Regulation of endothelial cell shape and barrier function by chromogranin A.
We have found that chromogranin A (CgA), a protein released in circulation by neuroendocrine cells and neurons, prevents the vascular leakage induced by tumor necrosis factor (TNF) in a mouse model. Studies of the mechanism of action showed that CgA and its NH(2)-terminal fragments inhibit TNF-induced vascular permeability by preventing endothelial cytoskeleton rearrangements. We propose that neuronal/endocrine secretion of CgA could contribute to the regulation of endothelial barrier function and the protection of vessels against plasma leakage in inflammatory diseases.
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DIBIT, San Raffaele H Scientific Institute, via Olgettina 58, 20132 Milan, Italy.
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D000818:Animals; D002478:Cells, Cultured; D053379:Chromogranin A; D002864:Chromogranins / Q000502:physiology*; D004730:Endothelium, Vascular / Q000166:cytology*; D006801:Humans; D007249:Inflammation; D051379:Mice; D008807:Mice, Inbred BALB C; D017434:Protein Structure, Tertiary; D011994:Recombinant Proteins / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
C506150:CHGA protein, human; D053379:Chromogranin A; D002864:Chromogranins; D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha; C506155:chromogranin A, mouse