Abstract
Chromogranin A (CgA) is an acidic glycoprotein belonging to a family of regulated secretory proteins stored in the dense core granules of many neuroendocrine cells and neurons. This protein is produced, in certain conditions also by cardiomyocytes, keratinocytes and granulocytes. Upon secretion CgA is released in the extracellular environment and then in circulation. Increased levels of circulating CgA have been detected in patients with cancer, heart failure, hypertension, atrophic gastritis, renal failure, giant cell artheritis, rheumatoid arthritis, sepsis and other inflammatory diseases. Endothelial cells, either those located in the close proximity of secretory cells or in distant tissues, may be exposed, therefore, to variable levels of CgA. In this review we discuss recent findings that implicate CgA and its fragments as a modulators of the physiology of endothelial cells in normal and in pathological conditions. In particular, we review data that suggest that CgA and its N-terminal fragment, called vasostatin-1, are important modulators of the endothelial barrier function and potent inhibitors of the endothelial cell activation caused by inflammatory and pro-angiogenic cytokines, with potential implications in angiogenesis, inflammation and cancer.
Keywords: Chromogranin A, vasostatin-1, TNF, NGR-TNF, VEGF, endothelial cell, vascular leakage, angiogenesis, VE-cadherin, endothelial barrier function, cancer, neuroendocrine tumors.
Current Medicinal Chemistry
Title:Chromogranin A and the Endothelial Barrier Function
Volume: 19 Issue: 24
Author(s): A. Corti and E. Ferrero
Affiliation:
Keywords: Chromogranin A, vasostatin-1, TNF, NGR-TNF, VEGF, endothelial cell, vascular leakage, angiogenesis, VE-cadherin, endothelial barrier function, cancer, neuroendocrine tumors.
Abstract: Chromogranin A (CgA) is an acidic glycoprotein belonging to a family of regulated secretory proteins stored in the dense core granules of many neuroendocrine cells and neurons. This protein is produced, in certain conditions also by cardiomyocytes, keratinocytes and granulocytes. Upon secretion CgA is released in the extracellular environment and then in circulation. Increased levels of circulating CgA have been detected in patients with cancer, heart failure, hypertension, atrophic gastritis, renal failure, giant cell artheritis, rheumatoid arthritis, sepsis and other inflammatory diseases. Endothelial cells, either those located in the close proximity of secretory cells or in distant tissues, may be exposed, therefore, to variable levels of CgA. In this review we discuss recent findings that implicate CgA and its fragments as a modulators of the physiology of endothelial cells in normal and in pathological conditions. In particular, we review data that suggest that CgA and its N-terminal fragment, called vasostatin-1, are important modulators of the endothelial barrier function and potent inhibitors of the endothelial cell activation caused by inflammatory and pro-angiogenic cytokines, with potential implications in angiogenesis, inflammation and cancer.
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Cite this article as:
Corti A. and Ferrero E., Chromogranin A and the Endothelial Barrier Function, Current Medicinal Chemistry 2012; 19 (24) . https://dx.doi.org/10.2174/092986712802429975
DOI https://dx.doi.org/10.2174/092986712802429975 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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