|
|
||||||||
1 and hyperosmolarity
1 Department of Medicine, Kolling Institute: Renal Research Group, and 2 Department of Immunology, Royal North Shore Hospital, St Leonards, 2065; and 3 Department of Physiology, University of Sydney, New South Wales 2006, Australia
Human endothelial cells were
exposed to 5 mM glucose (control), 25 mM (high) glucose, or osmotic
control for 72 h. TGF-
1 production, cell growth, death, and
cell cycle progression, and the effects of TGF-
1 and TGF-
neutralization on these parameters were studied. High glucose and
hyperosmolarity increased endothelial TGF-
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-
antibody only reversed the antiproliferative and
hypertrophic effects of high glucose. High glucose altered cell cycle
progression and cyclin-dependent kinase inhibitor expression
independently of hyperosmolarity. High glucose increased endothelial
cell apoptosis (P < 0.01), whereas
hyperosmolarity induced endothelial cell necrosis (P < 0.001). TGF-
antibody did not reverse the apoptotic effects
observed with high glucose. Exogenous TGF-
1 mimicked the increased S
phase delay but not endoreduplication observed with high glucose. High glucose altered endothelial cell growth, apoptosis, and cell
cycle progression. These growth effects occurred principally via a
TGF-
1 autocrine pathway. In contrast, apoptosis and
endoreduplication occurred independently of this cytokine and hyperosmolarity.
endothelial cells; diabetes mellitus; apoptosis; endoreduplication; transforming growth factor-
1
This article has been cited by other articles:
![]() |
J. L. Vega, C. Puebla, R. Vasquez, M. Farias, J. Alarcon, M. Pastor-Anglada, B. Krause, P. Casanello, and L. Sobrevia TGF-{beta}1 inhibits expression and activity of hENT1 in a nitric oxide-dependent manner in human umbilical vein endothelium Cardiovasc Res, June 1, 2009; 82(3): 458 - 467. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Varma, B. K. Lal, R. Zheng, J. W. Breslin, S. Saito, P. J. Pappas, R. W. Hobson II, and W. N. Duran Hyperglycemia alters PI3k and Akt signaling and leads to endothelial cell proliferative dysfunction Am J Physiol Heart Circ Physiol, October 1, 2005; 289(4): H1744 - H1751. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. McGinn, S. Saad, P. Poronnik, and C. A. Pollock High glucose-mediated effects on endothelial cell proliferation occur via p38 MAP kinase Am J Physiol Endocrinol Metab, October 1, 2003; 285(4): E708 - E717. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |