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Effects of Aging on Wire Injury‐induced Neointimal Hyperplasia: An in vitro and in vivo Study
Author(s) -
Wu ChiehHsi,
Pan ChunHsu,
Wu ChiHan
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.lb601
Subject(s) - neointimal hyperplasia , restenosis , senescence , hyperplasia , vascular smooth muscle , immunohistochemistry , in vivo , medicine , cell growth , endocrinology , pathology , cancer research , smooth muscle , biology , biochemistry , stent , microbiology and biotechnology
In the balloon angioplasty‐injured vascular tissues, abnormal cell proliferation and migration of smooth muscle cells have been believed to play an important role during the disease progression. It still lacks final conclusion and research evidences at present to clarify whether possessing the characteristics of advanced aging will become a susceptibility factor of restenosis. Therefore, the senescence accelerated mouse‐prone 8 (SAMP8) was applied as animal model to induce neointimal hyperplasia by wire injury in this project. The statistical results suggested that the ratio of neointimal‐to‐medial area (N/M ratio) was lower in the SAMP8 mice than in the wild‐type mice of the same age, which implicated that the aging factor may reduce the severity of neointimal hyperplasia. The immunohistochemistry staining was further used to examine the expression of β‐galactosidase, a senescence marker, in the vascular tissues. The level of β‐galactosidase was higher in SAMP8 mice than in the wild‐type mice of the same age. Hence, a cellular senescence model was induced by CoCl 2 treatment in the vascular smooth muscle cells (VSMCs) to investigate the regulations and mechanisms of senescence in the cell proliferation and migration of VSMCs. We found that CoCl 2 ‐induced senescent VSMCs to the serum‐triggered stimulations in the cell growth and migration were negatively correlated with treatment concentration of CoCl 2 . Similarly, this phenomenon was also found in the regulation of AKT and ERK 1/2. Thus, aging factor may reduce the sensitivity of VSMCs to the exogenous stimulatory factors with consistent results to the in vivo study.