Journal
ARCHIVES OF PHYSIOLOGY AND BIOCHEMISTRY
Volume 117, Issue 5, Pages 270-282Publisher
INFORMA HEALTHCARE
DOI: 10.3109/13813455.2011.599844
Keywords
-
Funding
- NHLBI NIH HHS [HL-104103, R01 HL104103, HL-71010, R01 HL104103-02, R01 HL071010-08, R01 HL071010, R01 HL088012, R01 HL088012-04, HL-88012] Funding Source: Medline
Ask authors/readers for more resources
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 beta-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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available