Endothelin signaling via guanine exchange factor C3G in renal glomerular mesangial cellsThis article is one of a selection of papers published in the two-part special issue entitled 20 Years of Endothelin Research.

Rufanova, Victoriya A.; Alexanian, Anna; Ostendorf, Tammo; Bokemeyer, Dirk; Prosser, Simon; Miller, Bradley; Sorokin, Andrey

doi:10.1139/y10-056

Cited by 4 publications

(2 citation statements)

References 30 publications

(49 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…110 Expression of C3G caused enhanced and prolonged Rap1 activation in response to ET-1 in rat GMC 110 but not in immortalized human GMC. 107 In primary GMC of rat origin, C3G overexpression led to significant changes in cell spreading and migration patterns in response to ET-1 stimulation and also increased stress fiber formation, phenomena which were mimicked by Rap1A overexpression.…”

Section: Glomerular Activities Of Endothelin In Health and Diseasementioning

confidence: 96%

See 1 more Smart Citation

Endothelin and the Glomerulus in Chronic Kidney Disease

Barton

Sorokin

2015

Seminars in Nephrology

Self Cite

View full text Add to dashboard Cite

Summary Endothelin-1 (ET-1) is a 21-amino acid peptide with mitogenic and powerful vasoconstricting properties. Under healthy conditions, ET-1 is constitutively expressed in all cells of the glomerulus and participates in homeostasis of glomerular structure and filtration function. Under disease conditions, increases in ET-1 are critically involved in initiating and maintaining glomerular inflammation, glomerular basement membrane hypertrophy, and injury of podocytes (visceral epithelial cells), thereby promoting proteinuria and glomerulosclerosis. Here, we review the role of ET-1 in the function of glomerular endothelial cells, visceral (podocytes) and parietal epithelial cells, mesangial cells, the glomerular basement membrane, stromal cells, inflammatory cells, and mesenchymal stem cells. We also discuss molecular mechanisms by which ET-1 – predominantly through activation of the ETA receptor - contributes to injury to glomerular cells and review preclinical and clinical evidence supporting its pathogenic role in glomerular injury in chronic renal disease. Finally, the therapeutic rationale for endothelin antagonists as a new class of antiproteinuric drugs is discussed.

show abstract

Section: Glomerular Activities Of Endothelin In Health and Diseasementioning

confidence: 96%

“…107 Thus, an increase in the C3G protein level contributes to the resolution stage of mesangioproliferative glomerulonephritis by modulating cellular motility and actin dynamics. 110 …”

Section: Glomerular Activities Of Endothelin In Health and Diseasementioning

confidence: 99%

Endothelin and the Glomerulus in Chronic Kidney Disease

Barton

Sorokin

2015

Seminars in Nephrology

Self Cite

View full text Add to dashboard Cite

show abstract

Substance-specific importance of EGFR for vascular smooth muscle cells motility in primary culture

Schreier

Schwerdt

Heise

et al. 2016

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

View full text Add to dashboard Cite

Besides their importance for the vascular tone, vascular smooth muscle cells (VSMC) also contribute to pathophysiological vessel alterations. Various G-protein coupled receptor ligands involved in vascular dysfunction and remodeling can transactivate the epidermal growth factor receptor (EGFR) of VSMC, yet the importance of EGFR transactivation for the VSMC phenotype is incompletely understood. The aims of this study were (i) to characterize further the importance of the VSMC-EGFR for proliferation, migration and marker gene expression for inflammation, fibrosis and reactive oxygen species (ROS) homeostasis and (ii) to test the hypothesis that vasoactive substances (endothelin-1, phenylephrine, thrombin, vasopressin and ATP) rely differentially on the EGFR with respect to the abovementioned phenotypic alterations. In primary, aortic VSMC from mice without conditional deletion of the EGFR, proliferation, migration, marker gene expression (inflammation, fibrosis and ROS homeostasis) and cell signaling (ERK 1/2, intracellular calcium) were analyzed. VSMC-EGFR loss reduced collective cell migration and single cell migration probability, while no difference between the genotypes in single cell velocity, chemotaxis or marker gene expression could be observed under control conditions. EGF promoted proliferation, collective cell migration, chemokinesis and chemotaxis and leads to a proinflammatory gene expression profile in wildtype but not in knockout VSMC. Comparing the impact of five vasoactive substances (all reported to transactivate EGFR and all leading to an EGFR dependent increase in ERK1/2 phosphorylation), we demonstrate that the importance of EGFR for their action is substance-dependent and most apparent for crowd migration but plays a minor role for gene expression regulation.

show abstract

Role of guanine-nucleotide exchange factor Epac in renal physiology and pathophysiology

Yang

Xiao

et al. 2013

American Journal of Physiology-Renal Physiology

View full text Add to dashboard Cite

Exchange proteins directly activated by cAMP [Epac(s)] were discovered more than a decade ago as new sensors for the second messenger cAMP. The Epac family members, including Epac1 and Epac2, are guanine nucleotide exchange factors for the Ras-like small GTPases Rap1 and Rap2, and they function independently of protein kinase A. Given the importance of cAMP in kidney homeostasis, several molecular and cellular studies using specific Epac agonists have analyzed the role and regulation of Epac proteins in renal physiology and pathophysiology. The specificity of the functions of Epac proteins may depend upon their expression and localization in the kidney as well as their abundance in the microcellular environment. This review discusses recent literature data concerning the involvement of Epac in renal tubular transport physiology and renal glomerular cells where various signaling pathways are known to be operative. In addition, the potential role of Epac in kidney disorders, such as diabetic kidney disease and ischemic kidney injury, is discussed.

show abstract

Endothelin signaling via guanine exchange factor C3G in renal glomerular mesangial cellsThis article is one of a selection of papers published in the two-part special issue entitled 20 Years of Endothelin Research.

Cited by 4 publications

References 30 publications

Endothelin and the Glomerulus in Chronic Kidney Disease

Endothelin and the Glomerulus in Chronic Kidney Disease

Substance-specific importance of EGFR for vascular smooth muscle cells motility in primary culture

Role of guanine-nucleotide exchange factor Epac in renal physiology and pathophysiology

Contact Info

Product

Resources

About