Literature DB >> 31511362

Inhibition of Endocytosis of Clathrin-Mediated Angiotensin II Receptor Type 1 in Podocytes Augments Glomerular Injury.

Kazunori Inoue1, Xuefei Tian1, Heino Velazquez1, Keita Soda1, Zhen Wang1, Christopher E Pedigo1, Ying Wang1, Elizabeth Cross1, Marwin Groener1, Jee-Won Shin1, Wei Li1, Hossam Hassan1, Koichi Yamamoto2, Peter Mundel3, Shuta Ishibe4.   

Abstract

BACKGROUND: Inhibition of the renin-angiotensin system remains a cornerstone in reducing proteinuria and progression of kidney failure, effects believed to be the result of reduction in BP and glomerular hyperfiltration. However, studies have yielded conflicting results on whether podocyte-specific angiotensin II (AngII) signaling directly induces podocyte injury. Previous research has found that after AngII stimulation, β-arrestin-bound angiotensin II receptor type 1 (AT1R) is internalized in a clathrin- and dynamin-dependent manner, and that Dynamin1 and Dynamin2 double-knockout mice exhibit impaired clathrin-mediated endocytosis.
METHODS: We used podocyte-specific Dyn double-knockout mice to examine AngII-stimulated AT1R internalization and signaling in primary podocytes and controls. We also examined the in vivo effect of AngII in these double-knockout mice through renin-angiotensin system blockers and through deletion of Agtr1a (which encodes the predominant AT1R isoform expressed in kidney, AT1aR). We tested calcium influx, Rac1 activation, and lamellipodial extension in control and primary podocytes of Dnm double-knockout mice treated with AngII.
RESULTS: We confirmed augmented AngII-stimulated AT1R signaling in primary Dnm double-knockout podocytes resulting from arrest of clathrin-coated pit turnover. Genetic ablation of podocyte Agtr1a in Dnm double-knockout mice demonstrated improved albuminuria and kidney function compared with the double-knockout mice. Isolation of podocytes from Dnm double-knockout mice revealed abnormal membrane dynamics, with increased Rac1 activation and lamellipodial extension, which was attenuated in Dnm double-knockout podocytes lacking AT1aR.
CONCLUSIONS: Our results indicate that inhibiting aberrant podocyte-associated AT1aR signaling pathways has a protective effect in maintaining the integrity of the glomerular filtration barrier.
Copyright © 2019 by the American Society of Nephrology.

Entities:  

Keywords:  endocytosis; podocyte; proteinuria

Year:  2019        PMID: 31511362      PMCID: PMC6900791          DOI: 10.1681/ASN.2019010053

Source DB:  PubMed          Journal:  J Am Soc Nephrol        ISSN: 1046-6673            Impact factor:   10.121


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Authors:  Ying Wang; Christopher E Pedigo; Kazunori Inoue; Xuefei Tian; Elizabeth Cross; Karen Ebenezer; Wei Li; Zhen Wang; Jee Won Shin; Eike Schwartze; Marwin Groener; Shuta Ishibe
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