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AMP-activated protein kinase inhibits TGF-β-, angiotensin II-, aldosterone-, high glucose- and albumin-induced epithelial-mesenchymal transition.

Am J Physiol Renal Physiol. 2013 Jan 16;

Authors: Lee JH, Kim JH, Kim JS, Chang JW, Kim SB, Park JS, Lee SK


Epithelial-mesenchymal transition (EMT) is a novel mechanism that promotes renal fibrosis. TGF-β, angiotensin II, aldosterone, high glucose and urinary albumin are well known cause of EMT and renal fibrosis. We examined whether and how activation of AMP-activated protein kinase (AMPK) suppressed EMT induced by the above agents in tubular epithelial cells. All experiments were performed using HK-2 cells. Protein expression was measured by Western blot analysis. Intracellular reactive oxygen species (ROS) were analyzed by flow cytometry. Exposure of tubular cells to TGF-β (10 ng/ml), angiotensin II (1 μM), aldosterone (100 nM), high glucose (30 mM) and albumin (5 mg/ml) for 5 days induced EMT, as shown by up-regulation of α-smooth muscle actin and down-regulation of E-cadherin. ROS and Nox4 expression were increased and anti-oxidants such as tiron and N-acetylcysteine inhibited EMT-induction. Metformin (the best known clinical activator of AMPK) suppressed EMT-induction through inhibition of ROS via induction of heme oxygenase-1 and endogenous anti-oxidant thioredoxin. AMPK inhibitor (compound C)and AMPK siRNA blocked the effect of metformin and another AMPK activator (AICAR) exerted the same effects as metformin. In conclusion, AMPK activation might be beneficial in attenuating the tubulointerstitial fibrosis induced by TGF-β, angiotensin II, aldosterone, high glucose and urinary albumin.

PMID: 23324179 [PubMed - as supplied by publisher]