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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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| Published in: | Molecular and cellular endocrinology 2013-04, Vol.369 (1-2), p.35-41 |
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| container_end_page | 41 |
| container_issue | 1-2 |
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| container_title | Molecular and cellular endocrinology |
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| creator | Weaver, J.R. Taylor-Fishwick, D.A. |
| description | ► 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 |
| doi_str_mv | 10.1016/j.mce.2013.01.011 |
| format | article |
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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<0.05). Regulation of NOX-1 expression in beta cells followed modulation of cellular reactive oxygen species (ROS); pro-oxidants increased NOX-1 (p<0.001) and anti-oxidants decreased NOX-1 (p<0.05). Activation of Src-kinase followed ROS elevation. Inhibition of Src-kinase decreased NOX-1 expression (p<0.01). Beta cell dysfunction, measured by elevated MCP-1 expression, loss of glucose-sensitive insulin secretion or cell death, was induced by pro-inflammatory cytokine stimulation. Importantly, inhibition of Src-kinase or NOX-1 preserved beta cell function and survival. Collectively, these data indicate that expression of NOX-1 in beta cells is regulated in a feed-forward loop mediated by ROS and Src-kinase. Uncoupling of this feed-forward activation could provide new approaches to preserve and protect beta cells in diabetes.</description><identifier>ISSN: 0303-7207</identifier><identifier>EISSN: 1872-8057</identifier><identifier>DOI: 10.1016/j.mce.2013.01.011</identifier><identifier>PMID: 23410839</identifier><language>eng</language><publisher>Ireland: Elsevier Ireland Ltd</publisher><subject>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</subject><ispartof>Molecular and cellular endocrinology, 2013-04, Vol.369 (1-2), p.35-41</ispartof><rights>2013 Elsevier Ireland Ltd</rights><rights>Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c443t-c741fabfea07034d66351302d0b7d48f532a5fb0594eaa2ef4628f5eca4e6bf43</citedby><cites>FETCH-LOGICAL-c443t-c741fabfea07034d66351302d0b7d48f532a5fb0594eaa2ef4628f5eca4e6bf43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27922,27923</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23410839$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Weaver, J.R.</creatorcontrib><creatorcontrib>Taylor-Fishwick, D.A.</creatorcontrib><title>Regulation of NOX-1 expression in beta cells: A positive feedback loop involving the Src-kinase signaling pathway</title><title>Molecular and cellular endocrinology</title><addtitle>Mol Cell Endocrinol</addtitle><description>► 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<0.05). Regulation of NOX-1 expression in beta cells followed modulation of cellular reactive oxygen species (ROS); pro-oxidants increased NOX-1 (p<0.001) and anti-oxidants decreased NOX-1 (p<0.05). Activation of Src-kinase followed ROS elevation. Inhibition of Src-kinase decreased NOX-1 expression (p<0.01). Beta cell dysfunction, measured by elevated MCP-1 expression, loss of glucose-sensitive insulin secretion or cell death, was induced by pro-inflammatory cytokine stimulation. Importantly, inhibition of Src-kinase or NOX-1 preserved beta cell function and survival. Collectively, these data indicate that expression of NOX-1 in beta cells is regulated in a feed-forward loop mediated by ROS and Src-kinase. Uncoupling of this feed-forward activation could provide new approaches to preserve and protect beta cells in diabetes.</description><subject>antioxidants</subject><subject>Apoptosis</subject><subject>Beta cells</subject><subject>cell death</subject><subject>Cell Line</subject><subject>Cell Survival</subject><subject>Cytokines</subject><subject>Diabetes</subject><subject>Feed-forward regulation</subject><subject>Feedback, Physiological</subject><subject>Gene Expression Regulation</subject><subject>Humans</subject><subject>inflammation</subject><subject>insulin secretion</subject><subject>Insulin-Secreting Cells - cytology</subject><subject>Insulin-Secreting Cells - enzymology</subject><subject>NAD(P)H oxidase (H2O2-forming)</subject><subject>NADH, NADPH Oxidoreductases - metabolism</subject><subject>NADPH Oxidase 1</subject><subject>reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Signal Transduction</subject><subject>src-Family Kinases - antagonists & inhibitors</subject><subject>src-Family Kinases - metabolism</subject><subject>Src-kinase</subject><issn>0303-7207</issn><issn>1872-8057</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><recordid>eNp9kE1v1DAQhi0EokvhB3ABH3vJMuOPTQqnquKjUkUlSiVuluOMt95m49TObum_x9EWjkgjjTTzzCv7YewtwhIBVx82y62jpQCUS8BS-IwtsKlF1YCun7MFSJBVLaA-Yq9y3gBArUXzkh0JqRAaebpg9z9ovevtFOLAo-ffr35VyOn3mCjneRYG3tJkuaO-zx_5GR9jDlPYE_dEXWvdHe9jHAu3j_0-DGs-3RK_Tq66C4PNxHNYD7afF6Odbh_s42v2wts-05unfsxuvnz-ef6turz6enF-dlk5peRUuVqht60nCzVI1a1WUqME0UFbd6rxWgqrfQv6VJG1grxaiTIlZxWtWq_kMTs55I4p3u8oT2Yb8vwNO1DcZYMS60ZrLWVB8YC6FHNO5M2YwtamR4NgZtNmY4ppM5s2gKWw3Lx7it-1W-r-XfxVW4D3B8DbaOw6hWxurkuCBsAGhZqJTweCioZ9oGSyCzQ46kIiN5kuhv884A-U8Zg7</recordid><startdate>20130430</startdate><enddate>20130430</enddate><creator>Weaver, J.R.</creator><creator>Taylor-Fishwick, D.A.</creator><general>Elsevier Ireland Ltd</general><scope>FBQ</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20130430</creationdate><title>Regulation of NOX-1 expression in beta cells: A positive feedback loop involving the Src-kinase signaling pathway</title><author>Weaver, J.R. ; Taylor-Fishwick, D.A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c443t-c741fabfea07034d66351302d0b7d48f532a5fb0594eaa2ef4628f5eca4e6bf43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>antioxidants</topic><topic>Apoptosis</topic><topic>Beta cells</topic><topic>cell death</topic><topic>Cell Line</topic><topic>Cell Survival</topic><topic>Cytokines</topic><topic>Diabetes</topic><topic>Feed-forward regulation</topic><topic>Feedback, Physiological</topic><topic>Gene Expression Regulation</topic><topic>Humans</topic><topic>inflammation</topic><topic>insulin secretion</topic><topic>Insulin-Secreting Cells - cytology</topic><topic>Insulin-Secreting Cells - enzymology</topic><topic>NAD(P)H oxidase (H2O2-forming)</topic><topic>NADH, NADPH Oxidoreductases - metabolism</topic><topic>NADPH Oxidase 1</topic><topic>reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Signal Transduction</topic><topic>src-Family Kinases - antagonists & inhibitors</topic><topic>src-Family Kinases - metabolism</topic><topic>Src-kinase</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Weaver, J.R.</creatorcontrib><creatorcontrib>Taylor-Fishwick, D.A.</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular and cellular endocrinology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Weaver, J.R.</au><au>Taylor-Fishwick, D.A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regulation of NOX-1 expression in beta cells: A positive feedback loop involving the Src-kinase signaling pathway</atitle><jtitle>Molecular and cellular endocrinology</jtitle><addtitle>Mol Cell Endocrinol</addtitle><date>2013-04-30</date><risdate>2013</risdate><volume>369</volume><issue>1-2</issue><spage>35</spage><epage>41</epage><pages>35-41</pages><issn>0303-7207</issn><eissn>1872-8057</eissn><abstract>► 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<0.05). Regulation of NOX-1 expression in beta cells followed modulation of cellular reactive oxygen species (ROS); pro-oxidants increased NOX-1 (p<0.001) and anti-oxidants decreased NOX-1 (p<0.05). Activation of Src-kinase followed ROS elevation. Inhibition of Src-kinase decreased NOX-1 expression (p<0.01). Beta cell dysfunction, measured by elevated MCP-1 expression, loss of glucose-sensitive insulin secretion or cell death, was induced by pro-inflammatory cytokine stimulation. Importantly, inhibition of Src-kinase or NOX-1 preserved beta cell function and survival. Collectively, these data indicate that expression of NOX-1 in beta cells is regulated in a feed-forward loop mediated by ROS and Src-kinase. Uncoupling of this feed-forward activation could provide new approaches to preserve and protect beta cells in diabetes.</abstract><cop>Ireland</cop><pub>Elsevier Ireland Ltd</pub><pmid>23410839</pmid><doi>10.1016/j.mce.2013.01.011</doi><tpages>7</tpages></addata></record> |
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| source | ScienceDirect Freedom Collection |
| subjects | 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 |
| title | Regulation of NOX-1 expression in beta cells: A positive feedback loop involving the Src-kinase signaling pathway |
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