MafA is required for postnatal proliferation of pancreatic β-cells
The postnatal proliferation and maturation of insulin-secreting pancreatic β-cells are critical for glucose metabolism and disease development in adults. Elucidation of the molecular mechanisms underlying these events will be beneficial to direct the differentiation of stem cells into functional β-c...
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| Veröffentlicht in: | PloS one 2014-08, Vol.9 (8), p.e104184-e104184 |
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| creator | Eto, Koki Nishimura, Wataru Oishi, Hisashi Udagawa, Haruhide Kawaguchi, Miho Hiramoto, Masaki Fujiwara, Toshiyoshi Takahashi, Satoru Yasuda, Kazuki |
| description | The postnatal proliferation and maturation of insulin-secreting pancreatic β-cells are critical for glucose metabolism and disease development in adults. Elucidation of the molecular mechanisms underlying these events will be beneficial to direct the differentiation of stem cells into functional β-cells. Maturation of β-cells is accompanied by increased expression of MafA, an insulin gene transcription factor. Transcriptome analysis of MafA knockout islets revealed MafA is required for the expression of several molecules critical for β-cell function, including Glut2, ZnT8, Granuphilin, Vdr, Pcsk1 and Urocortin 3, as well as Prolactin receptor (Prlr) and its downstream target Cyclin D2 (Ccnd2). Inhibition of MafA expression in mouse islets or β-cell lines resulted in reduced expression of Prlr and Ccnd2, and MafA transactivated the Prlr promoter. Stimulation of β-cells by prolactin resulted in the phosphorylation and translocation of Stat5B and an increased nuclear pool of Ccnd2 via Prlr and Jak2. Consistent with these results, the loss of MafA resulted in impaired proliferation of β-cells at 4 weeks of age. These results suggest that MafA regulates the postnatal proliferation of β-cells via prolactin signaling. |
| doi_str_mv | 10.1371/journal.pone.0104184 |
| format | Article |
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Elucidation of the molecular mechanisms underlying these events will be beneficial to direct the differentiation of stem cells into functional β-cells. Maturation of β-cells is accompanied by increased expression of MafA, an insulin gene transcription factor. Transcriptome analysis of MafA knockout islets revealed MafA is required for the expression of several molecules critical for β-cell function, including Glut2, ZnT8, Granuphilin, Vdr, Pcsk1 and Urocortin 3, as well as Prolactin receptor (Prlr) and its downstream target Cyclin D2 (Ccnd2). Inhibition of MafA expression in mouse islets or β-cell lines resulted in reduced expression of Prlr and Ccnd2, and MafA transactivated the Prlr promoter. Stimulation of β-cells by prolactin resulted in the phosphorylation and translocation of Stat5B and an increased nuclear pool of Ccnd2 via Prlr and Jak2. Consistent with these results, the loss of MafA resulted in impaired proliferation of β-cells at 4 weeks of age. These results suggest that MafA regulates the postnatal proliferation of β-cells via prolactin signaling.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0104184</identifier><identifier>PMID: 25126749</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adults ; Animals ; Animals, Newborn ; Binding sites ; Biology and Life Sciences ; Cell division ; Cell growth ; Cell Line ; Cell lines ; Cell Proliferation ; Cyclin D2 ; Cyclin D2 - genetics ; Cyclin D2 - metabolism ; Dentistry ; Deoxyribonucleic acid ; Diabetes ; DNA ; Embryology ; Endocrinology ; Gene Expression ; Gene Expression Profiling ; Gene Expression Regulation ; Genes, Reporter ; Glucose ; Glucose metabolism ; Glucose transporter ; Growth hormones ; Homeostasis ; Humans ; Insulin ; Insulin resistance ; Insulin-Secreting Cells - metabolism ; Islets of Langerhans - metabolism ; Janus kinase 2 ; Kinases ; Maf Transcription Factors, Large - genetics ; Maf Transcription Factors, Large - metabolism ; Male ; Maturation ; Medicine ; Medicine and Health Sciences ; Metabolic disorders ; Metabolism ; Mice ; Mice, Knockout ; Molecular modelling ; Newborn babies ; Pancreas ; Pharmaceutical sciences ; Phosphorylation ; Pregnancy ; Prolactin ; Promoter Regions, Genetic ; Rats ; Receptors, Prolactin - genetics ; Rodents ; Signal Transduction ; Signaling ; Stem cell transplantation ; Stem cells ; Transcription factors ; Transcriptome ; Translocation ; Urocortin ; Vitamin D receptors</subject><ispartof>PloS one, 2014-08, Vol.9 (8), p.e104184-e104184</ispartof><rights>2014 Eto et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 Eto et al 2014 Eto et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c526t-a15dd09fbbba767ec15a93bf63212c30a3161ccb097105e2538ef2e674ce0a973</citedby><cites>FETCH-LOGICAL-c526t-a15dd09fbbba767ec15a93bf63212c30a3161ccb097105e2538ef2e674ce0a973</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4134197/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4134197/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2095,2914,23846,27903,27904,53769,53771,79346,79347</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25126749$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Abderrahmani, Amar</contributor><creatorcontrib>Eto, Koki</creatorcontrib><creatorcontrib>Nishimura, Wataru</creatorcontrib><creatorcontrib>Oishi, Hisashi</creatorcontrib><creatorcontrib>Udagawa, Haruhide</creatorcontrib><creatorcontrib>Kawaguchi, Miho</creatorcontrib><creatorcontrib>Hiramoto, Masaki</creatorcontrib><creatorcontrib>Fujiwara, Toshiyoshi</creatorcontrib><creatorcontrib>Takahashi, Satoru</creatorcontrib><creatorcontrib>Yasuda, Kazuki</creatorcontrib><title>MafA is required for postnatal proliferation of pancreatic β-cells</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>The postnatal proliferation and maturation of insulin-secreting pancreatic β-cells are critical for glucose metabolism and disease development in adults. Elucidation of the molecular mechanisms underlying these events will be beneficial to direct the differentiation of stem cells into functional β-cells. Maturation of β-cells is accompanied by increased expression of MafA, an insulin gene transcription factor. Transcriptome analysis of MafA knockout islets revealed MafA is required for the expression of several molecules critical for β-cell function, including Glut2, ZnT8, Granuphilin, Vdr, Pcsk1 and Urocortin 3, as well as Prolactin receptor (Prlr) and its downstream target Cyclin D2 (Ccnd2). Inhibition of MafA expression in mouse islets or β-cell lines resulted in reduced expression of Prlr and Ccnd2, and MafA transactivated the Prlr promoter. Stimulation of β-cells by prolactin resulted in the phosphorylation and translocation of Stat5B and an increased nuclear pool of Ccnd2 via Prlr and Jak2. Consistent with these results, the loss of MafA resulted in impaired proliferation of β-cells at 4 weeks of age. These results suggest that MafA regulates the postnatal proliferation of β-cells via prolactin signaling.</description><subject>Adults</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Binding sites</subject><subject>Biology and Life Sciences</subject><subject>Cell division</subject><subject>Cell growth</subject><subject>Cell Line</subject><subject>Cell lines</subject><subject>Cell Proliferation</subject><subject>Cyclin D2</subject><subject>Cyclin D2 - genetics</subject><subject>Cyclin D2 - metabolism</subject><subject>Dentistry</subject><subject>Deoxyribonucleic acid</subject><subject>Diabetes</subject><subject>DNA</subject><subject>Embryology</subject><subject>Endocrinology</subject><subject>Gene Expression</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation</subject><subject>Genes, Reporter</subject><subject>Glucose</subject><subject>Glucose metabolism</subject><subject>Glucose transporter</subject><subject>Growth hormones</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Insulin-Secreting Cells - metabolism</subject><subject>Islets of Langerhans - metabolism</subject><subject>Janus kinase 2</subject><subject>Kinases</subject><subject>Maf Transcription Factors, Large - genetics</subject><subject>Maf Transcription Factors, Large - metabolism</subject><subject>Male</subject><subject>Maturation</subject><subject>Medicine</subject><subject>Medicine and Health Sciences</subject><subject>Metabolic disorders</subject><subject>Metabolism</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Molecular modelling</subject><subject>Newborn babies</subject><subject>Pancreas</subject><subject>Pharmaceutical sciences</subject><subject>Phosphorylation</subject><subject>Pregnancy</subject><subject>Prolactin</subject><subject>Promoter Regions, Genetic</subject><subject>Rats</subject><subject>Receptors, Prolactin - genetics</subject><subject>Rodents</subject><subject>Signal Transduction</subject><subject>Signaling</subject><subject>Stem cell transplantation</subject><subject>Stem cells</subject><subject>Transcription factors</subject><subject>Transcriptome</subject><subject>Translocation</subject><subject>Urocortin</subject><subject>Vitamin D 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is required for postnatal proliferation of pancreatic β-cells</title><author>Eto, Koki ; Nishimura, Wataru ; Oishi, Hisashi ; Udagawa, Haruhide ; Kawaguchi, Miho ; Hiramoto, Masaki ; Fujiwara, Toshiyoshi ; Takahashi, Satoru ; Yasuda, Kazuki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c526t-a15dd09fbbba767ec15a93bf63212c30a3161ccb097105e2538ef2e674ce0a973</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Adults</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Binding sites</topic><topic>Biology and Life Sciences</topic><topic>Cell division</topic><topic>Cell growth</topic><topic>Cell Line</topic><topic>Cell lines</topic><topic>Cell Proliferation</topic><topic>Cyclin D2</topic><topic>Cyclin D2 - genetics</topic><topic>Cyclin D2 - metabolism</topic><topic>Dentistry</topic><topic>Deoxyribonucleic acid</topic><topic>Diabetes</topic><topic>DNA</topic><topic>Embryology</topic><topic>Endocrinology</topic><topic>Gene Expression</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation</topic><topic>Genes, Reporter</topic><topic>Glucose</topic><topic>Glucose metabolism</topic><topic>Glucose transporter</topic><topic>Growth hormones</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Insulin</topic><topic>Insulin resistance</topic><topic>Insulin-Secreting Cells - metabolism</topic><topic>Islets of Langerhans - metabolism</topic><topic>Janus kinase 2</topic><topic>Kinases</topic><topic>Maf Transcription Factors, Large - genetics</topic><topic>Maf Transcription Factors, Large - metabolism</topic><topic>Male</topic><topic>Maturation</topic><topic>Medicine</topic><topic>Medicine and Health Sciences</topic><topic>Metabolic disorders</topic><topic>Metabolism</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Molecular 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Toshiyoshi</au><au>Takahashi, Satoru</au><au>Yasuda, Kazuki</au><au>Abderrahmani, Amar</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MafA is required for postnatal proliferation of pancreatic β-cells</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2014-08-15</date><risdate>2014</risdate><volume>9</volume><issue>8</issue><spage>e104184</spage><epage>e104184</epage><pages>e104184-e104184</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>The postnatal proliferation and maturation of insulin-secreting pancreatic β-cells are critical for glucose metabolism and disease development in adults. Elucidation of the molecular mechanisms underlying these events will be beneficial to direct the differentiation of stem cells into functional β-cells. Maturation of β-cells is accompanied by increased expression of MafA, an insulin gene transcription factor. Transcriptome analysis of MafA knockout islets revealed MafA is required for the expression of several molecules critical for β-cell function, including Glut2, ZnT8, Granuphilin, Vdr, Pcsk1 and Urocortin 3, as well as Prolactin receptor (Prlr) and its downstream target Cyclin D2 (Ccnd2). Inhibition of MafA expression in mouse islets or β-cell lines resulted in reduced expression of Prlr and Ccnd2, and MafA transactivated the Prlr promoter. Stimulation of β-cells by prolactin resulted in the phosphorylation and translocation of Stat5B and an increased nuclear pool of Ccnd2 via Prlr and Jak2. Consistent with these results, the loss of MafA resulted in impaired proliferation of β-cells at 4 weeks of age. These results suggest that MafA regulates the postnatal proliferation of β-cells via prolactin signaling.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25126749</pmid><doi>10.1371/journal.pone.0104184</doi><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2014-08, Vol.9 (8), p.e104184-e104184 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1553532855 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS); PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Adults Animals Animals, Newborn Binding sites Biology and Life Sciences Cell division Cell growth Cell Line Cell lines Cell Proliferation Cyclin D2 Cyclin D2 - genetics Cyclin D2 - metabolism Dentistry Deoxyribonucleic acid Diabetes DNA Embryology Endocrinology Gene Expression Gene Expression Profiling Gene Expression Regulation Genes, Reporter Glucose Glucose metabolism Glucose transporter Growth hormones Homeostasis Humans Insulin Insulin resistance Insulin-Secreting Cells - metabolism Islets of Langerhans - metabolism Janus kinase 2 Kinases Maf Transcription Factors, Large - genetics Maf Transcription Factors, Large - metabolism Male Maturation Medicine Medicine and Health Sciences Metabolic disorders Metabolism Mice Mice, Knockout Molecular modelling Newborn babies Pancreas Pharmaceutical sciences Phosphorylation Pregnancy Prolactin Promoter Regions, Genetic Rats Receptors, Prolactin - genetics Rodents Signal Transduction Signaling Stem cell transplantation Stem cells Transcription factors Transcriptome Translocation Urocortin Vitamin D receptors |
| title | MafA is required for postnatal proliferation of pancreatic β-cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-24T02%3A23%3A03IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=MafA%20is%20required%20for%20postnatal%20proliferation%20of%20pancreatic%20%CE%B2-cells&rft.jtitle=PloS%20one&rft.au=Eto,%20Koki&rft.date=2014-08-15&rft.volume=9&rft.issue=8&rft.spage=e104184&rft.epage=e104184&rft.pages=e104184-e104184&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0104184&rft_dat=%3Cproquest_plos_%3E1554473393%3C/proquest_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1553532855&rft_id=info:pmid/25126749&rft_doaj_id=oai_doaj_org_article_c9f4d253b5bf4608a4f03cdc52bdc1a1&rfr_iscdi=true |