽  
Author(s):  
Gunter Wolf ◽  
Karel J.M. Assmann ◽  
Rolf A.K. Stahl
Keyword(s):  
Angiotensin Ii ◽  
Mesangial Cells ◽  
Aminopeptidase A ◽  
Growth Promoting
Sign in / Sign up

Export Citation Format

Share Document