title: [The phenotypic switching of vascular smooth muscle cells induced by cholesterol].
abstract: OBJECTIVE
  To observe the effect of cholesterol on phenotypic switching of human vascular smooth muscle cells (VSMCs) in vitro.
  
  
  METHODS
  VSMCs were treated with cholesterol at 12.5, 25.0 and 50.0 mg/L for 48 hours and at 50 mg/L for 24, 48 and 72 hours. Real-time quantitative PCR and Western blotting were respectively applied to detect the mRNA expressions of smooth muscle alpha-actin (α-SMA), smooth muscle 22 alpha (SM22α) and the protein expressions of SM22α, monocyte chemotactic protein-1 induced protein (MCPIP). CCK-8 assay was performed to analyze the viability of VSMCs.
  
  
  RESULTS
  Compared with control groups, cholesterol treatments resulted in a significant down-regulation of both mRNA and protein expressions of endogenous α-SMA and SM22α in VSMCs at 48 hours (P<0.05), and the expressions were lowest when cholesterol was 50.0 mg/L. At 48 and 72 hours, 50.0 mg/L cholesterol significantly decreased the expressions of α-SMA and SM22α (P<0.05). The proliferation of VSMCs in cholesterol groups was promoted significantly compared with control groups (P<0.05). Cholesterol at 50.0 mg/L was also able to induce MCPIP protein expression in VSMCs at 48 hours (P<0.05).
  
  
  CONCLUSIONS
  Cholesterol can decrease the expressions of α-SMA and SM22α and enhance the proliferation of VSMCs, which suggests that cholesterol induces phenotypic switching of VSMCs.
authors.affiliation: Shanghai University of Traditional Chinese Medicine, Shanghai 200032; Department of Biochemistry, Zunyi Medical College, Zunyi 563003, China.
authors.forename: Bo
authors.initials: B
authors.lastname: Shu
authors.affiliation: Department of Biochemistry, Zunyi Medical College, Zunyi 563003, China.
authors.forename: Yijun
authors.initials: Y
authors.lastname: Yang
authors.affiliation: Department of Biochemistry, Zunyi Medical College, Zunyi 563003, China.
authors.forename: Minzhang
authors.initials: M
authors.lastname: Qian
mesh_terms: D000199:Actins / Q000235:genetics / Q000378:metabolism; D015153:Blotting, Western; D049109:Cell Proliferation / Q000187:drug effects*; D002478:Cells, Cultured; D002784:Cholesterol / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D015870:Gene Expression / Q000187:drug effects; D006801:Humans; D008840:Microfilament Proteins / Q000235:genetics / Q000378:metabolism; D009124:Muscle Proteins / Q000235:genetics / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000737:chemistry / Q000166:cytology*; D032389:Myocytes, Smooth Muscle / Q000187:drug effects* / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012260:Ribonucleases; D013997:Time Factors; D014157:Transcription Factors / Q000378:metabolism
chemical_list: D000199:Actins; D008840:Microfilament Proteins; D009124:Muscle Proteins; D014157:Transcription Factors; C051615:transgelin; D002784:Cholesterol; D012260:Ribonucleases; C510646:ZC3H12A protein, human