Abstract
Vessel calcification involves an active cellular process. However, the events by which calcification occurs in vascular endothelial cells have not been sufficiently studied. We performed experiments that evaluated the effect of osteogenic medium (OM) on alkaline phosphatase activity, signaling pathways and cell death in human umbilical vein endothelial cells (HUVEC). We found that OM emits a survival signal at the beginning of cell culture and then causes massive cell death. The formation of intracellular calcium accumulation led to complete calcification spread by alkaline phosphatase produced in stimulated cells. To better understand the signaling networks involved, we analyzed the HUVEC- and HUVEC-treated cell lysates using the Kinexus™ KPSS 1.3 phospho-site pathway screen. Our studies revealed that STAT3 Serine 727 phosphorylation is enhanced in HUVEC. Treatment with 5-aza-2-deoxycytidine led up to inhibition of calcium accumulation induced by OM. These data suggest that under calcifying conditions, STAT3 is a potential important mediator of calcium uptake in endothelial cells. Continuing research is revealing the similarities, differences and deficiencies of STAT3 activities in diverse processes including the calcification of vessels.
Keywords: Vascular calcification, STAT3, Alkaline Phosphatase, 5-aza-2'-deoxycytidine, autophagy
Current Chemical Biology
Title: Enhanced Activity of pSTAT-3 Ser-727 in Functional Endothelial Cells Under Calcifying Conditions
Volume: 4 Issue: 2
Author(s): Jorge Flavio Mendoza-Rincon, Arturo Gonzalez-Robles, Rebeca Lopez-Marure and Julio Roberto Caceres-Cortes
Affiliation:
Keywords: Vascular calcification, STAT3, Alkaline Phosphatase, 5-aza-2'-deoxycytidine, autophagy
Abstract: Vessel calcification involves an active cellular process. However, the events by which calcification occurs in vascular endothelial cells have not been sufficiently studied. We performed experiments that evaluated the effect of osteogenic medium (OM) on alkaline phosphatase activity, signaling pathways and cell death in human umbilical vein endothelial cells (HUVEC). We found that OM emits a survival signal at the beginning of cell culture and then causes massive cell death. The formation of intracellular calcium accumulation led to complete calcification spread by alkaline phosphatase produced in stimulated cells. To better understand the signaling networks involved, we analyzed the HUVEC- and HUVEC-treated cell lysates using the Kinexus™ KPSS 1.3 phospho-site pathway screen. Our studies revealed that STAT3 Serine 727 phosphorylation is enhanced in HUVEC. Treatment with 5-aza-2-deoxycytidine led up to inhibition of calcium accumulation induced by OM. These data suggest that under calcifying conditions, STAT3 is a potential important mediator of calcium uptake in endothelial cells. Continuing research is revealing the similarities, differences and deficiencies of STAT3 activities in diverse processes including the calcification of vessels.
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Cite this article as:
Flavio Mendoza-Rincon Jorge, Gonzalez-Robles Arturo, Lopez-Marure Rebeca and Roberto Caceres-Cortes Julio, Enhanced Activity of pSTAT-3 Ser-727 in Functional Endothelial Cells Under Calcifying Conditions, Current Chemical Biology 2010; 4 (2) . https://dx.doi.org/10.2174/2212796811004020133
DOI https://dx.doi.org/10.2174/2212796811004020133 |
Print ISSN 2212-7968 |
Publisher Name Bentham Science Publisher |
Online ISSN 1872-3136 |
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