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Am J Physiol Cell Physiol (September 18, 2002). doi:10.1152/ajpcell.00192.2002
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Articles in PresS, published online ahead of print September 18, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00192.2002
Submitted on April 24, 2002
Accepted on September 16, 2002

High Glucose Induced, Endothelin Dependent, Extracellular Matrix Protein Synthesis is Mediated via Nuclear Factor-kappa B and Activating Protein-1

Shali Chen1, Suranjana Mukherjee1, Chandan Chakraborty1, and Subrata Chakrabarti1*

1 Pathology, The University of Western Ontario, London, Ontario, Canada

* To whom correspondence should be addressed. E-mail: schakrab{at}uwo.ca.

Human endothelial cells cultured under high glucose (HG) conditions were shown before to upregulate several basement membrane proteins, including fibronectin (FN); thus mimicking effects of diabetes. Using a human macrovascular (HUVEC) and a microvascular (HMEC) endothelial cell lines, we evaluated in the present study, some of the key molecular signaling events involved in HG-induced FN overexpression. This expression was shown to be dependent on endogenous endothelin (ET)-receptor-mediated signaling. We also examined the roles played by protein kinase-C (PKC), and the transcription factors nuclear factor kappa -{kappa}B (NF-{kappa}B) and activating protein (AP)-1 with respect to such changes. HG, PKC activators and ETs (ET-1 and ET-3) which increased FN expression also caused activation of NF-{kappa}B and AP-1. Inhibitors of both NF-{kappa}B and AP-1 prevented HG- and ET-induced FN production. ET-receptor blockade also prevented these HG-and ET-mediated changes. The results of this study indicate that glucose-induced increased FN production in diabetes may be mediated via ET-dependent NF-{kappa}B and AP-1 activation.




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