Ultrasound‑targeted microbubble destruction‑mediated Galectin‑7‑siRNA promotes the homing of bone marrow mesenchymal stem cells to alleviate acute myocardial infarction in rats
- Xin Wei
- Yan Zheng
- Weilin Zhang
- Jing Tan
- Hong Zheng
Affiliations: Department of Ultrasound, People's Hospital of Deyang City, Deyang, Sichuan 618000, P.R. China, Department of Cardiology, Guizhou Provincial People's Hospital, Guiyang, Guizhou 550002, P.R. China
- Published online on: December 23, 2020 https://doi.org/10.3892/ijmm.2020.4830
Copyright: © Wei
et al. This is an open access article distributed under the
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Bone marrow mesenchymal stem cells (BMSCs) are accepted as a form of cellular therapy to improve cardiac function following acute myocardial infarction (AMI). The present study was performed to investigate the synergistic effect of ultrasound‑targeted microbubble destruction (UTMD)‑mediated Galectin‑7‑small interfering (si)RNA with the homing of BMSCs for AMI. The rat model of AMI was established, followed by identification of BMSCs. Rats with AMI received BMSC transplantation, BMSC transplantation + UTMD + siRNA negative control, or BMSC transplantation + UTMD + Galectin‑7‑siRNA. The cardiac function, hemodynamics indexes, degree of myocardial fiber injury and expression of apoptosis‑related proteins in myocardial tissues of rats were detected. The homing of BMSCs was observed, and the indexes of myocardial microenvironment and the TGF‑β/Smads pathway‑related proteins in myocardial tissues were determined. AMI rats treated with UTMD‑mediated Galectin‑7‑siRNA exhibited improved cardiac function and hemodynamics‑related indices, decreased myocardial fiber injury and apoptotic cells, as well as enhanced homing ability of BMSCs, improved myocardial microenvironment, and suppressed TGF‑β1/Smads pathway activation. In conclusion, the present study demonstrated that UTMD‑mediated Galectin‑7‑siRNA treatment could enhance the homing ability of BMSCs, thus alleviating AMI in rats.