Exosomes from adipose-derived mesenchymal stem cells ameliorate cardiac damage after myocardial infarction by activating S1P/SK1/S1PR1 signaling and promoting macrophage M2 polarization

被引:189
|
作者
Deng, Shengqiong [1 ]
Zhou, Xianjin [2 ]
Ge, Zhiru [3 ]
Song, Yuting [4 ,5 ]
Wang, Hairong [3 ]
Liu, Xinghui [1 ]
Zhang, Denghai [5 ]
机构
[1] Second Mil Med Univ, Shanghai Gongli Hosp, Dept Clin Lab, Shanghai 200135, Peoples R China
[2] Tongji Univ, Shanghai Matern & Infant Hosp 1, Sch Med, Shanghai 200135, Peoples R China
[3] Second Mil Med Univ, Shanghai Gongli Hosp, Dept Cardiol, Shanghai 200135, Peoples R China
[4] Ningxia Med Univ, Ningxia 750000, Peoples R China
[5] Secondary Mil Med Univ, Shanghai Gongli Hosp, Sinofrench Cooperat Cent Lab, Shanghai 200135, Peoples R China
来源
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY | 2019年 / 114卷
基金
中国国家自然科学基金;
关键词
ADSCs; Sphingosine; 1-phosphate; Macrophage; Exosome; Myocardial infarction; INTERCELLULAR COMMUNICATION; SPHINGOSINE; 1-PHOSPHATE; INFLAMMATION; KINASE; REPAIR;
D O I
10.1016/j.biocel.2019.105564
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Exosomes derived from mesenchymal stem cells (MSCs) are known to participate in myocardial repair after myocardial infarction (MI), but the mechanism remains unclear. Here, we isolated exosomes from adipose-derived MSCs (ADSCs) and examined their effect on MI-induced cardiac damage. To examine the underlying mechanism, H9c2 cells, cardiac fibroblasts, and HAPI cells were used to study the effect of ADSC-exosomes on hypoxia-induced H9c2 apoptosis, TGF-beta 1-induced fibrosis of cardiac fibroblasts, and hypoxia-induced macrophage M1 polarization using qRT-PCR, western blot, ELISA, immunohistochemistry, immunofluorescence and flow cytometry. ADSC-exosome treatment mitigated MI-induced cardiac damage by suppressing cardiac dysfunction, cardiac apoptosis, cardiac fibrosis, and inflammatory responses in vitro and in vivo. In addition, ADSC-exosome treatment promoted macrophage M2 polarization. Further experiments found that S1P/SK1/S1PR1 signaling was involved in the ADSC-exosome-mediated myocardial repair. Silencing of S1PR1 reversed the inhibitory effect of ADSC-exosomes on MI-induced cardiac apoptosis and fibrosis in vitro. ADSC-exosome-induced macrophage M2 polarization was also reversed after downregulation of S1PR1 under hypoxia conditions, which promoted NF kappa B and TGF-beta 1 expression, and suppressed the MI-induced cardiac fibrosis and inflammatory response. In sum, these results indicate that ADSC-derived exosomes ameliorate cardiac damage after MI by activating S1P/SK1/S1PR1 signaling and promoting macrophage M2 polarization.
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页数:9
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