期刊
INTERNATIONAL JOURNAL OF LOWER EXTREMITY WOUNDS
卷 14, 期 1, 页码 73-86出版社
SAGE PUBLICATIONS INC
DOI: 10.1177/1534734615569053
关键词
nonhealing wound; diabetes mellitus; hyperglycemia; chronic inflammation; oxidative stress; mesenchymal stem cell-conditioned medium; Erk signaling pathway
资金
- National Basic Science and Development Program [2012CB518103, 2012CB518105]
- 863 Projects of Ministry of Science and Technology of China [2013AA020105, 2012AA020502]
- National Natural Science Foundation of China [81201479, 81121004, 81230041]
- Military Medical Foundation [AWS11J008]
- Key Sciences and Technology Project in Hainan Province [ZDZX2013003]
The impairment of wound healing in diabetic patients is an important clinical problem. Proper keratinocyte migration and proliferation are the crucial steps during reepithelialization, and these steps may be impaired in diabetes mellitus (DM) due to hyperglycemia and chronic inflammation in wound site. In this study, we explored the effects of diabetes-like microenvironment with high glucose (HG) and intense inflammation on the migration and proliferation of keratinocytes in vitro. We found that the migration and proliferation of rat keratinocytes were reduced with HG and lipopolysaccharide (LPS) stimulation via Erk signaling pathway in a reactive oxygen species (ROS)-dependent manner. Nevertheless, mesenchymal stem cell-conditioned medium (MSC-CM) counteracts the effects of HG and LPS. Treatment of rat keratinocyte with MSC-CM decreased HG- and/or LPS-induced ROS overproduction. Furthermore, MSC-CM reversed the downregulation of phosphorylation of MEK 1/2 and Erk 1/2, which was induced by HG and/or LPS without affecting total levels. Our results may provide a possible mechanism for delayed wound healing in DM and provide a foundation to develop MSC-CM as an alternative therapeutic strategy to ameliorate the poor wound-healing conditions.
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