Comparative proteomic study reveals 17β-HSD13 as a pathogenic protein in nonalcoholic fatty liver disease
Nonalcoholic fatty liver disease (NAFLD) is characterized by a massive accumulation of lipid droplets (LDs). The aim of this study was to determine the function of 17β-hydroxysteroid dehydrogenase-13 (17β-HSD13), one of our newly identified LD-associated proteins in human subjects with normal liver...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2014-08, Vol.111 (31), p.11437-11442 |
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| creator | Su, Wen Wang, Yang Jia, Xiao Wu, Wenhan Li, Linghai Tian, Xiaodong Li, Sha Wang, Chunjiong Xu, Huamin Cao, Jiaqi Han, Qifei Xu, Shimeng Chen, Yong Zhong, Yanfeng Zhang, Xiaoyan Liu, Pingsheng Gustafsson, Jan-Åke Guan, Youfei |
| description | Nonalcoholic fatty liver disease (NAFLD) is characterized by a massive accumulation of lipid droplets (LDs). The aim of this study was to determine the function of 17β-hydroxysteroid dehydrogenase-13 (17β-HSD13), one of our newly identified LD-associated proteins in human subjects with normal liver histology and simple steatosis, in NAFLD development. LDs were isolated from 21 human liver biopsies, including 9 cases with normal liver histology (group 1) and 12 cases with simple steatosis (group 2). A complete set of LD-associated proteins from three liver samples of group 1 or group 2 were determined by 2D LC-MS/MS. By comparing the LD-associated protein profiles between subjects with or without NAFLD, 54 up-regulated and 35 down-regulated LD-associated proteins were found in NAFLD patients. Among them, 17β-HSD13 represents a previously unidentified LD-associated protein with a significant up-regulation in NAFLD. Because the 17β-HSD family plays an important role in lipid metabolism, 17β-HSD13 was selected for validating the proteomic findings and exploring its role in the pathogenesis of NAFLD. Increased hepatic 17β-HSD13 and its LD surface location were confirmed in db/db (diabetic) and high-fat diet-fed mice. Adenovirus-mediated hepatic overexpression of human 17β-HSD13 induced a fatty liver phenotype in C57BL/6 mice, with a significant increase in mature sterol regulatory element-binding protein 1 and fatty acid synthase levels. The present study reports an extensive set of human liver LD proteins and an array of proteins differentially expressed in human NAFLD. We also identified 17β-HSD13 as a pathogenic protein in the development of NAFLD. |
| doi_str_mv | 10.1073/pnas.1410741111 |
| format | Article |
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The aim of this study was to determine the function of 17β-hydroxysteroid dehydrogenase-13 (17β-HSD13), one of our newly identified LD-associated proteins in human subjects with normal liver histology and simple steatosis, in NAFLD development. LDs were isolated from 21 human liver biopsies, including 9 cases with normal liver histology (group 1) and 12 cases with simple steatosis (group 2). A complete set of LD-associated proteins from three liver samples of group 1 or group 2 were determined by 2D LC-MS/MS. By comparing the LD-associated protein profiles between subjects with or without NAFLD, 54 up-regulated and 35 down-regulated LD-associated proteins were found in NAFLD patients. Among them, 17β-HSD13 represents a previously unidentified LD-associated protein with a significant up-regulation in NAFLD. Because the 17β-HSD family plays an important role in lipid metabolism, 17β-HSD13 was selected for validating the proteomic findings and exploring its role in the pathogenesis of NAFLD. Increased hepatic 17β-HSD13 and its LD surface location were confirmed in db/db (diabetic) and high-fat diet-fed mice. Adenovirus-mediated hepatic overexpression of human 17β-HSD13 induced a fatty liver phenotype in C57BL/6 mice, with a significant increase in mature sterol regulatory element-binding protein 1 and fatty acid synthase levels. The present study reports an extensive set of human liver LD proteins and an array of proteins differentially expressed in human NAFLD. We also identified 17β-HSD13 as a pathogenic protein in the development of NAFLD.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.1410741111</identifier><identifier>PMID: 25028495</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>17-Hydroxysteroid Dehydrogenases - metabolism ; Animals ; Biological Sciences ; biopsy ; Cell lines ; Cells, Cultured ; Diet, High-Fat ; droplets ; Epithelial cells ; Fatty liver ; Fatty Liver - enzymology ; Fatty Liver - pathology ; fatty-acid synthase ; gene expression regulation ; gene overexpression ; Hepatocytes ; Hepatocytes - enzymology ; Hepatocytes - pathology ; histology ; Humans ; Lipid metabolism ; Lipids ; Lipids - chemistry ; Lipogenesis ; Liver ; Liver - enzymology ; Liver - pathology ; Male ; Mice ; Mice, Inbred C57BL ; Non-alcoholic Fatty Liver Disease ; Pathogenesis ; patients ; phenotype ; proteins ; Proteome - metabolism ; Proteomics ; Proteomics - methods ; Reproducibility of Results ; Up-Regulation</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2014-08, Vol.111 (31), p.11437-11442</ispartof><rights>copyright © 1993—2008 National Academy of Sciences of the United States of America</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c497t-8c9430f8cd65c0c579324f2b811a9956da17ba62fe31bdeaa1e7baefb5a09aa83</citedby><cites>FETCH-LOGICAL-c497t-8c9430f8cd65c0c579324f2b811a9956da17ba62fe31bdeaa1e7baefb5a09aa83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/111/31.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/23805811$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/23805811$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,723,776,780,799,881,27901,27902,53766,53768,57992,58225</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25028495$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Su, Wen</creatorcontrib><creatorcontrib>Wang, Yang</creatorcontrib><creatorcontrib>Jia, Xiao</creatorcontrib><creatorcontrib>Wu, Wenhan</creatorcontrib><creatorcontrib>Li, Linghai</creatorcontrib><creatorcontrib>Tian, Xiaodong</creatorcontrib><creatorcontrib>Li, Sha</creatorcontrib><creatorcontrib>Wang, Chunjiong</creatorcontrib><creatorcontrib>Xu, Huamin</creatorcontrib><creatorcontrib>Cao, Jiaqi</creatorcontrib><creatorcontrib>Han, Qifei</creatorcontrib><creatorcontrib>Xu, Shimeng</creatorcontrib><creatorcontrib>Chen, Yong</creatorcontrib><creatorcontrib>Zhong, Yanfeng</creatorcontrib><creatorcontrib>Zhang, Xiaoyan</creatorcontrib><creatorcontrib>Liu, Pingsheng</creatorcontrib><creatorcontrib>Gustafsson, Jan-Åke</creatorcontrib><creatorcontrib>Guan, Youfei</creatorcontrib><title>Comparative proteomic study reveals 17β-HSD13 as a pathogenic protein in nonalcoholic fatty liver disease</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>Nonalcoholic fatty liver disease (NAFLD) is characterized by a massive accumulation of lipid droplets (LDs). The aim of this study was to determine the function of 17β-hydroxysteroid dehydrogenase-13 (17β-HSD13), one of our newly identified LD-associated proteins in human subjects with normal liver histology and simple steatosis, in NAFLD development. LDs were isolated from 21 human liver biopsies, including 9 cases with normal liver histology (group 1) and 12 cases with simple steatosis (group 2). A complete set of LD-associated proteins from three liver samples of group 1 or group 2 were determined by 2D LC-MS/MS. By comparing the LD-associated protein profiles between subjects with or without NAFLD, 54 up-regulated and 35 down-regulated LD-associated proteins were found in NAFLD patients. Among them, 17β-HSD13 represents a previously unidentified LD-associated protein with a significant up-regulation in NAFLD. Because the 17β-HSD family plays an important role in lipid metabolism, 17β-HSD13 was selected for validating the proteomic findings and exploring its role in the pathogenesis of NAFLD. Increased hepatic 17β-HSD13 and its LD surface location were confirmed in db/db (diabetic) and high-fat diet-fed mice. Adenovirus-mediated hepatic overexpression of human 17β-HSD13 induced a fatty liver phenotype in C57BL/6 mice, with a significant increase in mature sterol regulatory element-binding protein 1 and fatty acid synthase levels. The present study reports an extensive set of human liver LD proteins and an array of proteins differentially expressed in human NAFLD. We also identified 17β-HSD13 as a pathogenic protein in the development of NAFLD.</description><subject>17-Hydroxysteroid Dehydrogenases - metabolism</subject><subject>Animals</subject><subject>Biological Sciences</subject><subject>biopsy</subject><subject>Cell lines</subject><subject>Cells, Cultured</subject><subject>Diet, High-Fat</subject><subject>droplets</subject><subject>Epithelial cells</subject><subject>Fatty liver</subject><subject>Fatty Liver - enzymology</subject><subject>Fatty Liver - pathology</subject><subject>fatty-acid synthase</subject><subject>gene expression regulation</subject><subject>gene overexpression</subject><subject>Hepatocytes</subject><subject>Hepatocytes - enzymology</subject><subject>Hepatocytes - pathology</subject><subject>histology</subject><subject>Humans</subject><subject>Lipid metabolism</subject><subject>Lipids</subject><subject>Lipids - chemistry</subject><subject>Lipogenesis</subject><subject>Liver</subject><subject>Liver - enzymology</subject><subject>Liver - pathology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Non-alcoholic Fatty Liver Disease</subject><subject>Pathogenesis</subject><subject>patients</subject><subject>phenotype</subject><subject>proteins</subject><subject>Proteome - metabolism</subject><subject>Proteomics</subject><subject>Proteomics - methods</subject><subject>Reproducibility of Results</subject><subject>Up-Regulation</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1u1DAUhSMEotPCmhXgJZu09_onsTdI1UApUiUWpWvrJnFmMsrEwc6MNK_Fg_BMeDrDFFZYlq7t-51jWyfL3iBcIpTiahwoXqJMa4lpPMtmCAbzQhp4ns0AeJlryeVZdh7jCgCM0vAyO-MKuJZGzbLV3K9HCjR1W8fG4Cfn113N4rRpdiy4raM-Mix__cxv7z-hYBQZsZGmpV-4IYGPkm5gaQ5-oL72S9-n85amacf65BpY00VH0b3KXrTJzb0-1ovs4ebz9_ltfvfty9f59V1eS1NOua6NFNDquilUDbUqjeCy5ZVGJGNU0RCWFRW8dQKrxhGhS3vXVorAEGlxkX08-I6bau2a2g1ToN6OoVtT2FlPnf23M3RLu_BbK5FrMHuDD0eD4H9sXJzsuou163sanN9EixoECiwV_z-qFGquCw4JvTqgdfAxBteeXoRg92HafZj2KcykePf3R078n_QSwI7AXnmyQ7QCU5GiTMjbA7KKkw9PFkKD0o93vD_0W_KWFqGL9uGeAxYAKKVQIH4Dc9O6uA</recordid><startdate>20140805</startdate><enddate>20140805</enddate><creator>Su, Wen</creator><creator>Wang, Yang</creator><creator>Jia, Xiao</creator><creator>Wu, Wenhan</creator><creator>Li, Linghai</creator><creator>Tian, Xiaodong</creator><creator>Li, Sha</creator><creator>Wang, Chunjiong</creator><creator>Xu, Huamin</creator><creator>Cao, Jiaqi</creator><creator>Han, Qifei</creator><creator>Xu, Shimeng</creator><creator>Chen, Yong</creator><creator>Zhong, Yanfeng</creator><creator>Zhang, Xiaoyan</creator><creator>Liu, Pingsheng</creator><creator>Gustafsson, Jan-Åke</creator><creator>Guan, Youfei</creator><general>National Academy of Sciences</general><general>National Acad Sciences</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><scope>7S9</scope><scope>L.6</scope><scope>5PM</scope></search><sort><creationdate>20140805</creationdate><title>Comparative proteomic study reveals 17β-HSD13 as a pathogenic protein in nonalcoholic fatty liver disease</title><author>Su, Wen ; Wang, Yang ; Jia, Xiao ; Wu, Wenhan ; Li, Linghai ; Tian, Xiaodong ; Li, Sha ; Wang, Chunjiong ; Xu, Huamin ; Cao, Jiaqi ; Han, Qifei ; Xu, Shimeng ; Chen, Yong ; Zhong, Yanfeng ; Zhang, Xiaoyan ; Liu, Pingsheng ; Gustafsson, Jan-Åke ; Guan, Youfei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c497t-8c9430f8cd65c0c579324f2b811a9956da17ba62fe31bdeaa1e7baefb5a09aa83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>17-Hydroxysteroid Dehydrogenases - metabolism</topic><topic>Animals</topic><topic>Biological Sciences</topic><topic>biopsy</topic><topic>Cell lines</topic><topic>Cells, Cultured</topic><topic>Diet, High-Fat</topic><topic>droplets</topic><topic>Epithelial cells</topic><topic>Fatty liver</topic><topic>Fatty Liver - enzymology</topic><topic>Fatty Liver - pathology</topic><topic>fatty-acid synthase</topic><topic>gene expression regulation</topic><topic>gene overexpression</topic><topic>Hepatocytes</topic><topic>Hepatocytes - enzymology</topic><topic>Hepatocytes - pathology</topic><topic>histology</topic><topic>Humans</topic><topic>Lipid metabolism</topic><topic>Lipids</topic><topic>Lipids - chemistry</topic><topic>Lipogenesis</topic><topic>Liver</topic><topic>Liver - enzymology</topic><topic>Liver - pathology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Non-alcoholic Fatty Liver Disease</topic><topic>Pathogenesis</topic><topic>patients</topic><topic>phenotype</topic><topic>proteins</topic><topic>Proteome - metabolism</topic><topic>Proteomics</topic><topic>Proteomics - methods</topic><topic>Reproducibility of Results</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Su, Wen</creatorcontrib><creatorcontrib>Wang, Yang</creatorcontrib><creatorcontrib>Jia, Xiao</creatorcontrib><creatorcontrib>Wu, Wenhan</creatorcontrib><creatorcontrib>Li, Linghai</creatorcontrib><creatorcontrib>Tian, Xiaodong</creatorcontrib><creatorcontrib>Li, Sha</creatorcontrib><creatorcontrib>Wang, Chunjiong</creatorcontrib><creatorcontrib>Xu, Huamin</creatorcontrib><creatorcontrib>Cao, Jiaqi</creatorcontrib><creatorcontrib>Han, Qifei</creatorcontrib><creatorcontrib>Xu, Shimeng</creatorcontrib><creatorcontrib>Chen, Yong</creatorcontrib><creatorcontrib>Zhong, Yanfeng</creatorcontrib><creatorcontrib>Zhang, Xiaoyan</creatorcontrib><creatorcontrib>Liu, Pingsheng</creatorcontrib><creatorcontrib>Gustafsson, Jan-Åke</creatorcontrib><creatorcontrib>Guan, Youfei</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><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Su, Wen</au><au>Wang, Yang</au><au>Jia, Xiao</au><au>Wu, Wenhan</au><au>Li, Linghai</au><au>Tian, Xiaodong</au><au>Li, Sha</au><au>Wang, Chunjiong</au><au>Xu, Huamin</au><au>Cao, Jiaqi</au><au>Han, Qifei</au><au>Xu, Shimeng</au><au>Chen, Yong</au><au>Zhong, Yanfeng</au><au>Zhang, Xiaoyan</au><au>Liu, Pingsheng</au><au>Gustafsson, Jan-Åke</au><au>Guan, Youfei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Comparative proteomic study reveals 17β-HSD13 as a pathogenic protein in nonalcoholic fatty liver disease</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>2014-08-05</date><risdate>2014</risdate><volume>111</volume><issue>31</issue><spage>11437</spage><epage>11442</epage><pages>11437-11442</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><abstract>Nonalcoholic fatty liver disease (NAFLD) is characterized by a massive accumulation of lipid droplets (LDs). The aim of this study was to determine the function of 17β-hydroxysteroid dehydrogenase-13 (17β-HSD13), one of our newly identified LD-associated proteins in human subjects with normal liver histology and simple steatosis, in NAFLD development. LDs were isolated from 21 human liver biopsies, including 9 cases with normal liver histology (group 1) and 12 cases with simple steatosis (group 2). A complete set of LD-associated proteins from three liver samples of group 1 or group 2 were determined by 2D LC-MS/MS. By comparing the LD-associated protein profiles between subjects with or without NAFLD, 54 up-regulated and 35 down-regulated LD-associated proteins were found in NAFLD patients. Among them, 17β-HSD13 represents a previously unidentified LD-associated protein with a significant up-regulation in NAFLD. Because the 17β-HSD family plays an important role in lipid metabolism, 17β-HSD13 was selected for validating the proteomic findings and exploring its role in the pathogenesis of NAFLD. Increased hepatic 17β-HSD13 and its LD surface location were confirmed in db/db (diabetic) and high-fat diet-fed mice. Adenovirus-mediated hepatic overexpression of human 17β-HSD13 induced a fatty liver phenotype in C57BL/6 mice, with a significant increase in mature sterol regulatory element-binding protein 1 and fatty acid synthase levels. The present study reports an extensive set of human liver LD proteins and an array of proteins differentially expressed in human NAFLD. We also identified 17β-HSD13 as a pathogenic protein in the development of NAFLD.</abstract><cop>United States</cop><pub>National Academy of Sciences</pub><pmid>25028495</pmid><doi>10.1073/pnas.1410741111</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 17-Hydroxysteroid Dehydrogenases - metabolism Animals Biological Sciences biopsy Cell lines Cells, Cultured Diet, High-Fat droplets Epithelial cells Fatty liver Fatty Liver - enzymology Fatty Liver - pathology fatty-acid synthase gene expression regulation gene overexpression Hepatocytes Hepatocytes - enzymology Hepatocytes - pathology histology Humans Lipid metabolism Lipids Lipids - chemistry Lipogenesis Liver Liver - enzymology Liver - pathology Male Mice Mice, Inbred C57BL Non-alcoholic Fatty Liver Disease Pathogenesis patients phenotype proteins Proteome - metabolism Proteomics Proteomics - methods Reproducibility of Results Up-Regulation |
| title | Comparative proteomic study reveals 17β-HSD13 as a pathogenic protein in nonalcoholic fatty liver disease |
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