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Pubmed for Handhelds

PUBMED FOR HANDHELDS

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  • Title: Chronic hyperhomocysteinemia causes vascular remodelling by instigating vein phenotype in artery.
    Author: Basu P, Qipshidze N, Sen U, Givvimani S, Munjal C, Mishra PK, Tyagi SC.
    Journal: Arch Physiol Biochem; 2011 Dec; 117(5):270-82. PubMed ID: 21838575.
    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.
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