Experimental and Molecular Medicine

Korean Society for Biochemistry and Molecular Biongy (생화학분자생물학회)
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TGF-$\beta$1-induced PINCH-1-ILK-$\alpha$-parvin complex formation regulates mesangial cell proliferation and hypertrophy

Kim, Sung-Min;Kim, Na-Ri;Lee, Seoul;Kim, Do-Kyung;Lee, Yu-Min;Ahn, Seon-Ho;Song, Ju-Hung;Choi, Bong-Kyu;Wu, Chuan-Yue;Jung, Kyu-Yong

  • Published : 20070800
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Abstract

TGF-β1-induced glomerular mesangial cell (GMC) in-jury is a prominent characteristic of renal pathology in several kidney diseases, and a ternary protein com-plex consisting of PINCH-1, integrin-linked kinase (ILK) and α-parvin plays a pivotal role in the regulation of cell behavior such as cel proliferation and hyper-trophy. We report here that PINCH-1-ILK-α-parvin (PIP) complex regulates the TGF-βliferation and hypertrophy in cultured rat GMCs. When GMCs were treated with TGF-β1 for 1, 2 and 3 days, the PIP complex formation was up-regulated after 1 day, but it was down-regulated on day 2. Cell numbers were significantly elevated on day 2, but dramatically decreased on day 3. In contrast, a sig-nificant increase in cellular protein contents was ob-served 3 days after TGF-β1-treatment. TGF-β1 in-duced early increase of caspase-3 activity. In GMCs β1 for 2 days, cytosolic ex-pression of p27Kip1 was dramatically reduced, but its nuclear expression was remarkably elevated. A sig-nificantly decreased expression of phospho-Akt (Ser 473) was observed in the cells treated with TGF-β1 for 1 day. TGF-β1 induced early increase of phos-pho-p27Kip1(Thr 157) expression with subsequent de-crease, and similar responses to TGF-β1 were ob-Taken together, TGF-β1 differently regulates the PIP complex formation of GMCs in an incubation peri-od-dependant fashion. The TGF-β1-induced up- and down-regulation of the PIP complex formation likely contributes to the pleiotropic efects of TGF-β1 on mesangial cell proliferation and hypertrophy through cellular localization of p27Kip1and alteration of Akt and p38 phosphorylation. TGF-β1-induced alteration implicated in the development and progression of glomerular failure shown in several kidney diseases.

Keywords

References

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