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Scientists at Catholic University, Medical Department report research in cellular physiology



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2007 NOV 20 -- According to a study from Santiago, Chile, "Elevated extracellular D-glucose increases transforming growth factor P I (TGF-P 1) release from human umbilical vein endothelium (HUVEC). TGF-P 1, via TGF-P receptors I (T beta RI) and T beta RII, activates Smad2 and mitogen -activated protein kinases p44 and p42 (p42/44 (mapk))."

"We studied whether D-glucose-stimulation Of L-arginine transport and nitric oxide synthesis involves TGF-beta 1 in primary cultures of HUVEC. TGF-P I release was higher (similar to 1.6-fold) in 25 mM (high) compared with 5 mM (normal) D-glucose. TGF-P I increases L-arginine transport (half maximal effect similar to 1.6 ng/ml) in normal D-glucose, but did not alter high D-glucose-increased L-arginine transport. TGF-P I and high D-glucose increased hCAT- I mRNA expression (similar to 8-fold) and maximal transport velocity (V-max), L- [(3) H]citrulline formation from L- [3 H]arginine (index of NO synthesis) and endothelial NO synthase (eNOS) protein abundance, but did not alter eNOS phosphorylation. TGF-beta 1 I and high D-gludose increased p42/44 mapk and Smad2 phosphorylation, an effect blocked by PD-98059 (MEK 1 /2 inhibitor). However, TGF-P I and high D-glucose were ineffective in cells expressing a truncated, negative dominant T beta RII High D-glucose increases L-arginine transport and eNOS expression following T beta RII activation by TGF-P I involving p42/44 (mapk) and Smad2 in HUVEC," wrote R. Vaquez and colleagues, Catholic University, Medical Department.

The researchers concluded: "Thus, TGF-P I could play a crucial role under conditions of hyperglycemia, such as gestational diabetes mellitus, which is'."

Vaquez and colleagues published their study in the Journal of Cellular Physiology (D-Glucose stimulation of L-arginine transport and nitric oxicle synthesis results from activation of mitogen-activated protein kinases p42/44 and smad2 requiring functional type II TGF-beta receptors in human umbilical vein endothelium. Journal of Cellular Physiology, 2007;212(3):626-632).

For more information, contact L. Sobrevia, Pontifical Catholic University, Faculty Medical, Dept. of Obstetrics & Gynecology, Cellular & Molecular Physiol Laboratory, School Medical, Medical Research Center, POB 114-D, Santiago, Chile.

Publisher contact information for the Journal of Cellular Physiology is: Wiley-Liss, Division John Wiley & Sons Inc., 111 River St., Hoboken, NJ 07030, USA.

Keywords: Chile, Santiago, Life Sciences, Nitric Oxide, Pharmaceuticals, Drugs, Therapy, Treatment, Cellular Physiology, Catholic University, Medical Department.

This article was prepared by Science Letter editors from staff and other reports. Copyright 2007, Science Letter via NewsRx.com.