Defective differentiation of adipose precursor cells from lipodystrophic mice lacking perilipin 1
Perilipin 1 (Plin1) localizes at the surface of lipid droplets to regulate triglyceride storage and hydrolysis in adipocytes. Plin1 defect leads to low adiposity in mice and partial lipodystrophy in human. This study investigated the roles of Plin1 in adipocyte differentiation. Plin1 null (-/-) mice...
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| description | Perilipin 1 (Plin1) localizes at the surface of lipid droplets to regulate triglyceride storage and hydrolysis in adipocytes. Plin1 defect leads to low adiposity in mice and partial lipodystrophy in human. This study investigated the roles of Plin1 in adipocyte differentiation. Plin1 null (-/-) mice showed plenty of multilocular adipocytes and small unilocular adipocytes in adipose tissue, along with lack of a subpopulation of adipose progenitor cells capable of in vivo adipogenesis and along with downregulation of adipogenic pathway. Before initiation of differentiation, adipose stromal-vascular cells (SVCs) from Plin1-/- mice already accumulated numerous tiny lipid droplets, which increased in number and size during the first 12-h induction but thereafter became disappeared at day 1 of differentiation. The adipogenic signaling was dysregulated despite protein level of PPARγ was near normal in Plin1-/- SVCs like in Plin1-/- adipose tissue. Heterozygous Plin1+/- SVCs were able to develop lipid droplets, with both the number and size more than in Plin1-/- SVCs but less than in Plin1+/+ SVCs, indicating that Plin1 haploinsufficiency accounts for attenuated adipogenesis. Aberrant lipid droplet growth and differentiation of Plin1-/- SVCs were rescued by adenoviral Plin1 expression and were ameliorated by enhanced or prolonged adipogenic stimulation. Our finding suggests that Plin1 plays an important role in adipocyte differentiation and provides an insight into the pathology of partial lipodystrophy in patients with Plin1 mutation. |
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Plin1 defect leads to low adiposity in mice and partial lipodystrophy in human. This study investigated the roles of Plin1 in adipocyte differentiation. Plin1 null (-/-) mice showed plenty of multilocular adipocytes and small unilocular adipocytes in adipose tissue, along with lack of a subpopulation of adipose progenitor cells capable of in vivo adipogenesis and along with downregulation of adipogenic pathway. Before initiation of differentiation, adipose stromal-vascular cells (SVCs) from Plin1-/- mice already accumulated numerous tiny lipid droplets, which increased in number and size during the first 12-h induction but thereafter became disappeared at day 1 of differentiation. The adipogenic signaling was dysregulated despite protein level of PPARγ was near normal in Plin1-/- SVCs like in Plin1-/- adipose tissue. Heterozygous Plin1+/- SVCs were able to develop lipid droplets, with both the number and size more than in Plin1-/- SVCs but less than in Plin1+/+ SVCs, indicating that Plin1 haploinsufficiency accounts for attenuated adipogenesis. Aberrant lipid droplet growth and differentiation of Plin1-/- SVCs were rescued by adenoviral Plin1 expression and were ameliorated by enhanced or prolonged adipogenic stimulation. Our finding suggests that Plin1 plays an important role in adipocyte differentiation and provides an insight into the pathology of partial lipodystrophy in patients with Plin1 mutation.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0117536</identifier><identifier>PMID: 25695774</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>1-Methyl-3-isobutylxanthine - pharmacology ; Adenoviruses ; Adipocytes ; Adipogenesis ; Adipogenesis - drug effects ; Adipose tissue ; Adipose Tissue - cytology ; Adipose Tissue - metabolism ; Animals ; Biosynthesis ; Body fat ; Carrier Proteins - genetics ; Carrier Proteins - metabolism ; CCAAT-Enhancer-Binding Proteins - genetics ; CCAAT-Enhancer-Binding Proteins - metabolism ; Cells (biology) ; Cytoplasm ; Diabetes ; Differentiation ; Droplets ; Gene expression ; Haploinsufficiency ; Immunoglobulins ; Kinases ; Lipid Metabolism - physiology ; Lipids ; Lipodystrophy ; Lipodystrophy - metabolism ; Lipodystrophy - pathology ; Lipolysis - physiology ; Metabolism ; Mice ; Mice, Knockout ; Microscopy, Fluorescence ; Mutation ; Perilipin-1 ; Phosphodiesterase Inhibitors - pharmacology ; Phosphoproteins - genetics ; Phosphoproteins - metabolism ; Physiology ; PPAR gamma - genetics ; PPAR gamma - metabolism ; Progenitor cells ; Proteins ; Rodents ; Signal Transduction ; Stem cells ; Stem Cells - cytology ; Stem Cells - metabolism ; Sterol Regulatory Element Binding Protein 1 - genetics ; Sterol Regulatory Element Binding Protein 1 - metabolism ; Triglycerides</subject><ispartof>PloS one, 2015-02, Vol.10 (2), p.e0117536-e0117536</ispartof><rights>COPYRIGHT 2015 Public Library of Science</rights><rights>2015 Lyu 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>2015 Lyu et al 2015 Lyu et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-9110d91b27ca752019a3d8343c830913e42f96e8969ceb9b56c7a37f74d4e8ee3</citedby><cites>FETCH-LOGICAL-c692t-9110d91b27ca752019a3d8343c830913e42f96e8969ceb9b56c7a37f74d4e8ee3</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/PMC4335001/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4335001/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25695774$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Yang, Hongyuan</contributor><creatorcontrib>Lyu, Ying</creatorcontrib><creatorcontrib>Su, Xueying</creatorcontrib><creatorcontrib>Deng, Jingna</creatorcontrib><creatorcontrib>Liu, Shangxin</creatorcontrib><creatorcontrib>Zou, Liangqiang</creatorcontrib><creatorcontrib>Zhao, Xiaojing</creatorcontrib><creatorcontrib>Wei, Suning</creatorcontrib><creatorcontrib>Geng, Bin</creatorcontrib><creatorcontrib>Xu, Guoheng</creatorcontrib><title>Defective differentiation of adipose precursor cells from lipodystrophic mice lacking perilipin 1</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Perilipin 1 (Plin1) localizes at the surface of lipid droplets to regulate triglyceride storage and hydrolysis in adipocytes. Plin1 defect leads to low adiposity in mice and partial lipodystrophy in human. This study investigated the roles of Plin1 in adipocyte differentiation. Plin1 null (-/-) mice showed plenty of multilocular adipocytes and small unilocular adipocytes in adipose tissue, along with lack of a subpopulation of adipose progenitor cells capable of in vivo adipogenesis and along with downregulation of adipogenic pathway. Before initiation of differentiation, adipose stromal-vascular cells (SVCs) from Plin1-/- mice already accumulated numerous tiny lipid droplets, which increased in number and size during the first 12-h induction but thereafter became disappeared at day 1 of differentiation. The adipogenic signaling was dysregulated despite protein level of PPARγ was near normal in Plin1-/- SVCs like in Plin1-/- adipose tissue. Heterozygous Plin1+/- SVCs were able to develop lipid droplets, with both the number and size more than in Plin1-/- SVCs but less than in Plin1+/+ SVCs, indicating that Plin1 haploinsufficiency accounts for attenuated adipogenesis. Aberrant lipid droplet growth and differentiation of Plin1-/- SVCs were rescued by adenoviral Plin1 expression and were ameliorated by enhanced or prolonged adipogenic stimulation. Our finding suggests that Plin1 plays an important role in adipocyte differentiation and provides an insight into the pathology of partial lipodystrophy in patients with Plin1 mutation.</description><subject>1-Methyl-3-isobutylxanthine - pharmacology</subject><subject>Adenoviruses</subject><subject>Adipocytes</subject><subject>Adipogenesis</subject><subject>Adipogenesis - drug effects</subject><subject>Adipose tissue</subject><subject>Adipose Tissue - cytology</subject><subject>Adipose Tissue - metabolism</subject><subject>Animals</subject><subject>Biosynthesis</subject><subject>Body fat</subject><subject>Carrier Proteins - genetics</subject><subject>Carrier Proteins - metabolism</subject><subject>CCAAT-Enhancer-Binding Proteins - genetics</subject><subject>CCAAT-Enhancer-Binding Proteins - metabolism</subject><subject>Cells (biology)</subject><subject>Cytoplasm</subject><subject>Diabetes</subject><subject>Differentiation</subject><subject>Droplets</subject><subject>Gene expression</subject><subject>Haploinsufficiency</subject><subject>Immunoglobulins</subject><subject>Kinases</subject><subject>Lipid Metabolism - physiology</subject><subject>Lipids</subject><subject>Lipodystrophy</subject><subject>Lipodystrophy - metabolism</subject><subject>Lipodystrophy - pathology</subject><subject>Lipolysis - physiology</subject><subject>Metabolism</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Microscopy, Fluorescence</subject><subject>Mutation</subject><subject>Perilipin-1</subject><subject>Phosphodiesterase Inhibitors - pharmacology</subject><subject>Phosphoproteins - genetics</subject><subject>Phosphoproteins - metabolism</subject><subject>Physiology</subject><subject>PPAR gamma - genetics</subject><subject>PPAR gamma - metabolism</subject><subject>Progenitor cells</subject><subject>Proteins</subject><subject>Rodents</subject><subject>Signal Transduction</subject><subject>Stem cells</subject><subject>Stem Cells - cytology</subject><subject>Stem Cells - metabolism</subject><subject>Sterol Regulatory Element Binding Protein 1 - genetics</subject><subject>Sterol Regulatory Element Binding Protein 1 - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lyu, Ying</au><au>Su, Xueying</au><au>Deng, Jingna</au><au>Liu, Shangxin</au><au>Zou, Liangqiang</au><au>Zhao, Xiaojing</au><au>Wei, Suning</au><au>Geng, Bin</au><au>Xu, Guoheng</au><au>Yang, Hongyuan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Defective differentiation of adipose precursor cells from lipodystrophic mice lacking perilipin 1</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2015-02-19</date><risdate>2015</risdate><volume>10</volume><issue>2</issue><spage>e0117536</spage><epage>e0117536</epage><pages>e0117536-e0117536</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Perilipin 1 (Plin1) localizes at the surface of lipid droplets to regulate triglyceride storage and hydrolysis in adipocytes. Plin1 defect leads to low adiposity in mice and partial lipodystrophy in human. This study investigated the roles of Plin1 in adipocyte differentiation. Plin1 null (-/-) mice showed plenty of multilocular adipocytes and small unilocular adipocytes in adipose tissue, along with lack of a subpopulation of adipose progenitor cells capable of in vivo adipogenesis and along with downregulation of adipogenic pathway. Before initiation of differentiation, adipose stromal-vascular cells (SVCs) from Plin1-/- mice already accumulated numerous tiny lipid droplets, which increased in number and size during the first 12-h induction but thereafter became disappeared at day 1 of differentiation. The adipogenic signaling was dysregulated despite protein level of PPARγ was near normal in Plin1-/- SVCs like in Plin1-/- adipose tissue. Heterozygous Plin1+/- SVCs were able to develop lipid droplets, with both the number and size more than in Plin1-/- SVCs but less than in Plin1+/+ SVCs, indicating that Plin1 haploinsufficiency accounts for attenuated adipogenesis. Aberrant lipid droplet growth and differentiation of Plin1-/- SVCs were rescued by adenoviral Plin1 expression and were ameliorated by enhanced or prolonged adipogenic stimulation. Our finding suggests that Plin1 plays an important role in adipocyte differentiation and provides an insight into the pathology of partial lipodystrophy in patients with Plin1 mutation.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25695774</pmid><doi>10.1371/journal.pone.0117536</doi><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_plos_journals_1656299173 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS); EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | 1-Methyl-3-isobutylxanthine - pharmacology Adenoviruses Adipocytes Adipogenesis Adipogenesis - drug effects Adipose tissue Adipose Tissue - cytology Adipose Tissue - metabolism Animals Biosynthesis Body fat Carrier Proteins - genetics Carrier Proteins - metabolism CCAAT-Enhancer-Binding Proteins - genetics CCAAT-Enhancer-Binding Proteins - metabolism Cells (biology) Cytoplasm Diabetes Differentiation Droplets Gene expression Haploinsufficiency Immunoglobulins Kinases Lipid Metabolism - physiology Lipids Lipodystrophy Lipodystrophy - metabolism Lipodystrophy - pathology Lipolysis - physiology Metabolism Mice Mice, Knockout Microscopy, Fluorescence Mutation Perilipin-1 Phosphodiesterase Inhibitors - pharmacology Phosphoproteins - genetics Phosphoproteins - metabolism Physiology PPAR gamma - genetics PPAR gamma - metabolism Progenitor cells Proteins Rodents Signal Transduction Stem cells Stem Cells - cytology Stem Cells - metabolism Sterol Regulatory Element Binding Protein 1 - genetics Sterol Regulatory Element Binding Protein 1 - metabolism Triglycerides |
| title | Defective differentiation of adipose precursor cells from lipodystrophic mice lacking perilipin 1 |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-07T11%3A12%3A13IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Defective%20differentiation%20of%20adipose%20precursor%20cells%20from%20lipodystrophic%20mice%20lacking%20perilipin%201&rft.jtitle=PloS%20one&rft.au=Lyu,%20Ying&rft.date=2015-02-19&rft.volume=10&rft.issue=2&rft.spage=e0117536&rft.epage=e0117536&rft.pages=e0117536-e0117536&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0117536&rft_dat=%3Cgale_plos_%3EA423951044%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1656299173&rft_id=info:pmid/25695774&rft_galeid=A423951044&rft_doaj_id=oai_doaj_org_article_9eafb28360a447c69c492c8b403d9ce3&rfr_iscdi=true |