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Published on: March 30, 2022
FoxC1-Induced Vascular Niche Improves Survival and Myocardial Repair of Mesenchymal Stem Cells in Infarcted Hearts
Lan Zhao1,2, Rui Zhang1, Feng Su3
1Department of Cardiology, GuangZhou Red Cross Hospital Medical College of Ji-Nan University, 396 Tongfuzhong Road, Haizhu District, Guangzhou 510220, China.
Insights
Forkhead box C1 (FoxC1) maintains the stem cell niche in infarcted hearts, improving mesenchymal stem cell (MSC) survival and myocardial repair. FoxC1 is crucial for MSC therapy efficacy after myocardial infarction (MI).
Area of Science:
- Cardiovascular Biology
- Stem Cell Biology
- Molecular Mechanisms
Background:
- Forkhead box C1 (FoxC1) is vital for hair follicle stem cell niche maintenance.
- The function of FoxC1 in mesenchymal stem cell (MSC) niches post-myocardial infarction (MI) remains unclear.
- Investigating FoxC1's role in ischemic niches is crucial for understanding MSC survival and function.
Purpose of the Study:
- To elucidate the role and mechanisms of FoxC1 in maintaining MSC survival and function within the ischemic niche after MI.
- To determine if FoxC1 influences MSC capacity and myocardial repair in infarcted hearts.
Main Methods:
- Established a myocardial infarction (MI) model in animals.
- Manipulated FoxC1 expression levels via transfection and siRNA (siFoxC1).
- Administered phosphate-buffered saline (PBS) or MSCs post-MI, assessing outcomes 15 days later.
Main Results:
- FoxC1 regulates the vascular niche in infarcted hearts by modulating proangiogenic and anti-inflammatory factors.
- FoxC1 enhances MSC survival and function in the ischemic environment.
- FoxC1 is essential for vessel specification and differentiation of transplanted MSCs, promoting myocardial repair.
Conclusions:
- FoxC1 signaling is critical for maintaining the ischemic vascular niche.
- FoxC1 plays a key role in enhancing MSC therapy for myocardial repair.
Aims:
Forkhead box C1 (FoxC1) is essential for maintaining the hair follicle stem cell niche. The role of FoxC1 in maintaining mesenchymal stem cell (MSC) niches after myocardial infarction (MI) has not been directly determined to date. In this study, we determined to explore the possible roles and mechanisms of FoxC1 on MSC survival and function in the ischemic niche.
Methods And Results:
MI model was established in this study, and expression level of FoxC1 was overexpressed or knocked down through efficient delivery of FoxC1 transfection or siFoxC1. Fifteen days later, the animals were allocated randomly to receive phosphate-buffered saline (PBS) injection or MSC transplantation. We identified FoxC1 as a key regulator of maintaining the vascular niche in the infarcted hearts (IHs) by driving proangiogenic and anti-inflammatory cytokines while repressing inflammatory and fibrotic factor expression. This vascular niche improved MSC survival and capacity in the IHs. Importantly, FoxC1 interacted with MSCs and was required for vessel specification and differentiation of engrafted MSCs in the ischemic niches, promoting myocardial repair. Inhibiting FoxC1 abolished these effects.
Conclusion:
These results definitively implicate FoxC1 signaling in maintaining ischemic vascular niche, which may be helpful in myocardial repair induced by MSC therapy.
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01:19Mesenchymal Stem Cells
01:26Stem Cell Niche