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논문 기본 정보

자료유형
학술저널
저자정보
Li Na (Department of Cardiology Beijing Chaoyang Hospital Capital Medical University) Guo Xue-Yuan (Beijing Institute of Heart Lung and Blood Vessel Diseases Capital Medical University) Zhou Jian (Department of Cardiology Beijing Chaoyang Hospital Capital Medical University) Yan Xian-Liang (Beijing Institute of Heart Lung and Blood Vessel Diseases Capital Medical University) Yu Fang-Fang (Department of Radiology Beijing Chaoyang Hospital Capital Medical University)
저널정보
한국조직공학과 재생의학회 조직공학과 재생의학 조직공학과 재생의학 제18권 제5호
발행연도
2021.10
수록면
863 - 873 (11page)
DOI
10.1007/s13770-021-00362-z

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BACKGROUND: We previously found that atorvastatin (ATV) enhanced mesenchymal stem cells (MSCs) migration, by a yet unknown mechanism. CXC chemokine receptor 4 (CXCR4) is critical to cell migration and regulated by microRNA-146a (miR-146a). Therefore, this study aimed to assess whether ATV ameliorates MSCs migration through miR-146a/CXCR4 signaling. METHODS: Expression of CXCR4 was evaluated by flow cytometry. Expression of miR-146a was examined by reverse transcription-quantitative polymerase chain reaction. A transwell system was used to assess the migration ability of MSCs. Recruitment of systematically delivered MSCs to the infarcted heart was evaluated in Sprague?Dawley rats with acute myocardial infarction (AMI). Mimics of miR-146a were used in vitro, and miR-146a overexpression lentivirus was used in vivo, to assess the role of miR-146a in the migration ability of MSCs. RESULTS: The results showed that ATV pretreatment in vitro upregulated CXCR4 and induced MSCs migration. In addition, flow cytometry demonstrated that miR-146a mimics suppressed CXCR4, and ATV pretreatment no longer ameliorated MSCs migration because of decreased CXCR4. In the AMI model, miR-146a-overexpressing MSCs increased infarct size and fibrosis. CONCLUSION: The miR-146a/CXCR4 signaling pathway contributes to MSCs migration and homing induced by ATV pretreatment. miR-146a may be a novel therapeutic target for stimulating MSCs migration to the ischemic tissue for improved repair.

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