These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: Time courses of vascular endothelial growth factor and intercellular adhesion molecule-1 expressions in aortas of atherosclerotic rats.
    Author: Yang PY, Rui YC, Lu L, Li TJ, Liu SQ, Yan HX, Wang HY.
    Journal: Life Sci; 2005 Sep 30; 77(20):2529-39. PubMed ID: 16005023.
    Abstract:
    An increasing number of studies have focused on the expressions of growth factors and adhesion molecules in atherosclerotic lesions, which are confirmed to play central roles in angiogenesis and endothelial dysfunction, including vascular endothelial growth factor (VEGF) and intercellular adhesion molecule-1 (ICAM-1). However, the difference of growth factor and adhesion molecule expression time courses has not been determined in vivo. This study aimed to determine the expression patterns and expression curves of ICAM-1 and VEGF in atherosclerotic rats during the time course. An experiment atherosclerotic model in rats was established by combining the high fat/cholesterol diets with injection of vitamin D3. In situ hybridization was used to determine the expression patterns of VEGF and ICAM-1 in aortas of normal or atherosclerotic rats in 8 weeks. There was a massive increase in reactivity for both ICAM-1 and VEGF in atherosclerotic plaques. Northern blot, Western blot and ELISA analysis were used to quantify VEGF and ICAM-1 expressions in time course. In rat aorta, the expression curves in time course showed that ICAM-1, not VEGF, was up-regulated in mRNA levels significantly in 2 weeks; while VEGF expression was hysteresis than ICAM-1, which showed maximum expression level in 8 weeks. Our results provide the evidence of VEGF and ICAM-1 expression curves in time course in atherosclerotic rats, which indicated different regulatory mechanisms of VEGF and ICAM-1 expression in atherogenesis.
    [Abstract] [Full Text] [Related] [New Search]