Chronic hyperhomocysteinemia causes vascular remodelling by instigating vein phenotype in artery

Poulami Basu, Natia Qipshidze, Utpal Sen, Srikanth Givvimani, Charu Munjal, Paras K. Mishra, Suresh C. Tyagi

Research output: Contribution to journalArticle

7 Scopus citations

Abstract

In the present study we tested the hypothesis whether hyperhomocysteinemia, an elevated homocysteine level, induces venous phenotype in artery. To test our hypothesis, we employed wild type (WT) and cystathionine β-synthase heterozygous (+/-) (CBS +/-) mice treatment with or without folic acid (FA). Aortic blood flow and velocity were significantly lower in CBS+/- mice compared to WT. Aortic lumen diameter was significantly decreased in CBS +/- mice, whereas FA treatment normalized it. Medial thickness and collagen were significantly increased in CBS +/- aorta, whereas elastin/collagen ratio was significantly decreased. Superoxide and gelatinase activity was significantly high in CBS +/- aorta vs WT. Western blot showed significant increase in MMP-2, -9,-12, TIMP-2 and decrease in TIMP-4 in aorta. RT-PCR revealed significant increase of vena cava marker EphB4, MMP-13 and TIMP-3 in aorta. We summarize that chronic HHcy causes vascular remodelling that transduces changes in vascular wall in a way that artery expresses vein phenotype.

Original languageEnglish (US)
Pages (from-to)270-282
Number of pages13
JournalArchives of Physiology and Biochemistry
Volume117
Issue number5
DOIs
StatePublished - Dec 2011

Keywords

  • Collagen
  • Cystathionine β-synthase
  • Elastin
  • EphB4 and Ephrin B2
  • Folic acid
  • Homocysteine
  • Matrix metalloproteinase

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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