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- W79118575 abstract "Tubulointerstitial fibrosis is a main pathological feature of progressive renal disease. Transforming growth factor beta (TGF-β) induces mesencymal cell characteristics in tubular epithelial cells including increased expression of fibronectin and α-smooth muscle actin (α-SMA). We report that in cultured murine and primary human proximal tubular epithelial cells (PTECs), TGF-β results in a decrease in AMPK phosphorylation on active site (Thr172) associated with increased fibronectin and α-SMA. Activation of AMPK with AICAR or metformin or overexpression of constitutively active AMPK markedly reduced TGF-β-induced fibronectin and α-SMA. Conversely, inhibition of AMPK with ARA or AMPK knockdown by siRNA enhanced basal as well as TGF-β-induced fibronectin and α-SMA. The decrease in AMPK phosphorylation with TGF-β was accompanied by a decrease in tuberin phosphorylation on Ser1387, the AMPK phosphorylated site that keeps tuberin active. Moreover, tuberin knockdown by siRNA in PTECs enhanced basal as well TGF-β-induced fibronectin and α-SMACollectively, the data indicate that TGF-β exerts its profibrotic actions via inactivation of AMPK and tuberin, and that AMPK activation attenuates PTECs injury. Our results suggest that AMPK activation represents a potential therapeutic target to prevent mesenchymal cell transition including extracellular matrix accumulation in progressive renal disease. This work was supported by NIH-NIDDK grant RO1 DK078971 to HEA." @default.
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- W79118575 date "2013-04-01" @default.
- W79118575 modified "2023-09-23" @default.
- W79118575 title "AMP‐activated Protein Kinase (AMPK) regulates TGF‐β1 Induced Fibronectin Expression in Renal Tubular Epithelial Cells" @default.
- W79118575 doi "https://doi.org/10.1096/fasebj.27.1_supplement.601.10" @default.
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