Bioactive compound reveals a novel function for ribosomal protein S5 in hepatic stellate cell activation and hepatic fibrosis
Liver fibrosis and its endstage, cirrhosis, represent a major public health problem worldwide. Activation of hepatic stellate cells (HSCs) is a central event in hepatic fibrosis. However, the proteins that control HSC activation are incompletely understood. Here we show that (6aS, 10S, 11aR, 11bR, 1...
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| Veröffentlicht in: | Hepatology (Baltimore, Md.) Md.), 2014-08, Vol.60 (2), p.648-660 |
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| creator | Xu, Wei‐Heng Hu, Hong‐Gang Tian, Yuan Wang, Shao‐Zhan Li, Jie Li, Jian‐Zhong Deng, Xing Qian, Hui Qiu, Lei Hu, Zhen‐Lin Wu, Qiu‐Ye Chai, Yi‐Feng Guo, Cheng Xie, Wei‐Fen Zhang, Jun‐Ping |
| description | Liver fibrosis and its endstage, cirrhosis, represent a major public health problem worldwide. Activation of hepatic stellate cells (HSCs) is a central event in hepatic fibrosis. However, the proteins that control HSC activation are incompletely understood. Here we show that (6aS, 10S, 11aR, 11bR, 11cS)‐10‐methylamino‐dodecahydro‐3a, 7a‐diaza‐benzo [de]anthracene‐8‐thione (MASM) exhibits potent inhibitory activity against liver fibrosis in vitro and in vivo associated with the reduction of Akt phosphorylation. Furthermore, ribosomal protein S5 (RPS5) was identified as a direct target of MASM, which stabilized RPS5 in cultured HSCs and in the liver of experimental animals after dimethylnitrosamine (DMN) or bile duct ligation (BDL). Functional studies revealed that RPS5 could prevent HSC activation. RPS5 overexpression in HSCs resulted in Akt dephosphorylation at both Ser473 and Thr308, and led to subsequent dephosphorylation of GSK3β or P70S6K. Progression of DMN‐ and BDL‐induced hepatic fibrosis was aggravated by Rps5 knockdown and alleviated by RPS5 overexpression, which correlated with the modulation of Akt phosphorylation and HSC number in the fibrotic livers. Moreover, RPS5 was substantially reduced in the transdifferentiated HSCs, experimental fibrotic livers, and human cirrhosis samples. Conclusion: These results demonstrate that RPS5 is implicated in hepatic fibrogenesis and may represent a promising target for potential therapeutic intervention in liver fibrotic diseases. (Hepatology 2014;60:648–660) |
| doi_str_mv | 10.1002/hep.27138 |
| format | Article |
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Activation of hepatic stellate cells (HSCs) is a central event in hepatic fibrosis. However, the proteins that control HSC activation are incompletely understood. Here we show that (6aS, 10S, 11aR, 11bR, 11cS)‐10‐methylamino‐dodecahydro‐3a, 7a‐diaza‐benzo [de]anthracene‐8‐thione (MASM) exhibits potent inhibitory activity against liver fibrosis in vitro and in vivo associated with the reduction of Akt phosphorylation. Furthermore, ribosomal protein S5 (RPS5) was identified as a direct target of MASM, which stabilized RPS5 in cultured HSCs and in the liver of experimental animals after dimethylnitrosamine (DMN) or bile duct ligation (BDL). Functional studies revealed that RPS5 could prevent HSC activation. RPS5 overexpression in HSCs resulted in Akt dephosphorylation at both Ser473 and Thr308, and led to subsequent dephosphorylation of GSK3β or P70S6K. Progression of DMN‐ and BDL‐induced hepatic fibrosis was aggravated by Rps5 knockdown and alleviated by RPS5 overexpression, which correlated with the modulation of Akt phosphorylation and HSC number in the fibrotic livers. Moreover, RPS5 was substantially reduced in the transdifferentiated HSCs, experimental fibrotic livers, and human cirrhosis samples. Conclusion: These results demonstrate that RPS5 is implicated in hepatic fibrogenesis and may represent a promising target for potential therapeutic intervention in liver fibrotic diseases. (Hepatology 2014;60:648–660)</description><identifier>ISSN: 0270-9139</identifier><identifier>EISSN: 1527-3350</identifier><identifier>DOI: 10.1002/hep.27138</identifier><identifier>PMID: 24668691</identifier><identifier>CODEN: HPTLD9</identifier><language>eng</language><publisher>United States: Wolters Kluwer Health, Inc</publisher><subject>Adenoviridae - genetics ; Alkaloids - pharmacology ; Animals ; Bile ; Cell Line, Transformed ; Disease Models, Animal ; Gene Knockdown Techniques ; Hepatic Stellate Cells - drug effects ; Hepatic Stellate Cells - pathology ; Hepatic Stellate Cells - physiology ; Hepatology ; Heterocyclic Compounds, 4 or More Rings - pharmacology ; Liver cirrhosis ; Liver Cirrhosis - drug therapy ; Liver Cirrhosis - pathology ; Liver Cirrhosis - physiopathology ; Male ; Medicine, Chinese Traditional - methods ; Myofibroblasts - drug effects ; Myofibroblasts - pathology ; Myofibroblasts - physiology ; Phosphorylation ; Phosphorylation - drug effects ; Phosphorylation - physiology ; Primary Cell Culture ; Quinolizines - pharmacology ; Rats ; Rats, Sprague-Dawley ; Ribosomal Proteins - genetics ; Ribosomal Proteins - physiology ; Signal Transduction - drug effects ; Signal Transduction - physiology</subject><ispartof>Hepatology (Baltimore, Md.), 2014-08, Vol.60 (2), p.648-660</ispartof><rights>2014 by the American Association for the Study of Liver Diseases</rights><rights>2014 by the American Association for the Study of Liver Diseases.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4208-afced3c798bc8d80fc0dda42cee6b55e281de69731030d0fe8fb7799cccdcb203</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fhep.27138$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fhep.27138$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24668691$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xu, Wei‐Heng</creatorcontrib><creatorcontrib>Hu, Hong‐Gang</creatorcontrib><creatorcontrib>Tian, Yuan</creatorcontrib><creatorcontrib>Wang, Shao‐Zhan</creatorcontrib><creatorcontrib>Li, Jie</creatorcontrib><creatorcontrib>Li, Jian‐Zhong</creatorcontrib><creatorcontrib>Deng, Xing</creatorcontrib><creatorcontrib>Qian, Hui</creatorcontrib><creatorcontrib>Qiu, Lei</creatorcontrib><creatorcontrib>Hu, Zhen‐Lin</creatorcontrib><creatorcontrib>Wu, Qiu‐Ye</creatorcontrib><creatorcontrib>Chai, Yi‐Feng</creatorcontrib><creatorcontrib>Guo, Cheng</creatorcontrib><creatorcontrib>Xie, Wei‐Fen</creatorcontrib><creatorcontrib>Zhang, Jun‐Ping</creatorcontrib><title>Bioactive compound reveals a novel function for ribosomal protein S5 in hepatic stellate cell activation and hepatic fibrosis</title><title>Hepatology (Baltimore, Md.)</title><addtitle>Hepatology</addtitle><description>Liver fibrosis and its endstage, cirrhosis, represent a major public health problem worldwide. Activation of hepatic stellate cells (HSCs) is a central event in hepatic fibrosis. However, the proteins that control HSC activation are incompletely understood. Here we show that (6aS, 10S, 11aR, 11bR, 11cS)‐10‐methylamino‐dodecahydro‐3a, 7a‐diaza‐benzo [de]anthracene‐8‐thione (MASM) exhibits potent inhibitory activity against liver fibrosis in vitro and in vivo associated with the reduction of Akt phosphorylation. Furthermore, ribosomal protein S5 (RPS5) was identified as a direct target of MASM, which stabilized RPS5 in cultured HSCs and in the liver of experimental animals after dimethylnitrosamine (DMN) or bile duct ligation (BDL). Functional studies revealed that RPS5 could prevent HSC activation. RPS5 overexpression in HSCs resulted in Akt dephosphorylation at both Ser473 and Thr308, and led to subsequent dephosphorylation of GSK3β or P70S6K. Progression of DMN‐ and BDL‐induced hepatic fibrosis was aggravated by Rps5 knockdown and alleviated by RPS5 overexpression, which correlated with the modulation of Akt phosphorylation and HSC number in the fibrotic livers. Moreover, RPS5 was substantially reduced in the transdifferentiated HSCs, experimental fibrotic livers, and human cirrhosis samples. Conclusion: These results demonstrate that RPS5 is implicated in hepatic fibrogenesis and may represent a promising target for potential therapeutic intervention in liver fibrotic diseases. (Hepatology 2014;60:648–660)</description><subject>Adenoviridae - genetics</subject><subject>Alkaloids - pharmacology</subject><subject>Animals</subject><subject>Bile</subject><subject>Cell Line, Transformed</subject><subject>Disease Models, Animal</subject><subject>Gene Knockdown Techniques</subject><subject>Hepatic Stellate Cells - drug effects</subject><subject>Hepatic Stellate Cells - pathology</subject><subject>Hepatic Stellate Cells - physiology</subject><subject>Hepatology</subject><subject>Heterocyclic Compounds, 4 or More Rings - pharmacology</subject><subject>Liver cirrhosis</subject><subject>Liver Cirrhosis - drug therapy</subject><subject>Liver Cirrhosis - pathology</subject><subject>Liver Cirrhosis - physiopathology</subject><subject>Male</subject><subject>Medicine, Chinese Traditional - methods</subject><subject>Myofibroblasts - drug effects</subject><subject>Myofibroblasts - pathology</subject><subject>Myofibroblasts - physiology</subject><subject>Phosphorylation</subject><subject>Phosphorylation - drug effects</subject><subject>Phosphorylation - physiology</subject><subject>Primary Cell Culture</subject><subject>Quinolizines - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Ribosomal Proteins - genetics</subject><subject>Ribosomal Proteins - physiology</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - physiology</subject><issn>0270-9139</issn><issn>1527-3350</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkU1PwzAMhiMEYuPjwB9Akbhw6XCSfiRHmPiSJoEEnKs0cUVQ24ymHeLAfycbgwMX25Ifv35lE3LCYMYA-MUrLme8YELukCnLeJEIkcEumQIvIFFMqAk5COENAFTK5T6Z8DTPZa7YlHxdOa_N4FZIjW-Xfuws7XGFuglU086vsKH12EXCd7T2Pe1d5YNvdUOXvR_QdfQpozFGD3pwhoYBm0YPUS5mupHWm2EdlX-h2lW9Dy4ckb06bsLjbT4kLzfXz_O7ZPFwez-_XCQm5SATXRu0whRKVkZaCbUBa3XKDWJeZRlyySzmqhAMBFioUdZVUShljLGm4iAOyfmPbvT8PmIYytaFtUHdoR9DybJUMpXxVEb07B_65se-i-7WVCEEy9iaOt1SY9WiLZe9a3X_Wf4eNgIXP8CHa_Dzr8-gXH-sjIcoNx8r764fN4X4BrV6io4</recordid><startdate>201408</startdate><enddate>201408</enddate><creator>Xu, Wei‐Heng</creator><creator>Hu, Hong‐Gang</creator><creator>Tian, Yuan</creator><creator>Wang, Shao‐Zhan</creator><creator>Li, Jie</creator><creator>Li, Jian‐Zhong</creator><creator>Deng, Xing</creator><creator>Qian, Hui</creator><creator>Qiu, Lei</creator><creator>Hu, Zhen‐Lin</creator><creator>Wu, Qiu‐Ye</creator><creator>Chai, Yi‐Feng</creator><creator>Guo, Cheng</creator><creator>Xie, Wei‐Fen</creator><creator>Zhang, Jun‐Ping</creator><general>Wolters Kluwer Health, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>201408</creationdate><title>Bioactive compound reveals a novel function for ribosomal protein S5 in hepatic stellate cell activation and hepatic fibrosis</title><author>Xu, Wei‐Heng ; 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Activation of hepatic stellate cells (HSCs) is a central event in hepatic fibrosis. However, the proteins that control HSC activation are incompletely understood. Here we show that (6aS, 10S, 11aR, 11bR, 11cS)‐10‐methylamino‐dodecahydro‐3a, 7a‐diaza‐benzo [de]anthracene‐8‐thione (MASM) exhibits potent inhibitory activity against liver fibrosis in vitro and in vivo associated with the reduction of Akt phosphorylation. Furthermore, ribosomal protein S5 (RPS5) was identified as a direct target of MASM, which stabilized RPS5 in cultured HSCs and in the liver of experimental animals after dimethylnitrosamine (DMN) or bile duct ligation (BDL). Functional studies revealed that RPS5 could prevent HSC activation. RPS5 overexpression in HSCs resulted in Akt dephosphorylation at both Ser473 and Thr308, and led to subsequent dephosphorylation of GSK3β or P70S6K. Progression of DMN‐ and BDL‐induced hepatic fibrosis was aggravated by Rps5 knockdown and alleviated by RPS5 overexpression, which correlated with the modulation of Akt phosphorylation and HSC number in the fibrotic livers. Moreover, RPS5 was substantially reduced in the transdifferentiated HSCs, experimental fibrotic livers, and human cirrhosis samples. Conclusion: These results demonstrate that RPS5 is implicated in hepatic fibrogenesis and may represent a promising target for potential therapeutic intervention in liver fibrotic diseases. (Hepatology 2014;60:648–660)</abstract><cop>United States</cop><pub>Wolters Kluwer Health, Inc</pub><pmid>24668691</pmid><doi>10.1002/hep.27138</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adenoviridae - genetics Alkaloids - pharmacology Animals Bile Cell Line, Transformed Disease Models, Animal Gene Knockdown Techniques Hepatic Stellate Cells - drug effects Hepatic Stellate Cells - pathology Hepatic Stellate Cells - physiology Hepatology Heterocyclic Compounds, 4 or More Rings - pharmacology Liver cirrhosis Liver Cirrhosis - drug therapy Liver Cirrhosis - pathology Liver Cirrhosis - physiopathology Male Medicine, Chinese Traditional - methods Myofibroblasts - drug effects Myofibroblasts - pathology Myofibroblasts - physiology Phosphorylation Phosphorylation - drug effects Phosphorylation - physiology Primary Cell Culture Quinolizines - pharmacology Rats Rats, Sprague-Dawley Ribosomal Proteins - genetics Ribosomal Proteins - physiology Signal Transduction - drug effects Signal Transduction - physiology |
| title | Bioactive compound reveals a novel function for ribosomal protein S5 in hepatic stellate cell activation and hepatic fibrosis |
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