Title : 20-HETE-induced mitochondrial superoxide production and inflammatory phenotype in vascular smooth muscle is prevented by glucose-6-phosphate dehydrogenase inhibition.

Pub. Date : 2016 May 1

PMID : 26921441






4 Functional Relationships(s)
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1 20-HETE-induced mitochondrial superoxide production and inflammatory phenotype in vascular smooth muscle is prevented by glucose-6-phosphate dehydrogenase inhibition. Superoxides glucose-6-phosphate dehydrogenase Homo sapiens
2 Lipidomic analysis indicated that G6PD inhibition and knockdown decreased 20-HETE levels in pulmonary arteries as well as 20-HETE-induced 1) mitochondrial superoxide production, 2) activation of mitogen-activated protein kinase 1 and 3, 3) phosphorylation of ETS domain-containing protein Elk-1 that activate transcription of tumor necrosis factor-alpha gene (Tnfa), and 4) expression of tumor necrosis factor-alpha (TNF-alpha). Superoxides glucose-6-phosphate dehydrogenase Homo sapiens
3 Moreover, inhibition of G6PD increased protein kinase G1alpha activity, which, at least partially, mitigated superoxide production and Elk-1 and TNF-alpha expression. Superoxides glucose-6-phosphate dehydrogenase Homo sapiens
4 In summary, our findings indicate that 20-HETE elicited mitochondrial superoxide production and promoted secretory phenotype of vascular smooth muscle cells by activating MAPK1-Elk-1, all of which are blocked by inhibition of G6PD. Superoxides glucose-6-phosphate dehydrogenase Homo sapiens