title: RNA interference of myocyte enhancer factor 2A accelerates atherosclerosis in apolipoprotein E-deficient mice.
abstract: OBJECTIVE
  Myocyte enhancer factor-2A (MEF 2A) has been shown to be involved in atherosclerotic lesion development, but its role in preexisting lesions is still unclear. In the present study we aim to assess the role of MEF 2A in the progression of pre-existing atherosclerosis.
  
  
  METHODS
  Eighty apolipoprotein E-deficient mice (APOE KO) were randomly allocated to control, scramble and MEF 2A RNA interference (RNAi) groups, and constrictive collars were used to induce plaque formation. Six weeks after surgery, lentiviral shRNA construct was used to silence the expression of MEF 2A. Carotid plaques were harvested for analysis 4 weeks after viral vector transduction. Inflammatory gene expression in the plasma and carotid plaques was determined by using ELISAs and real-time RT-PCR.
  
  
  RESULTS
  The expression level of MEF 2A was significantly reduced in plasma and plaque in the RNAi group, compared to the control and NC groups, whereas the expression level of pro-inflammatory cytokines was markedly increased. Silencing MEF 2A using lentiviral shRNA significantly reduced the plaque collagen content and fibrous cap thickness, as well as increased plaque area. However, silencing MEF 2A had no obvious effect on plaque lipid content.
  
  
  CONCLUSIONS
  Lentivirus-mediated MEF 2A shRNA accelerates inflammation and atherosclerosis in APOE KO mice, but has no effect on lipoprotein levels in plasma.
authors: Department of Cardiology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.
authors: Wen-ping
authors: WP
authors: Zhou
authors: Department of Cardiology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.
authors: Hui
authors: H
authors: Zhang
authors: Department of Medical Equipment, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.
authors: Yu-xia
authors: YX
authors: Zhao
authors: Department of Cardiology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.
authors: Gang-qiong
authors: GQ
authors: Liu
authors: Department of Cardiology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.
authors: Jin-ying
authors: JY
authors: Zhang
mesh_terms: D000818:Animals; D001011:Aorta / Q000473:pathology; D001057:Apolipoproteins E / Q000172:deficiency*; D050197:Atherosclerosis / Q000097:blood / Q000473:pathology*; D015415:Biomarkers / Q000378:metabolism; D001835:Body Weight; D042783:Endothelial Cells / Q000378:metabolism; D055785:Gene Knockdown Techniques; D005822:Genetic Vectors / Q000378:metabolism; D007249:Inflammation / Q000235:genetics; D016086:Lentivirus / Q000378:metabolism; D008055:Lipids / Q000097:blood; D064326:MEF2 Transcription Factors / Q000378:metabolism*; D008297:Male; D018345:Mice, Knockout; D058226:Plaque, Atherosclerotic / Q000097:blood / Q000473:pathology; D034622:RNA Interference; D034741:RNA, Small Interfering / Q000378:metabolism; D014161:Transduction, Genetic; D015854:Up-Regulation / Q000235:genetics
chemical_list: D001057:Apolipoproteins E; D015415:Biomarkers; D008055:Lipids; D064326:MEF2 Transcription Factors; D034741:RNA, Small Interfering