Related Experiment Video

Updated: May 10, 2026

Implementing Patch Clamp and Live Fluorescence Microscopy to Monitor Functional Properties of Freshly Isolated PKD Epithelium
08:46

Implementing Patch Clamp and Live Fluorescence Microscopy to Monitor Functional Properties of Freshly Isolated PKD Epithelium

Published on: September 1, 2015

Effects of caveolin-1 and P-ERK1/2 on Ang II-induced glomerular mesangial cell proliferation

Na Zhang1, Zequan Ji

  • 1Department of Pediatrics, Second Affiliated Hospital of Guangzhou Medical University, No. 195 Dongfeng Xi Road, Guangzhou, China.

Renal Failure
|July 6, 2013
PubMed

Insights

Angiotensin II (Ang II) promotes glomerular mesangial cell proliferation, involving caveolin-1, p-ERK1/2, and TRPC6. Intact caveolae and ERK1/2 activation are crucial for Ang II-induced cell growth.

Area of Science:

  • Cell Biology
  • Physiology
  • Molecular Biology

Background:

  • Glomerular mesangial cells (GMCs) play a key role in kidney function and disease.
  • Angiotensin II (Ang II) is a potent regulator of cardiovascular and renal function, implicated in GMC proliferation.
  • Caveolin-1, p-ERK1/2, and TRPC6 are signaling molecules involved in cellular processes.

Purpose of the Study:

  • To investigate the effects of Ang II on GMC proliferation.
  • To explore the roles of caveolin-1, p-ERK1/2, and TRPC6 in Ang II-induced GMC proliferation.
  • To elucidate the signaling pathways linking these molecules in GMCs.

Main Methods:

  • GMC cultures were treated with Ang II, PD98059 (ERK inhibitor), or MβCD (cholesterol depletor).
  • Cell proliferation was assessed using MTT and trypan blue assays.
  • Expression and distribution of caveolin-1, p-ERK1/2, and TRPC6 were analyzed by immunocytochemistry, real-time PCR, and Western blot.

Main Results:

  • Ang II significantly promoted GMC proliferation.
  • PD98059 and MβCD inhibited Ang II-induced proliferation by 31.06% and 48.96%, respectively.
  • Ang II increased p-ERK1/2 and TRPC6 expression while decreasing caveolin-1 expression. PD98059 and MβCD reversed these changes, with MβCD not affecting caveolin-1 protein levels.

Conclusions:

  • Intact caveolae structure is associated with Ang II-induced GMC proliferation, ERK1/2 activation, and TRPC6 expression.
  • p-ERK1/2 acts as an upstream signaling molecule for TRPC6.
  • p-ERK1/2 and caveolin-1 exhibit reciprocal inhibition, collectively regulating GMC proliferation via TRPC6.

More Related Videos

Glomerular Outgrowth as an Ex Vivo Assay to Analyze Pathways Involved in Parietal Epithelial Cell Activation06:39

Glomerular Outgrowth as an Ex Vivo Assay to Analyze Pathways Involved in Parietal Epithelial Cell Activation

Published on: August 19, 2020

Single-channel Analysis and Calcium Imaging in the Podocytes of the Freshly Isolated Glomeruli12:19

Single-channel Analysis and Calcium Imaging in the Podocytes of the Freshly Isolated Glomeruli

Published on: June 27, 2015

Related Concept Videos

cAMP-dependent Protein Kinase Pathways01:25

cAMP-dependent Protein Kinase Pathways

Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
Two...
Antihypertensive Drugs: Angiotensin II Receptor Blockers01:30

Antihypertensive Drugs: Angiotensin II Receptor Blockers

In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
Endocrine Signaling01:45

Endocrine Signaling

Endocrine cells produce hormones to communicate with remote target cells found in other organs. The hormone reaches these distant areas using the circulatory system. This exposes the whole organism to the hormone but only those cells expressing hormone receptors or target cells are affected. Thus, endocrine signaling induces slow responses from its target cells but these effects also last longer.
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...