| Literature DB >> 17167153 |
Xueguang Zhang1, Xiangmei Chen, Quan Hong, Hongli Lin, Hanyu Zhu, Qingxin Liu, Jianzhong Wang, Yuansheng Xie, Xiyao Shang, Suozhu Shi, Yang Lu, Zhong Yin.
Abstract
Imbalance of matrix metalloproteinases and tissue inhibitors of metalloproteinases (MMPs/TIMPs) takes part in age-related renal fibrosis; so does molecular inflammation. As several inflammatory mediators including intercellular adhesion molecule-1 (ICAM-1) are substrates of MMPs, we speculated that TIMP-1 might affect ICAM-1 through MMPs and subsequently promote age-related renal fibrosis. Then, we observed changes of kidney in human TIMP-1 transgenic mice and wild-type mice of different ages. It was found that the expressions and activities of gelatinases were downregulated; the expressions of ICAM-1, collagen III, collagen IV, and transforming growth factor (TGF)-beta1 were upregulated; and the number of infiltrating macrophages was increased in kidneys of 24-month-old TIMP-1 transgenic mice with high expressions of TIMP-1, compared with wild-type mice. Our results indicated that TIMP-1 could promote age-related renal fibrosis, which was partly attributed to enhancing inflammation through upregulation of ICAM-1.Entities:
Mesh：
Substances：
Year: 2006 PMID： 17167153 DOI： 10.1093/gerona/61.11.1130
Source DB: PubMed Journal: J Gerontol A Biol Sci Med Sci ISSN： 1079-5006 Impact factor: 6.053