【摘 要】
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Aim Stable microtubules (MTs) is involved the mechanism of diabetic cardiomyopathy (DCM), which is induced by acetylation of αtubulin.The present study investigated whether SIRT2, a deacetylase, regul
【机 构】
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Dept of Pharmacology,Wuhan University of Science and Technology,Wuhan 430065,China;Brain and Cogniti
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Aim Stable microtubules (MTs) is involved the mechanism of diabetic cardiomyopathy (DCM), which is induced by acetylation of αtubulin.The present study investigated whether SIRT2, a deacetylase, regulates MT stability through αtubulin deacetylation in DCM and whether the receptor of advanced glycation end products(AGEs) signaling pathway is involved in this effect.Methods Type 1 diabetic mellitus (T1DM) rats model was established by a single intraperitoneal injection of streptozotocin (STZ, 65 mg · kg1), and neonatal rat cardiomyocytes were also cultured.Heart function was detected by Doppler.MT stability was elevated by 3tubulin expression density.The protein expression of SIRT2, acetylated αtubulin and AGEs receptor were detected by immunohistochemistry or Western blots.The interaction of SIRT2 and acetylated αtubulin was detected by Coimmunoprecipitation.Results In an animal model of T1 DM, Western blot and immunohistochemistry revealed downregulation of SIRT2 but upregulation of the acetylated αtubulin protein.These effects were reduced by treatment of aminoguanidine, an inhibitor of AGEs production.HDAC6 expression did not regulated in heart.In primary cultures of neonatal rat cardiomyocytes, the AGEs treatment impaired the SIRT2/acetylated αtubulin signaling pathway, and SIRT2overexpression reversed the function of AGEs on cardiomyocytes.In addition, gene silencing of AGEs receptor alleviated the impairment effect of AGEs on cardiomyocytes.Conclusion In conclusion, these data demonstrate that AGEs/AGEs receptor promote MT stabilization via the suppression of the SIRT2/acetylated αtubulin signaling pathway in DCM development.
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