scholarly journals Pyk2 mediates endothelin-1 signaling via p130Cas/BCAR3 cascade and regulates human glomerular mesangial cell adhesion and spreading

2009 ◽  
Vol 219 (1) ◽  
pp. 45-56 ◽  
Author(s):  
Victoriya A. Rufanova ◽  
Anna Alexanian ◽  
Tetsuro Wakatsuki ◽  
Adam Lerner ◽  
Andrey Sorokin
Keyword(s):  
Cell Adhesion ◽  
Mesangial Cell ◽  
Glomerular Mesangial Cell ◽  
Endothelin 1

Endothelin-1 activates mesangial cell ERK1/2 via EGF-receptor transactivation and caveolin-1 interaction

2003 ◽  
Vol 284 (2) ◽  
pp. F303-F312 ◽  
Author(s):  
Hong Hua ◽  
Snezana Munk ◽  
Catharine I. Whiteside
Keyword(s):  
Matrix Protein ◽  
Egf Receptor ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Extracellular Matrix Protein ◽  
Glomerular Mesangial Cell ◽  
Caveolin 1 ◽  
Endothelin 1 ◽  
Protein Transcription ◽  
Dependent Pathway

Endothelin-1 (ET-1) stimulates glomerular mesangial cell proliferation and extracellular matrix protein transcription through an ERK1/2-dependent pathway. In this study, we determined whether ET-1 activation of glomerular mesangial cell ERK1/2 is mediated through EGF receptor (EGF-R) transactivation and whether intact caveolae are required. We showed that ET-1 stimulated tyrosine phosphorylation of the EGF-R in primary cultured, growth-arrested rat mesangial cells. In response to ET-1, ERK1/2 phosphorylation was increased by 27 ± 1-fold and attenuated by AG-1478, a specific EGF-R inhibitor, to 9 ± 1-fold. Moreover, filipin III and β-cyclodextrin, two cholesterol-depleting drugs known to disrupt caveolae, significantly reduced ET-1-induced phosphorylation of ERK1/2. In addition, preincubation of mesangial cells with a myristoylated peptide that binds to the caveolin-1 scaffolding domain diminished ET-1 activation of ERK1/2. ET-1 caused interaction of caveolin-1 with phosphorylated ERK1/2 identified by coimmunoprecipitation. Activation of ERK1/2 and its interaction with caveolin-1 were reduced by AG-1478, β-cyclodextrin, or inhibition of PKC. Phosphorylated ERK1/2 localized at focal adhesion complexes along with phospho-caveolin-1, suggesting specific sites of compartmentalization of these signaling molecules. Hence, ET-1 activates mesangial cell ERK1/2 predominantly through a pathway involving EGF-R transactivation, leading to a mechanism involving attachment to caveolin-1, presumably in caveolae.

scholarly journals Doxorubicin-Induced Fetal Mesangial Cell Death Occurs Independently of TRPC6 Channel Upregulation but Involves Mitochondrial Generation of Reactive Oxygen Species

2021 ◽  
Vol 22 (14) ◽  
pp. 7589
Author(s):  
Anberitha T. Matthews ◽  
Hitesh Soni ◽  
Katherine E. Robinson-Freeman ◽  
Theresa A. John ◽  
Randal K. Buddington ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Transient Receptor Potential ◽  
Mesangial Cell ◽  
Reactive Oxygen ◽  
Receptor Potential ◽  
Oxygen Species ◽  
Glomerular Mesangial Cell ◽  
Trpc6 Channel ◽  
Fetal Pig

Doxorubicin (DOX), a category D pregnancy drug, is a chemotherapeutic agent that has been shown in animal studies to induce fetal toxicity, including renal abnormalities. Upregulation of the transient receptor potential cation (TRPC) 6 channel is involved in DOX-induced podocyte apoptosis. We have previously reported that TRPC6-mediated Ca2+ signaling promotes neonatal glomerular mesangial cell (GMC) death. However, it is unknown whether DOX alters mesangial TRPC expression or viability in the fetus. In this study, cell growth was tracked in control and DOX-treated primary GMCs derived from fetal pigs. Live-cell imaging demonstrated that exposure to DOX inhibited the proliferation of fetal pig GMCs and induced cell death. DOX did not alter the TRPC3 expression levels. By contrast, TRPC6 protein expression in the cells was markedly reduced by DOX. DOX treatment also attenuated the TRPC6-mediated intracellular Ca2+ elevation. DOX stimulated mitochondrial reactive oxygen species (mtROS) generation and mitophagy by the GMCs. The DOX-induced mtROS generation and apoptosis were reversed by the mitochondria-targeted antioxidant mitoquinone. These data suggest that DOX-induced fetal pig GMC apoptosis is independent of TRPC6 channel upregulation but requires mtROS production. The mtROS-dependent GMC death may contribute to DOX-induced fetal nephrotoxicity when administered prenatally.

High glucose-stimulated enhancer of zeste homolog-2 (EZH2) forces suppression of deptor to cause glomerular mesangial cell pathology

2021 ◽  
pp. 110072
Author(s):  
Falguni Das ◽  
Amit Bera ◽  
Nandini Ghosh-Choudhury ◽  
Kavitha Sataranatarajan ◽  
Amrita Kamat ◽  
...  
Keyword(s):  
High Glucose ◽  
Mesangial Cell ◽  
Glomerular Mesangial Cell ◽  
Enhancer Of Zeste

scholarly journals Sublytic C5b-9 Induces Glomerular Mesangial Cell Apoptosis through the Cascade Pathway of MEKK2–p38 MAPK–IRF-1–TRADD–Caspase 8 in Rat Thy-1 Nephritis

2016 ◽  
Vol 198 (3) ◽  
pp. 1104-1118 ◽  
Author(s):  
Ganqian Zhu ◽  
Wen Qiu ◽  
Yongting Li ◽  
Chenhui Zhao ◽  
Fengxia He ◽  
...  
Keyword(s):  
P38 Mapk ◽  
Cell Apoptosis ◽  
Mesangial Cell ◽  
Caspase 8 ◽  
Glomerular Mesangial Cell

Circulating asymmetric dimethylarginine, endothelin-1 and cell adhesion molecules in women with gestational diabetes

2009 ◽  
Vol 46 (4) ◽  
pp. 303-308 ◽  
Author(s):  
Beata Telejko ◽  
Anna Zonenberg ◽  
Mariusz Kuzmicki ◽  
Anna Modzelewska ◽  
Karolina Niedziolko-Bagniuk ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Gestational Diabetes ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Asymmetric Dimethylarginine ◽  
Endothelin 1
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