Ultrasound-Targeted Microbubble Destruction Improves the Migration and Homing of Mesenchymal Stem Cells after Myocardial Infarction by Upregulating SDF-1/CXCR4: A Pilot Study.
Ultrasound-Targeted Microbubble Destruction Improves the Migration and Homing of Mesenchymal Stem Cells after Myocardial Infarction by Upregulating SDF-1/CXCR4: A Pilot Study.
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超声靶向微泡破坏通过上调 SDF-1/CXCR4 改善心肌梗塞后间充质干细胞的迁移和归巢：一项初步研究
DOI：
10.1155/2015/691310
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发表时间：
2015
影响因子：
4.3
通讯作者：
Xu Y
中科院分区：
文献类型：
--
作者：
Li L;Wu S;Liu Z;Zhuo Z;Tan K;Xia H;Zhuo L;Deng X;Gao Y;Xu Y
间充质干细胞（MSC）疗法在治疗心肌梗塞（MI）方面显示出巨大的前景。然而，全身输注后间充质干细胞的低效迁移和归巢限制了其治疗应用。超声靶向微泡破坏（UTMD）已被证明有望改善间充质干细胞向缺血心肌的归巢，但具体机制仍不清楚。我们假设UTMD通过上调SDF-1/CXCR4来促进MSC归巢，本研究旨在探索这种潜在机制。我们分析了 UTMD 治疗后的体外和体内 SDF-1/CXCR4 表达，并计算了 MI 区域归巢 MSC 的数量。体外结果表明，UTMD不仅导致SDF-1分泌增加，而且导致表达表面CXCR4的MSC比例增加。体内研究结果显示，与其他组相比，UTMD联合MSCs输注组归巢的MSCs数量增加，SDF-1/CXCR4表达更高。总之，UTMD可以增加缺血心肌中SDF-1的表达，上调MSCs表面CXCR4的表达，这为UTMD通过SDF-1/CXCR4轴辅助MSCs归巢提供了分子机制。
Mesenchymal stem cell (MSC) therapy shows considerable promise for the treatment of myocardial infarction (MI). However, the inefficient migration and homing of MSCs after systemic infusion have limited their therapeutic applications. Ultrasound-targeted microbubble destruction (UTMD) has proven to be promising to improve the homing of MSCs to the ischemic myocardium, but the concrete mechanism remains unclear. We hypothesize that UTMD promotes MSC homing by upregulating SDF-1/CXCR4, and this study was aimed at exploring this potential mechanism. We analyzed SDF-1/CXCR4 expression after UTMD treatment in vitro and in vivo and counted the number of homing MSCs in MI areas. The in vitro results demonstrated that UTMD not only led to elevated secretion of SDF-1 but also resulted in an increased proportion of MSCs that expressed surface CXCR4. The in vivo findings show an increase in the number of homing MSCs and higher expression of SDF-1/CXCR4 in the UTMD combined with MSCs infusion group compared to other groups. In conclusion, UTMD can increase SDF-1 expression in the ischemic myocardium and upregulate the expression of surface CXCR4 on MSCs, which provides a molecular mechanism for the homing of MSCs assisted by UTMD via SDF-1/CXCR4 axis.
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影响因子：
5.2
作者：
Son, Bo-Ra;Marquez-Curtis, Leah A.;Janowska-Wieczorek, Anna
通讯作者：
Janowska-Wieczorek, Anna
DOI：
10.1161/01.atv.0000179768.06206.cb
发表时间：
2005-10-01
影响因子：
8.7
作者：
Imada, T;Tatsumi, T;Matsubara, H
通讯作者：
Matsubara, H
间充质干细胞通过分泌上皮生长因子保护足细胞免受高糖诱导的细胞凋亡
影响因子：
7.5
作者：
Li D;Wang N;Zhang L;Hanyu Z;Xueyuan B;Fu B;Shaoyuan C;Zhang W;Xuefeng S;Li R;Chen X
通讯作者：
Chen X
影响因子：
5.2
作者：
Honczarenko, Marek;Le, Yi;Silberstein, Leslie E.
通讯作者：
Silberstein, Leslie E.
影响因子：
37.8
作者：
Kraitchman, DL;Tatsumi, M;Bulte, JWM
通讯作者：
Bulte, JWM