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Effects of Angiotensin II on Podocyte Synaptopodin: Role of AMP Kinase
하태선,박혜영,최지영,남자애,안희열 충북대학교 동물의학연구소 2011 Journal of Biomedical and Translational Research Vol.12 No.4
AMP-activated protein kinase (AMPK), as a sensor of cellular energy status, plays an important role in the pathophysiology of diabetes and its complications. As AMPK is also expressed in podocytes, podocyte AMPK would be an important contributing factor in the development of podocyte injury. We investigated the roles of AMPK in the pathological changes of podocyte synaptopodin induced by angiotensin II (Ang II), a major injury inducer. Mouse podocytes were incubated in media containing various concentrations of Ang II and AMPK-modulating agents, and the changes of synaptopodin were analyzed by confocal imaging and Western blotting. Ang II and compound C, an AMPK inhibitor, concentrated and re-localized synaptopodin from peripheral cytoplasm to internal cytoplasm portion in podocytes. Ang II also reduced synaptopodin protein and mRNA, which were reversed by metformin and 5-aminoimidazole-4-carboxamide ribonucleoside. Losartan, an Ang II type 1 receptor antagonist, also recovered synaptopodin mRNA, which was suppressed by Ang II. We suggest that Ang II induces the relocation and suppression of podocyte synaptopodin by the suppression of AMPK and via Ang II type 1 receptor, which would be an important mechanism in Ang II-induced podocyte phenotypical changes.
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Effects of Interleukin-13 and Montelukast on the Expression of Zonula Occludens-1 in Human Podocytes
박세진,하태선,Moin A. Saleem,남자애,신재일 연세대학교의과대학 2015 Yonsei medical journal Vol.56 No.2
Purpose: The aim of this study was to investigate whether pathologic changes in zonula occludens-1 (ZO-1) are induced by interleukin-13 (IL-13) in the experimentalminimal-change nephrotic syndrome (MCNS) model and to determine whether montelukast, a leukotriene receptor antagonist, has an effect on ZO-1 restorationin cultured human podocytes. Materials and Methods: Human podocytescultured on bovine serum albumin-coated plates were treated with different doses of IL-13 and montelukast and then examined for distribution using confocal microscopy and for ZO-1 protein levels using Western blotting. Results: ZO-1 was internalized and shown to accumulate in the cytoplasm of human podocytes in an IL-13 dose-dependent manner. High doses (50 and 100 ng/mL) of IL-13 decreasedthe levels of ZO-1 protein at 12 and 24 h (both p<0.01; n=3), which were significantly reversed by a high dose (0.5 μM) montelukast treatment (p<0.01; n=3). Conclusion: Our results suggest that IL-13 alters the expression of ZO-1, and such alterations in the content and distribution of ZO-1 may be relevant in the pathogenesis of proteinuria in the MCNS model.
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