AI Article Synopsis
- Microvascular hyperpermeability after a burn injury causes shock and cardiovascular collapse if not treated properly.
- GM-CSF has been shown to decrease this permeability and protect microvessels, but its exact mechanism was not previously understood.
- This study found that GM-CSF enhances endothelial cell stability by inhibiting RhoA activity and preserving VE-cadherin localization, which helps prevent cell death and maintain cell connections after burn injury.
Article Abstract
Microvascular hyperpermeability followed by burn injury is the main cause of shock, and cardiovascular collapse can result if the condition is treated improperly. Our previous studies demonstrated that granulocyte/macrophage colony-stimulating factor (GM-CSF) clearly reduces microvascular permeability and protects microvessels against burn injury. However, the mechanism underlying the protective function of GM-CSF on burn-injured microvessels remains unknown. This study aimed to investigate the effect and mechanism of GM-CSF on endothelial cells after exposure to burn serum. We demonstrated that GM-CSF reduced post-burn endothelial "capillary leak" by inhibiting the activity of RhoA and maintaining the membrane localization of VE-cadherin. Membranous VE-cadherin enhances adherens junctions between endothelial cells and co-localizes with and activates VEGFR2, which protect cells from burn serum-induced apoptosis. Our findings suggest that the protective mechanism of GM-CSF on burn serum-injured endothelial monolayer hyperpermeability is achieved by strengthening cell adherens junctions and improving cell viability.
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Source |
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4448188 | PMC |
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