Upregulation of pancreatic derived factor (FAM3B) expression in pancreatic β-cells by MCP-1 (CCL2)
► PANDER is a peptide mainly synthesized and secreted by pancreatic β-cells. ► PANDER is involved in impairment of β-cell function under pathological conditions. ► MCP-1 induces PANDER expression at mRNA and protein levels in β-cells and islets. ► MCP-1 upregulates PANDER via Ca2+–ERK1/2–AP-1 and PK...
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| Veröffentlicht in: | Molecular and cellular endocrinology 2011-08, Vol.343 (1-2), p.18-24 |
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| container_title | Molecular and cellular endocrinology |
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| creator | Hou, Xinwei Wang, Oumei Li, Zongmeng Mou, Haiwei Chen, Juan Deng, Bo Qian, Lihua Liu, Xiaolong Le, Yingying |
| description | ► PANDER is a peptide mainly synthesized and secreted by pancreatic β-cells. ► PANDER is involved in impairment of β-cell function under pathological conditions. ► MCP-1 induces PANDER expression at mRNA and protein levels in β-cells and islets. ► MCP-1 upregulates PANDER via Ca2+–ERK1/2–AP-1 and PKC–JNK–AP-1 signaling pathways. ► Our findings are helpful for investigating the pathophysiological roles of PANDER.
Pancreatic derived factor (PANDER, FAM3B) is a peptide mainly synthesized and secreted by pancreatic β-cells. PANDER is proposed to be involved in regulation of β-cell function under physiological conditions and impairment of β-cell function under pathological conditions. MCP-1 (CCL2) is expressed by normal pancreatic islets and has been implicated in inflammation related pancreatic disorders. We examined the effect of MCP-1 on PANDER expression by using murine pancreatic β-cell line MIN6 and pancreatic islets. We found that MCP-1 induced PANDER mRNA transcription and protein synthesis in MIN6 cells and islets. By using calcium chelator (EGTA); inhibitors for PKC (Go6976), MEK1/2 (PD98059) or c-Jun-N-terminal kinase (JNK) (SP600125); c-Jun dominant-negative construct; PANDER promoter luciferase constructs; and islets isolated from Fos knockout mice; we demonstrated that MCP-1 induced PANDER gene expression in β-cells through Ca2+–ERK1/2–AP-1 and PKC–JNK–AP-1 signaling pathways. Our findings suggest a new link between the endocrine and immune systems and provide useful information for further investigating the physiological functions of PANDER and its involvement in inflammation-related pancreatic disorders. |
| doi_str_mv | 10.1016/j.mce.2011.05.039 |
| format | Article |
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Pancreatic derived factor (PANDER, FAM3B) is a peptide mainly synthesized and secreted by pancreatic β-cells. PANDER is proposed to be involved in regulation of β-cell function under physiological conditions and impairment of β-cell function under pathological conditions. MCP-1 (CCL2) is expressed by normal pancreatic islets and has been implicated in inflammation related pancreatic disorders. We examined the effect of MCP-1 on PANDER expression by using murine pancreatic β-cell line MIN6 and pancreatic islets. We found that MCP-1 induced PANDER mRNA transcription and protein synthesis in MIN6 cells and islets. By using calcium chelator (EGTA); inhibitors for PKC (Go6976), MEK1/2 (PD98059) or c-Jun-N-terminal kinase (JNK) (SP600125); c-Jun dominant-negative construct; PANDER promoter luciferase constructs; and islets isolated from Fos knockout mice; we demonstrated that MCP-1 induced PANDER gene expression in β-cells through Ca2+–ERK1/2–AP-1 and PKC–JNK–AP-1 signaling pathways. Our findings suggest a new link between the endocrine and immune systems and provide useful information for further investigating the physiological functions of PANDER and its involvement in inflammation-related pancreatic disorders.</description><identifier>ISSN: 0303-7207</identifier><identifier>EISSN: 1872-8057</identifier><identifier>DOI: 10.1016/j.mce.2011.05.039</identifier><identifier>PMID: 21664946</identifier><language>eng</language><publisher>Ireland: Elsevier Ireland Ltd</publisher><subject>Animals ; calcium ; Calcium - metabolism ; CCL2 ; Cell Line ; chelating agents ; chemokine CCL2 ; Chemokine CCL2 - pharmacology ; Cytokines - genetics ; Cytokines - metabolism ; Enzyme Activation ; ethylene glycol tetraacetic acid ; Extracellular Signal-Regulated MAP Kinases - metabolism ; FAM3B ; gene expression ; Gene Expression - drug effects ; immune system ; inflammation ; Insulin-Secreting Cells - cytology ; Insulin-Secreting Cells - drug effects ; Insulin-Secreting Cells - metabolism ; islets of Langerhans ; JNK Mitogen-Activated Protein Kinases - metabolism ; luciferase ; messenger RNA ; Mice ; Mice, Inbred C57BL ; mitogen-activated protein kinase ; Pancreatic derived factor ; pancreatic diseases ; Pancreatic islet ; Promoter Regions, Genetic ; protein kinase C ; Protein Kinase C - antagonists & inhibitors ; Protein Kinase C - metabolism ; protein synthesis ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Signal transduction ; Signal Transduction - drug effects ; Up-Regulation - drug effects ; β-Cell</subject><ispartof>Molecular and cellular endocrinology, 2011-08, Vol.343 (1-2), p.18-24</ispartof><rights>2011 Elsevier Ireland Ltd</rights><rights>Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c376t-b53180726e47c10ca3daa7ef2df06dae11b384734442f4ae17b671ce5abd87173</citedby><cites>FETCH-LOGICAL-c376t-b53180726e47c10ca3daa7ef2df06dae11b384734442f4ae17b671ce5abd87173</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.mce.2011.05.039$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21664946$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hou, Xinwei</creatorcontrib><creatorcontrib>Wang, Oumei</creatorcontrib><creatorcontrib>Li, Zongmeng</creatorcontrib><creatorcontrib>Mou, Haiwei</creatorcontrib><creatorcontrib>Chen, Juan</creatorcontrib><creatorcontrib>Deng, Bo</creatorcontrib><creatorcontrib>Qian, Lihua</creatorcontrib><creatorcontrib>Liu, Xiaolong</creatorcontrib><creatorcontrib>Le, Yingying</creatorcontrib><title>Upregulation of pancreatic derived factor (FAM3B) expression in pancreatic β-cells by MCP-1 (CCL2)</title><title>Molecular and cellular endocrinology</title><addtitle>Mol Cell Endocrinol</addtitle><description>► PANDER is a peptide mainly synthesized and secreted by pancreatic β-cells. ► PANDER is involved in impairment of β-cell function under pathological conditions. ► MCP-1 induces PANDER expression at mRNA and protein levels in β-cells and islets. ► MCP-1 upregulates PANDER via Ca2+–ERK1/2–AP-1 and PKC–JNK–AP-1 signaling pathways. ► Our findings are helpful for investigating the pathophysiological roles of PANDER.
Pancreatic derived factor (PANDER, FAM3B) is a peptide mainly synthesized and secreted by pancreatic β-cells. PANDER is proposed to be involved in regulation of β-cell function under physiological conditions and impairment of β-cell function under pathological conditions. MCP-1 (CCL2) is expressed by normal pancreatic islets and has been implicated in inflammation related pancreatic disorders. We examined the effect of MCP-1 on PANDER expression by using murine pancreatic β-cell line MIN6 and pancreatic islets. We found that MCP-1 induced PANDER mRNA transcription and protein synthesis in MIN6 cells and islets. By using calcium chelator (EGTA); inhibitors for PKC (Go6976), MEK1/2 (PD98059) or c-Jun-N-terminal kinase (JNK) (SP600125); c-Jun dominant-negative construct; PANDER promoter luciferase constructs; and islets isolated from Fos knockout mice; we demonstrated that MCP-1 induced PANDER gene expression in β-cells through Ca2+–ERK1/2–AP-1 and PKC–JNK–AP-1 signaling pathways. Our findings suggest a new link between the endocrine and immune systems and provide useful information for further investigating the physiological functions of PANDER and its involvement in inflammation-related pancreatic disorders.</description><subject>Animals</subject><subject>calcium</subject><subject>Calcium - metabolism</subject><subject>CCL2</subject><subject>Cell Line</subject><subject>chelating agents</subject><subject>chemokine CCL2</subject><subject>Chemokine CCL2 - pharmacology</subject><subject>Cytokines - genetics</subject><subject>Cytokines - metabolism</subject><subject>Enzyme Activation</subject><subject>ethylene glycol tetraacetic acid</subject><subject>Extracellular Signal-Regulated MAP Kinases - metabolism</subject><subject>FAM3B</subject><subject>gene expression</subject><subject>Gene Expression - drug effects</subject><subject>immune system</subject><subject>inflammation</subject><subject>Insulin-Secreting Cells - cytology</subject><subject>Insulin-Secreting Cells - drug effects</subject><subject>Insulin-Secreting Cells - metabolism</subject><subject>islets of Langerhans</subject><subject>JNK Mitogen-Activated Protein Kinases - metabolism</subject><subject>luciferase</subject><subject>messenger RNA</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>mitogen-activated protein kinase</subject><subject>Pancreatic derived factor</subject><subject>pancreatic diseases</subject><subject>Pancreatic islet</subject><subject>Promoter Regions, Genetic</subject><subject>protein kinase C</subject><subject>Protein Kinase C - antagonists & inhibitors</subject><subject>Protein Kinase C - metabolism</subject><subject>protein synthesis</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Up-Regulation - drug effects</subject><subject>β-Cell</subject><issn>0303-7207</issn><issn>1872-8057</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMFO3DAQhq2KqizbPkAv4BtwSDq2k9iIE41YqLSISu2eLceeIK92k8XOovJaPEifqU4XECdO1kjf_3vmI-Qrg5wBq74t87XFnANjOZQ5iLMPZMKU5JmCUu6RCQgQmeQg98lBjEsAkCVXn8g-Z1VVnBXVhNjFJuDddmUG33e0b-nGdDZgGi11GPwDOtoaO_SBnswubsT3U4p_UiTGkffdW_7vU2ZxtYq0eaQ39c-M0ZO6nvPTz-Rja1YRvzy_U7KYXf6ur7P57dWP-mKeWSGrIWtKwRRIXmEhLQNrhDNGYstdC5UzyFgjVCFFURS8LdIsm0oyi6VpnJJMiik53vVuQn-_xTjotY_jRqbDfhu1Uv_zXCWS7Ugb-hgDtnoT_NqER81Aj2r1Uie1elSrodRJbcocPrdvmzW618SLywQc7YDW9NrcBR_14ldqKAHGu8T47fmOwGThwWPQ0XrsLDof0A7a9f6dBf4ButKRSQ</recordid><startdate>20110822</startdate><enddate>20110822</enddate><creator>Hou, Xinwei</creator><creator>Wang, Oumei</creator><creator>Li, Zongmeng</creator><creator>Mou, Haiwei</creator><creator>Chen, Juan</creator><creator>Deng, Bo</creator><creator>Qian, Lihua</creator><creator>Liu, Xiaolong</creator><creator>Le, Yingying</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>20110822</creationdate><title>Upregulation of pancreatic derived factor (FAM3B) expression in pancreatic β-cells by MCP-1 (CCL2)</title><author>Hou, Xinwei ; Wang, Oumei ; Li, Zongmeng ; Mou, Haiwei ; Chen, Juan ; Deng, Bo ; Qian, Lihua ; Liu, Xiaolong ; Le, Yingying</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c376t-b53180726e47c10ca3daa7ef2df06dae11b384734442f4ae17b671ce5abd87173</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>calcium</topic><topic>Calcium - metabolism</topic><topic>CCL2</topic><topic>Cell Line</topic><topic>chelating agents</topic><topic>chemokine CCL2</topic><topic>Chemokine CCL2 - pharmacology</topic><topic>Cytokines - genetics</topic><topic>Cytokines - metabolism</topic><topic>Enzyme Activation</topic><topic>ethylene glycol tetraacetic acid</topic><topic>Extracellular Signal-Regulated MAP Kinases - metabolism</topic><topic>FAM3B</topic><topic>gene expression</topic><topic>Gene Expression - drug effects</topic><topic>immune system</topic><topic>inflammation</topic><topic>Insulin-Secreting Cells - cytology</topic><topic>Insulin-Secreting Cells - drug effects</topic><topic>Insulin-Secreting Cells - metabolism</topic><topic>islets of Langerhans</topic><topic>JNK Mitogen-Activated Protein Kinases - metabolism</topic><topic>luciferase</topic><topic>messenger RNA</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>mitogen-activated protein kinase</topic><topic>Pancreatic derived factor</topic><topic>pancreatic diseases</topic><topic>Pancreatic islet</topic><topic>Promoter Regions, Genetic</topic><topic>protein kinase C</topic><topic>Protein Kinase C - antagonists & inhibitors</topic><topic>Protein Kinase C - metabolism</topic><topic>protein synthesis</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Up-Regulation - drug effects</topic><topic>β-Cell</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hou, Xinwei</creatorcontrib><creatorcontrib>Wang, Oumei</creatorcontrib><creatorcontrib>Li, Zongmeng</creatorcontrib><creatorcontrib>Mou, Haiwei</creatorcontrib><creatorcontrib>Chen, Juan</creatorcontrib><creatorcontrib>Deng, Bo</creatorcontrib><creatorcontrib>Qian, Lihua</creatorcontrib><creatorcontrib>Liu, Xiaolong</creatorcontrib><creatorcontrib>Le, Yingying</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>Hou, Xinwei</au><au>Wang, Oumei</au><au>Li, Zongmeng</au><au>Mou, Haiwei</au><au>Chen, Juan</au><au>Deng, Bo</au><au>Qian, Lihua</au><au>Liu, Xiaolong</au><au>Le, Yingying</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Upregulation of pancreatic derived factor (FAM3B) expression in pancreatic β-cells by MCP-1 (CCL2)</atitle><jtitle>Molecular and cellular endocrinology</jtitle><addtitle>Mol Cell Endocrinol</addtitle><date>2011-08-22</date><risdate>2011</risdate><volume>343</volume><issue>1-2</issue><spage>18</spage><epage>24</epage><pages>18-24</pages><issn>0303-7207</issn><eissn>1872-8057</eissn><abstract>► PANDER is a peptide mainly synthesized and secreted by pancreatic β-cells. ► PANDER is involved in impairment of β-cell function under pathological conditions. ► MCP-1 induces PANDER expression at mRNA and protein levels in β-cells and islets. ► MCP-1 upregulates PANDER via Ca2+–ERK1/2–AP-1 and PKC–JNK–AP-1 signaling pathways. ► Our findings are helpful for investigating the pathophysiological roles of PANDER.
Pancreatic derived factor (PANDER, FAM3B) is a peptide mainly synthesized and secreted by pancreatic β-cells. PANDER is proposed to be involved in regulation of β-cell function under physiological conditions and impairment of β-cell function under pathological conditions. MCP-1 (CCL2) is expressed by normal pancreatic islets and has been implicated in inflammation related pancreatic disorders. We examined the effect of MCP-1 on PANDER expression by using murine pancreatic β-cell line MIN6 and pancreatic islets. We found that MCP-1 induced PANDER mRNA transcription and protein synthesis in MIN6 cells and islets. By using calcium chelator (EGTA); inhibitors for PKC (Go6976), MEK1/2 (PD98059) or c-Jun-N-terminal kinase (JNK) (SP600125); c-Jun dominant-negative construct; PANDER promoter luciferase constructs; and islets isolated from Fos knockout mice; we demonstrated that MCP-1 induced PANDER gene expression in β-cells through Ca2+–ERK1/2–AP-1 and PKC–JNK–AP-1 signaling pathways. Our findings suggest a new link between the endocrine and immune systems and provide useful information for further investigating the physiological functions of PANDER and its involvement in inflammation-related pancreatic disorders.</abstract><cop>Ireland</cop><pub>Elsevier Ireland Ltd</pub><pmid>21664946</pmid><doi>10.1016/j.mce.2011.05.039</doi><tpages>7</tpages></addata></record> |
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| source | MEDLINE; Elsevier ScienceDirect Journals Complete |
| subjects | Animals calcium Calcium - metabolism CCL2 Cell Line chelating agents chemokine CCL2 Chemokine CCL2 - pharmacology Cytokines - genetics Cytokines - metabolism Enzyme Activation ethylene glycol tetraacetic acid Extracellular Signal-Regulated MAP Kinases - metabolism FAM3B gene expression Gene Expression - drug effects immune system inflammation Insulin-Secreting Cells - cytology Insulin-Secreting Cells - drug effects Insulin-Secreting Cells - metabolism islets of Langerhans JNK Mitogen-Activated Protein Kinases - metabolism luciferase messenger RNA Mice Mice, Inbred C57BL mitogen-activated protein kinase Pancreatic derived factor pancreatic diseases Pancreatic islet Promoter Regions, Genetic protein kinase C Protein Kinase C - antagonists & inhibitors Protein Kinase C - metabolism protein synthesis RNA, Messenger - genetics RNA, Messenger - metabolism Signal transduction Signal Transduction - drug effects Up-Regulation - drug effects β-Cell |
| title | Upregulation of pancreatic derived factor (FAM3B) expression in pancreatic β-cells by MCP-1 (CCL2) |
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