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• W2026273170 abstract "Our previous studies showed that lipopolysaccharide (LPS)-induced nitric oxide (NO) synthesis in cardiovascular tissues is attenuated by protein kinase C (PKC) inhibitors. In the current study, we identify a specific PKC isotype involved in the LPS signal transduction pathway that leads to NO formation in rat vascular smooth muscle cells (VSMC). VSMC were transfected with a mammalian expression vector containing a full length PKCα cDNA insert, and a stable transfectant overexpressing PKCα was obtained as evidenced by increased expression of PKCα mRNA and protein. In response to 100 ng/ml LPS stimulation, the PKCα transfectants showed a 1.8-fold increase in PKC activity at 30 min and a twofold increase in NO production over 24 hr compared with cells transfected with control plasmids. The LPS-stimulated increase in NO synthesis in PKCα transfectants was blocked by the specific PKCα inhibitor Gö 6976. After 6 hr LPS treatment, PKCα-transfected and control cells showed equivalent increases in mRNA and protein for the inducible NO synthase. NO synthase activity of the cell extracts assayed in the presence of excess substrate and cofactors was not significantly different between PKCα-transfected and control cells after LPS stimulation. However, mRNA levels for GTP cyclohydrolase I, a key enzyme in (6R)-tetrahydro-L-biopterin synthesis, and cationic amino acid transporter-2, involved in L-arginine transport, was enhanced in cells overexpressing PKCα compared with control cells. These results suggest that PKCα plays an important role in LPS-induced NO formation and that a significant portion of this effect may be by means of enhanced substrate availability to the inducible nitric oxide synthase enzyme. J. Cell. Physiol. 176:402–411, 1998. © 1998 Wiley-Liss, Inc." @default.
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• W2026273170 date "1998-08-01" @default.
• W2026273170 modified "2023-10-17" @default.
• W2026273170 title "Overexpression of protein kinase Cα enhances lipopolysaccharide-induced nitric oxide formation in vascular smooth muscle cells" @default.
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• W2026273170 doi "https://doi.org/10.1002/(sici)1097-4652(199808)176:2<402::aid-jcp19>3.0.co;2-4" @default.
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