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Am J Physiol Cell Physiol (January 22, 2003). doi:10.1152/ajpcell.00466.2002
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Submitted on October 3, 2002
Accepted on January 11, 2003

High glucose and endothelial cell growth: Novel effects independent of autocrine TGF{beta}1 and hyperosmolarity

Stella McGinn1, Philip Poronnik2, Malcolm King3, Eileen D Gallery1, and Carol A Pollock1*

1 Department of Medicine, Kolling Institute, Royal North Shore Hospital, Sydney, NSW, Australia
2 Department of Medicine, Kolling Institute, Royal North Shore Hospital, Sydney, NSW, Australia; Department of Physiology, University of Sydney, Sydney, NSW, Australia
3 Department of Immunology, Royal North Shore Hospital, Sydney, NSW, Australia

* To whom correspondence should be addressed. E-mail: carpol{at}med.usyd.edu.au.

Methods. Human endothelial cells were exposed to 5mM glucose (control), 25mM (high) glucose or osmotic control for 72 hours. TGF{beta}1 production, cell growth, death and cell cycle progression and the effects of TGF{beta}1 and TGF{beta} neutralisation on these parameters were studied. Results. High glucose and hyperosmolarity increased endothelial TGF{beta}1 secretion (P<0.0001) and bioactivity (P<0.0001). However high glucose had a greater effect on reducing endothelial cell number (P<0.001) and increasing cellular protein content (P < 0.001) than the osmotic control. TGF{beta} antibody only reversed high glucose's antiproliferative and hypertrophic effects. High glucose altered cell cycle progression and cyclin dependent kinase inhibitor (cdki) expression independent of hyperosmolarity. High glucose increased endothelial cell apoptosis (P < 0.01) while hyperosmolarity induced endothelial cell necrosis (P < 0.001). TGF{beta} antibody did not reverse the apoptotic effects observed with high glucose. Exogenous TGF{beta}1 mimicked the increased S phase delay but not endoreduplication observed with high glucose. Conclusion. High glucose altered endothelial cell growth, apoptosis and cell cycle progression. These growth effects occurred principally via a TGF{beta}1 autocrine pathway. In contrast, apoptosis and endoreduplication occurred independent of this cytokine and hyperosmolarity.




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