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Published on: February 26, 2021
Caspases and p38 MAPK regulate endothelial cell adhesiveness for mesenchymal stem cells
Irina A Potapova1, Ira S Cohen, Sergey V Doronin
1Department of Physiology and Biophysics, Institute of Molecular Cardiology, Stony Brook University, Stony Brook, New York, United States of America.
Mesenchymal stem cells (MSCs) specifically adhere to distressed endothelial cells. This adhesion is mediated by p38 MAPK activation and caspase potentiation in apoptotic endothelial cells, clarifying MSC homing mechanisms.
Area of Science:
- Cell biology
- Immunology
- Regenerative Medicine
Background:
- Mesenchymal stem cells (MSCs) are crucial for tissue repair and home to injury sites.
- The precise mechanisms governing MSC homing remain largely unknown.
- Endothelial cell distress is implicated in modulating MSC interactions.
Purpose of the Study:
- To elucidate the molecular mechanisms underlying mesenchymal stem cell (MSC) adhesion to endothelial cells at injury sites.
- To investigate the role of endothelial cell apoptosis and associated signaling pathways in MSC homing.
Main Methods:
- Utilized in vitro models of endothelial cell apoptosis.
- Assessed MSC adhesion to apoptotic endothelial cells.
- Investigated the involvement of endothelial caspases and p38 MAPK signaling pathways.
Main Results:
- Endothelial cell apoptosis significantly enhances endothelial cell adhesiveness for MSCs.
- MSC adhesion to apoptotic endothelial cells is dependent on endothelial caspase activation and p38 MAPK signaling.
- p38 MAPK activation is primary, while caspase activation potentiates the adhesion process.
Conclusions:
- MSCs specifically recognize and adhere to distressed or apoptotic endothelial cells.
- The findings reveal a novel mechanism for MSC homing to injury sites.
- This study provides critical insights into the cell-cell interactions governing regenerative processes.
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