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Updated: Aug 29, 2026

Delayed Intramyocardial Delivery of Stem Cells after Ischemia Reperfusion Injury in a Murine Model
Published on: September 3, 2020
Enhanced cytoprotection and angiogenesis by bone marrow cell transplantation may contribute to improved ischemic
Shaoheng Zhang1, Ping Zhang, Jingxuan Guo
1Stem Cell Research Center, Peking University, 38 Xue Yuan Road, Hai Dian District, 100083, Beijing, China
Insights
Bone marrow cell transplantation (BMT) improves heart function after infarction by boosting heat shock proteins (HSPs) and vascular endothelial growth factor (VEGF), promoting healing and cell repair.
Area of Science:
- Cardiovascular Research
- Regenerative Medicine
- Cell Biology
Background:
- Heat shock proteins (HSPs) offer cytoprotection, while vascular endothelial growth factor (VEGF) drives angiogenesis.
- Bone marrow cell transplantation (BMT) is explored for cardiac repair following myocardial infarction.
Purpose of the Study:
- To investigate the roles of cytoprotection and angiogenesis in cardiac function post-BMT.
- To assess the impact of BMT on HSP and VEGF expression and cardiac recovery.
Main Methods:
- Myocardial infarction induced in rats, followed by bone marrow-mononuclear cell transplantation.
- Cardiac function assessed via echocardiography; HSP32, HSP70, and VEGF expression analyzed by immunofluorescence and RT-PCR.
- Angiogenesis quantified by vessel count; transplanted cell differentiation examined.
Main Results:
- BMT significantly improved cardiac function (ejection fraction, fractional shortening).
- HSP32, HSP70, and VEGF expression increased in transplanted cells and cardiomyocytes.
- Enhanced angiogenesis and vessel formation observed in BMT group; transplanted cells showed myocardial and endothelial differentiation.
Conclusions:
- BMT upregulates HSPs and VEGF, enhancing cytoprotection and angiogenesis for early cardiac functional recovery.
- Transplanted cells may differentiate into myocardial and vascular cells, further improving cardiac function in the late phase.
Objectives:
Heat shock proteins (HSPs) are cytoprotective proteins. Vascular endothelial growth factor (VEGF) is the most potent angiogenic factor. This study aimed to elucidate the possible role of cytoprotection and angiogenesis on cardiac function after bone marrow cell transplantation (BMT).
Methods:
Myocardial infarction was induced in inbred Lewis rats by left anterior descending artery ligation. A total of 5 x 10(6) bone marrow-mononuclear cells were transplanted into the ischemic zone by direct injection. At 1, 3, 7, 14 and 28 days post-transplantation, cardiac function was evaluated by echocardiography. The expressions of HSP32, HSP70 and VEGF were assessed by immunofluorescence and RT-PCR. The number of vessels was examined by immunohistochemistry. The differentiation of the transplanted cells was determined by immunofluorescence.
Results:
Echocardiography showed BMT led to sustained improvement in cardiac function, as assessed by left ventricle ejection fraction and fraction of shortening. Immunofluorescence revealed that the expressions of HSP32, HSP70 and VEGF were promoted in both transplanted bone marrow cells and recipient cardiomyocytes. RT-PCR showed that the mRNA expression levels of HSP32, HSP70 and VEGF in the BMT group were markedly higher in comparison with injection of peripheral blood cells or saline (P<0.01) by day 7. Seven days later, the vessel count showed that angiogenesis had been induced to a significantly greater degree in the BMT groups. Fourteen days later, specific markers for myocardial or vascular endothelial cells were detected in the transplanted bone marrow cells.
Conclusions:
BMT upregulated the expressions of HSP32, HSP70 and VEGF in both transplanted bone marrow cells and recipient endogenous cardiomyocytes in the early phase post-transplantation. This enhanced cytoprotection and angiogenesis, and contributed to the functional recovery following cardiac infarction. In the late phase, the transplanted bone marrow cells might differentiate into both myocardial and vascular endothelial cells that enhanced the ischemic cardiac function further.
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