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Stem cell-based therapeutic strategies have obtained a significant breakthrough in the treatment of cardiovascular diseases, particularly in myocardial infarction (MI). Nevertheless, limited retention and poor migration of stem cells are still problems for stem cell therapeutic development. Hence, there is an urgent need to develop new strategies that can mobilize stem cells to infarcted myocardial tissues effectively. Electroacupuncture (EA) intervention can improve cardiac function and alleviate myocardial injury after MI, but its molecular mechanism is still unclear. This study is aimed at observing the effects of EA treatment on the stem cell mobilization and revealing possible mechanisms in the MI model of mice. EA treatment at Neiguan (PC6) and Xinshu (BL15) acupoints was conducted on the second day after the ligation surgery. Then, the number of stem cells in peripheral blood after EA in MI mice and their cardiac function, infarct size, and collagen deposition was observed. We found that the number of CD34-, CD117-, Sca-1-, and CD90-positive cells increased at 6 h and declined at 24 h after EA intervention in the blood of MI mice. The expression of CXC chemokine receptor-4 (CXCR4) protein was upregulated at 6 h after EA treatment, while the ratio of LC3B II/I or p-ERK/ERK showed a reverse trend. In addition, there was obvious difference in EF and FS between wild-type mice and CXCR4+/- mice. The infarct size, collagen deposition, and apoptosis of the injured myocardium in CXCR4+/- mice increased but could be ameliorated by EA. In a word, our study demonstrates that EA alleviates myocardial injury via stem cell mobilization which may be regulated by the SDF-1/CXCR4 axis. Copyright © 2022 Tian-tian Zhao et al.

Citation

Tian-Tian Zhao, Jia-Jia Liu, Jing Zhu, Han Li, Ya-Chao Wang, Yue Zhao, Shui-Jin Shao, Hai-Dong Guo, Fang-Fang Mou. SDF-1/CXCR4-Mediated Stem Cell Mobilization Involved in Cardioprotective Effects of Electroacupuncture on Mouse with Myocardial Infarction. Oxidative medicine and cellular longevity. 2022;2022:4455183

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PMID: 35982734

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