Regulation of NOX-1 expression in beta cells: A positive feedback loop involving the Src-kinase signaling pathway

► Pro-inflammatory cytokines induce NADPH oxidase-1 expression in beta cells. ► Inhibitors of NADPH oxidase block NOX-1 expression in beta cells. ► Cellular reactive oxygen species levels modulate NOX-1 expression in beta cells. ► Src-kinase activation by cellular reactive oxygen species activates N...

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Veröffentlicht in:	Molecular and cellular endocrinology 2013-04, Vol.369 (1-2), p.35-41
Hauptverfasser:	Weaver, J.R., Taylor-Fishwick, D.A.
Format:	Artikel
Sprache:	eng
Schlagworte:	antioxidants Apoptosis Beta cells cell death Cell Line Cell Survival Cytokines Diabetes Feed-forward regulation Feedback, Physiological Gene Expression Regulation Humans inflammation insulin secretion Insulin-Secreting Cells - cytology Insulin-Secreting Cells - enzymology NAD(P)H oxidase (H2O2-forming) NADH, NADPH Oxidoreductases - metabolism NADPH Oxidase 1 reactive oxygen species Reactive Oxygen Species - metabolism Signal Transduction src-Family Kinases - antagonists & inhibitors src-Family Kinases - metabolism Src-kinase
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Zusammenfassung:	► Pro-inflammatory cytokines induce NADPH oxidase-1 expression in beta cells. ► Inhibitors of NADPH oxidase block NOX-1 expression in beta cells. ► Cellular reactive oxygen species levels modulate NOX-1 expression in beta cells. ► Src-kinase activation by cellular reactive oxygen species activates NOX-1 expression. ► Feedback regulation of NOX-1 in β-cells, an enticing therapeutic target in diabetes. NADPH oxidase-1 (NOX-1) is upregulated in beta cells in response to pro-inflammatory cytokines. Inhibition of NADPH oxidase activity blocked stimulated NOX-1 expression (p
ISSN:	0303-7207 1872-8057
DOI:	10.1016/j.mce.2013.01.011