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Amadori‐glycated albumin‐induced vascular smooth muscle cell proliferation and expression of inhibitor of apoptosis protein‐1 and nerve growth factor‐γ
Author(s) -
Lee ByungWan,
Ihm Jahei,
Kang Jun Gu,
Choi Moon Gi,
Yoo Hyung Joon,
Ihm SungHee
Publication year - 2007
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.5520310301
Subject(s) - vascular smooth muscle , signal transduction , apoptosis , cell growth , endocrinology , superoxide dismutase , biology , growth factor , medicine , nerve growth factor , glycation , oxidative stress , microbiology and biotechnology , biochemistry , receptor , diabetes mellitus , smooth muscle
We investigated the effects of Amadori‐glycated serum albumin (GSA) on cell proliferation as well as expressions of antioxidant enzyme genes and marker genes associated with signal transduction pathways in rat aortic vascular smooth muscle cells (VSMCs). Quiescent VSMCs treated with GSA (0–500 μg/mL, 48 h) exhibited a dose‐dependent increase in proliferation that was prevented by PD98059 (25 μM), suggesting a MAPK‐dependent signaling pathway. Compared with bovine serum albumin (BSA)‐treated cells, the GSA (500 μg/mL, 24 h)‐treated VSMCs showed a higher superoxide dismutase 2 gene expression in quantitative RT‐PCR, suggesting the involvement of oxidative stress. In a focused oligonucleotide array containing 96 signal transduction‐related genes, expression of inhibitor of apoptosis protein‐1 (IAP‐1), nerve growth factorγ (NGF‐γ), and c‐jun genes was significantly higher in the GSA‐treated VSMCs. These results suggest that induction of antiapoptotic proteins like IAP‐1 and strong mitogens like NGF‐γ by GSA might further contribute to the VSMC proliferation and accelerated vascular remodeling in diabetes.