HDAC9, TWIST1 and FERD3L gene expression in asymptomatic stable and unstable carotid plaques

Inflamm Res. 2016 Apr;65(4):261-3. doi: 10.1007/s00011-015-0904-z. Epub 2015 Nov 30.

Abstract

Background and objectives: A variant located at the end of HDAC9 gene within clusters of DNAse I sensitivity zones and histone modification hotspots has been associated with large vessel stroke and could be linked to plaque instability. The aim of the study is to define if an altered expression of HDAC9, TWIST1 and FERD3L genes could be involved in plaque vulnerability.

Methods: Histological classification and gene expression analysis were performed in 6 stable and 16 unstable plaques obtained from asymptomatic patients undergoing endarterectomy. Gene expression was analysed by real-time PCR.

Results and conclusions: TWIST1 gene expression resulted higher in stable plaques (P < 0.02). HDAC9 gene expression followed a similar trend (P = 0.11). These results highlighting the significant correlation between TWIST and HDAC9 gene expression suggest that both genes may contribute to plaque stability in a coordinated way.

Keywords: Carotid plaques instability; HDAC9, TWIST1, FERD3L gene expression; Polymorphism.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Aged, 80 and over
  • Carotid Artery Diseases / genetics*
  • Female
  • Gene Expression
  • Histone Deacetylases / genetics*
  • Humans
  • Male
  • Myogenic Regulatory Factors / genetics*
  • Nuclear Proteins / genetics*
  • Plaque, Atherosclerotic / genetics*
  • Repressor Proteins / genetics*
  • Twist-Related Protein 1 / genetics*

Substances

  • FERD3L protein, human
  • Myogenic Regulatory Factors
  • Nuclear Proteins
  • Repressor Proteins
  • TWIST1 protein, human
  • Twist-Related Protein 1
  • HDAC9 protein, human
  • Histone Deacetylases