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CD31+ Circulating Angiogenic Cell Number and Subtypes are Reduced in Individuals with Chronic Stroke
Rian Q Landers-Ramos1, Katherine I Kim2, Brent Hickey1
1Department of Kinesiology, Towson University, Towson, MD, United States.
Insights
Chronic stroke patients have fewer CD31+ circulating angiogenic cells (CACs). These cell subtypes are reduced, but their function in forming vascular networks remains similar to controls, suggesting potential therapeutic targets for stroke recovery.
Area of Science:
- Vascular biology
- Regenerative medicine
- Neurology
Background:
- Reduced CD31+ circulating angiogenic cells (CACs) may underlie vascular issues in chronic stroke.
- Investigating CACs is crucial for understanding stroke pathophysiology.
Purpose of the Study:
- Quantify CD31+ CACs, their subtypes, and paracrine function in chronic stroke patients versus controls.
- Identify potential therapeutic targets for chronic stroke recovery.
Main Methods:
- Isolated peripheral blood mononuclear cells from chronic stroke patients and controls.
- Quantified CD31+ cells and their subtypes (CD14, CD3, CD11b, CD34) using flow cytometry.
- Assessed CD31+ CAC paracrine function via capillary-like network formation assay.
Main Results:
- Chronic stroke patients had significantly fewer CD31+ CACs (-24%, P=0.04).
- Specific subtypes (CD31+/CD14+, CD31+/CD11b+, CD31+/CD3+) were also significantly reduced in stroke patients.
- No significant difference in CD31+ CAC conditioned media's ability to form capillary-like networks was observed between groups.
Conclusions:
- CD31+ CACs and their subtypes are diminished in individuals with chronic stroke.
- These cells and their specific subtypes represent potential therapeutic targets for improving chronic stroke recovery.
Background And Purpose:
Reduced number and function of CD31+ circulating angiogenic cells (CACs) may explain vascular complications associated with the chronic phase stroke. The purpose of this study was to quantify CD31+ CAC paracrine function, total number and number of various subtypes of CD31+ CACs in individuals with chronic stroke compared with controls.
Methods:
Peripheral blood mononuclear cells were isolated from chronic stroke participants and controls. CD31+ cells were quantified by flow cytometry, as was co-expression of CD31 in combination with CD14, CD3, CD11b, or CD34. Immunomagnetically selected CD31+ cells were cultured, and conditioned medium was used in a capillary-like network assay.
Results:
Significantly lower levels of CD31+ CACs were found in stroke participants compared with controls (-24%; P=0.04). Additionally, CD31+/CD14+, CD31+/CD11b+ and CD31+/CD3+ cells were significantly lower in the chronic stroke group compared with controls (-45%, P=0.02; -47%, P=0.02 and -32%, P=0.03, respectively). There was no group effect on CD31+ CAC conditioned media-mediated capillary-like network formation.
Conclusion:
CD31+ CACs and subtypes may serve as potential therapeutic targets in chronic stroke recovery.
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