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Am J Physiol Endocrinol Metab (April 29, 2003). doi:10.1152/ajpendo.00509.2002
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Submitted on November 21, 2002
Accepted on April 21, 2003

Glucose-dependent Insulinotropic Peptide Stimulates 3H-thymidine Incorporation in Vascular Endothelial Cells: Role of Endothelin-1

Ke-Hong Ding1, Qing Zhong1, and Carlos M. Isales2*

1 Institute of Molecular Medicine and Genetics, Department of Medicine, Medical College of Georgia, Augusta, Georgia, USA
2 Institute of Molecular Medicine and Genetics, Department of Medicine, Medical College of Georgia, Augusta, Georgia, USA; Augusta VAMC, Augusta, Georgia, USA

* To whom correspondence should be addressed. E-mail: cisales{at}mail.mcg.edu.

We have previously characterized the receptor for glucose-dependent insulinotropic polypeptide (GIPR) in vascular endothelial cells (EC). Different EC types were found to contain distinct GIPR splice variants. In order to determine if activation of the GIPR splice variants resulted in different cellular responses we examined GIP effects on human umbilical vein endothelial cells (HUVEC- which contain two GIPR splice variants) compared to a spontaneously transformed human umbilical vein EC line, ECV 304 (which contain four GIPR splice variants). GIP dose-dependently stimulated HUVEC and ECV 304 proliferation as measured by [3H]-thymidine incorporation. GIP increased ET-1 secretion from HUVEC but not from ECV 304. Use of the ETbR blocker BQ-788 resulted in an inhibition of [3H]-thymidine incorporation in HUVEC but not in ECV 304. These findings suggest that although GIP increases [3H]-thymidine incorporation in both HUVEC and ECV 304 this proliferative response is mediated by ET-1 only in HUVEC. These differences in cellular response to GIP may be related to differences in activation of GIPR splice variants.




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