Ultrasound-Targeted Microbubble Destruction Improves the Migration and Homing of Mesenchymal Stem Cells after Myocardial Infarction by Upregulating SDF-1/CXCR4: A Pilot Study
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...
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| Main Authors: | , , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Wiley
2015-01-01
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| Series: | Stem Cells International |
| Online Access: | http://dx.doi.org/10.1155/2015/691310 |
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| Summary: | 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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| ISSN: | 1687-966X 1687-9678 |