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Regulation of endothelial cell shape and barrier function by chromogranin A
1DIBIT, San Raffaele H Scientific Institute, via Olgettina 58, 20132 Milan, Italy.
Annals of the New York Academy of Sciences
|November 20, 2002
Summary
Chromogranin A (CgA), a protein from neuroendocrine cells, was found to prevent vascular leakage caused by tumor necrosis factor (TNF). CgA achieves this by inhibiting endothelial cytoskeleton rearrangements, protecting vessels in inflammatory conditions.
Area of Science:
- Biochemistry
- Cell Biology
- Neuroendocrinology
Background:
- Neuroendocrine cells and neurons release chromogranin A (CgA) into circulation.
- Tumor necrosis factor (TNF) is known to induce vascular leakage.
- The role of CgA in regulating vascular permeability is not fully understood.
Purpose of the Study:
- To investigate the effect of chromogranin A (CgA) on TNF-induced vascular leakage.
- To elucidate the mechanism by which CgA influences endothelial barrier function.
Main Methods:
- Utilized a mouse model to study TNF-induced vascular leakage.
- Investigated the molecular mechanisms of CgA's action on endothelial cells.
- Analyzed the impact of CgA and its fragments on endothelial cytoskeleton rearrangements.
Main Results:
- Chromogranin A (CgA) was found to prevent vascular leakage induced by TNF in a mouse model.
- CgA and its NH(2)-terminal fragments inhibit TNF-induced vascular permeability.
- The mechanism involves the prevention of endothelial cytoskeleton rearrangements.
Conclusions:
- Neuronal and endocrine secretion of CgA may play a role in regulating endothelial barrier function.
- CgA could protect vessels against plasma leakage during inflammatory diseases.
- CgA represents a potential therapeutic target for managing vascular leakage in inflammation.