Angiotensin II Modulates p130Cas of Podocytes by the Suppression of AMP-Activated Protein Kinase

Angiotensin II (Ang II) induces the pathological process of vascular structures, including renal glomeruli by hemodynamic and nonhemodynamic direct effects. In kidneys, Ang II plays an important role in the development of proteinuria by the modification of podocyte molecules. We have previously foun...

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Main Authors:	Ha, Tae-Sun, Park, Hye-Young, Seong, Su-Bin, Ahn, Hee-Yul
Format:	Online
Language:	English
Published:	The Korean Academy of Medical Sciences 2016
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4810335/

id	pubmed-4810335
recordtype	oai_dc
spelling	pubmed-48103352016-04-05 Angiotensin II Modulates p130Cas of Podocytes by the Suppression of AMP-Activated Protein Kinase Ha, Tae-Sun Park, Hye-Young Seong, Su-Bin Ahn, Hee-Yul Original Article Angiotensin II (Ang II) induces the pathological process of vascular structures, including renal glomeruli by hemodynamic and nonhemodynamic direct effects. In kidneys, Ang II plays an important role in the development of proteinuria by the modification of podocyte molecules. We have previously found that Ang II suppressed podocyte AMP-activated protein kinase (AMPK) via Ang II type 1 receptor and MAPK signaling pathway. In the present study, we investigated the roles of AMPK on the changes of p130Cas of podocyte by Ang II. We cultured mouse podocytes and treated them with various concentrations of Ang II and AMPK-modulating agents and analyzed the changes of p130Cas by confocal imaging and western blotting. In immunofluorescence study, Ang II decreased the intensity of p130Cas and changed its localization from peripheral cytoplasm into peri-nuclear areas in a concentrated pattern in podocytes. Ang II also reduced the amount of p130Cas in time and dose-sensitive manners. AMPK activators, metformin and AICAR, restored the suppressed and mal-localized p130Cas significantly, whereas, compound C, an AMPK inhibitor, further aggravated the changes of p130Cas. Losartan, an Ang II type 1 receptor antagonist, recovered the abnormal changes of p130Cas suppressed by Ang II. These results suggest that Ang II induces the relocalization and suppression of podocyte p130Cas by the suppression of AMPK via Ang II type 1 receptor, which would contribute to Ang II-induced podocyte injury. The Korean Academy of Medical Sciences 2016-04 2016-03-02 /pmc/articles/PMC4810335/ /pubmed/27051236 http://dx.doi.org/10.3346/jkms.2016.31.4.535 Text en © 2016 The Korean Academy of Medical Sciences. http://creativecommons.org/licenses/by-nc/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Ha, Tae-Sun Park, Hye-Young Seong, Su-Bin Ahn, Hee-Yul
spellingShingle	Ha, Tae-Sun Park, Hye-Young Seong, Su-Bin Ahn, Hee-Yul Angiotensin II Modulates p130Cas of Podocytes by the Suppression of AMP-Activated Protein Kinase
author_facet	Ha, Tae-Sun Park, Hye-Young Seong, Su-Bin Ahn, Hee-Yul
author_sort	Ha, Tae-Sun
title	Angiotensin II Modulates p130Cas of Podocytes by the Suppression of AMP-Activated Protein Kinase
title_short	Angiotensin II Modulates p130Cas of Podocytes by the Suppression of AMP-Activated Protein Kinase
title_full	Angiotensin II Modulates p130Cas of Podocytes by the Suppression of AMP-Activated Protein Kinase
title_fullStr	Angiotensin II Modulates p130Cas of Podocytes by the Suppression of AMP-Activated Protein Kinase
title_full_unstemmed	Angiotensin II Modulates p130Cas of Podocytes by the Suppression of AMP-Activated Protein Kinase
title_sort	angiotensin ii modulates p130cas of podocytes by the suppression of amp-activated protein kinase
description	Angiotensin II (Ang II) induces the pathological process of vascular structures, including renal glomeruli by hemodynamic and nonhemodynamic direct effects. In kidneys, Ang II plays an important role in the development of proteinuria by the modification of podocyte molecules. We have previously found that Ang II suppressed podocyte AMP-activated protein kinase (AMPK) via Ang II type 1 receptor and MAPK signaling pathway. In the present study, we investigated the roles of AMPK on the changes of p130Cas of podocyte by Ang II. We cultured mouse podocytes and treated them with various concentrations of Ang II and AMPK-modulating agents and analyzed the changes of p130Cas by confocal imaging and western blotting. In immunofluorescence study, Ang II decreased the intensity of p130Cas and changed its localization from peripheral cytoplasm into peri-nuclear areas in a concentrated pattern in podocytes. Ang II also reduced the amount of p130Cas in time and dose-sensitive manners. AMPK activators, metformin and AICAR, restored the suppressed and mal-localized p130Cas significantly, whereas, compound C, an AMPK inhibitor, further aggravated the changes of p130Cas. Losartan, an Ang II type 1 receptor antagonist, recovered the abnormal changes of p130Cas suppressed by Ang II. These results suggest that Ang II induces the relocalization and suppression of podocyte p130Cas by the suppression of AMPK via Ang II type 1 receptor, which would contribute to Ang II-induced podocyte injury.
publisher	The Korean Academy of Medical Sciences
publishDate	2016
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4810335/
_version_	1613558654077763584

Angiotensin II Modulates p130Cas of Podocytes by the Suppression of AMP-Activated Protein Kinase

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