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The role of microparticles in inhibiting hypoxia and serum deprivation induced apoptosis of bone marrow mesenchymal stem cells |
JIN Peifeng1, JIANG Sheng1, WENG Jiakan1,2, WANG Lei1, Ding Lu3, ZHAO Kaixiang1, SUN Chengchao1 |
1.Department of Cardiothoracic Surgery, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325015, China; 2.Department of Cardiothoracic Surgery, Sir Run Run Shaw Hospital, Affiliated to Zhejiang University School of Medicine, Hangzhou 310000, China; 3.Department of Ergology, Wenzhou Medical University, Wenzhou 325035, China |
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Cite this article: |
JIN Peifeng1,JIANG Sheng,WENG Jiakan, et al. The role of microparticles in inhibiting hypoxia and serum deprivation induced apoptosis of bone marrow mesenchymal stem cells[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2019, 49(2): 79-84.
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Abstract Objective: To investigate the effects of myocardial infarction plasma-derived microparticles (MPs) on the hypoxia and serum deprivation induced apoptosis of bone marrow mesenchymal stem cells (BMSCs). Methods: Myocardial infarction (MI) was created by left anterior descending artery ligation in Lewis rats. The plasma-derived MPs were isolated 24 hours later from the blood. In order to study the protective effects of MPs on BMSCs under the conditions of hypoxia and serum deprivation (hypoxia/SD). BMSCs were pretreated with different concentrations (0.5 μg/mL, 1 μg/mL, and 2 μg/mL) of MPs before the apoptosis was induced. Cell apoptosis was evaluated by using flow cytometry of Annexin V/PI staining, Hoechst staining and the Tunel assay. Expression of cleavage of caspase-3 were assessed by Western blotting. The Akt pathway inhibitor AZD5363 was used to reveal the mechanism of MPs inhibiting BMSCs apoptosis. Results: The MPs derived from the myocardial infarction rats could remarkably prevent BMSCs from Hypoxia/SD induced apoptosis through activating Akt signaling pathway, and its anti-apoptosis effect showed a concentration dependence (0.5-2 μg/mL) (P<0.01). Conclusion: MPs derived from myocardial infarction could effectively inhibit hypoxia/SD induced apoptosis of BMSCs.
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