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Author (up) Azechi, T.; Kanehira, D.; Kobayashi, T.; Sudo, R.; Nishimura, A.; Sato, F.; Wachi, H.
url  openurl
  Title Trichostatin A, an HDAC Class I/II Inhibitor, Promotes Pi-Induced Vascular Calcification Via Up-Regulation of the Expression of Alkaline Phosphatase Type Journal Article
  Year 2013 Publication Journal of Atherosclerosis and Thrombosis Abbreviated Journal J Atheroscler Thromb  
  Volume Issue Pages  
  Abstract Aim: Vascular calcification, a major complication of chronic kidney disease (CKD), refers to the mineralization of vascular smooth muscle cells (VSMCs), resulting from a phenotypic change towards osteoblast-like cells. Histone deacetylase inhibitors (HDIs), potential therapeutic agents for CKD, are known to promote the differentiation and mineralization of osteoblasts. In this study, we aimed to determine the effects of an HDI on the phenotypic change of VSMCs and the development of vascular calcification.Methods: The effect of trichostatin A (TSA), an HDI, on human aortic smooth muscle cells (HASMCs) was determined. The mineralization of HASMCs was induced by inorganic phosphorus (Pi), and was confirmed by quantitation of Ca levels and by von Kossa staining. Furthermore, we examined the effect of alkaline phosphatase (ALP) suppression using siRNA on Pi-induced vascular calcification in the presence or absence of TSA.Results: TSA increased the expression and activity of ALP in HASMCs at a concentration which showed an inhibitory effect of histone deacetylase (HDAC) activity but not on cell viability. Moreover, TSA promoted the Pi-induced mineralization of HASMCs. In addition, both phosphonoformic acid (PFA), which is a sodium-dependent phosphate transporter inhibitor, and suppression of ALP expression by siRNA markedly inhibited the TSA-promoted mineralization of HASMCs.Conclusion: These data show that inhibition of HDAC activity promotes Pi-induced vascular calcification via the up-regulation of ALP expression. Taken together, HDIs may increase the risk of vascular calcification in CKD patients.  
  Address Department of Clinical Chemistry, Hoshi University School of Pharmacy and Pharmaceutical Sciences  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 1340-3478 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:23518467 Approved no  
  Call Number @ @ Serial 38637  
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