Leukemia inhibitory factor attenuates renal fibrosis through Stat3-miR-29c
Leukemia inhibitory factory (LIF), as a member of the IL-6 family, has been reported to ameliorate myocardial fibrosis and myocardial cell death. The purpose of the present study was to investigate the effect of LIF on renal fibrosis and its underlying mechanism. Our results showed, first, that LIF...
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| Veröffentlicht in: | American journal of physiology. Renal physiology 2015-10, Vol.309 (7), p.F595-F603 |
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| container_title | American journal of physiology. Renal physiology |
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| creator | Yu, Ying Wang, Yumei Niu, Yangyang Fu, Lanjun Chin, Y Eugene Yu, Chen |
| description | Leukemia inhibitory factory (LIF), as a member of the IL-6 family, has been reported to ameliorate myocardial fibrosis and myocardial cell death. The purpose of the present study was to investigate the effect of LIF on renal fibrosis and its underlying mechanism. Our results showed, first, that LIF inhibited collagen type 1 and collagen type 3 expression induced by ANG II in NRK-49F (rat kidney fibroblast) cells and in mice with unilateral ureteral obstruction. Second, LIF induced Stat3 Tyr(705) phosphorylation and inhibited Stat3 Tyr(705) and Ser(727) phosphorylation induced by ANG II in NRK-49F cells. Third, LIF exerted an antirenal fibrosis effect mainly through activation of Stat3 Tyr(705) phosphorylation in NRK-49F cells. These effects of LIF were not observed in Stat3(-/-) cells. Finally, LIF-Stat3 upregulated microRNA-29c expression, and the latter downregulated collagen type 1 and collagen type 3 expression in NRK-49F cells and in mice with unilateral ureteral obstruction. In conclusion, LIF played a role in antirenal fibrosis by competitively activating Stat3 Tyr(705) phosphorylation, which upregulated microRNA-29c to suppress collagen expression. |
| doi_str_mv | 10.1152/ajprenal.00634.2014 |
| format | Article |
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The purpose of the present study was to investigate the effect of LIF on renal fibrosis and its underlying mechanism. Our results showed, first, that LIF inhibited collagen type 1 and collagen type 3 expression induced by ANG II in NRK-49F (rat kidney fibroblast) cells and in mice with unilateral ureteral obstruction. Second, LIF induced Stat3 Tyr(705) phosphorylation and inhibited Stat3 Tyr(705) and Ser(727) phosphorylation induced by ANG II in NRK-49F cells. Third, LIF exerted an antirenal fibrosis effect mainly through activation of Stat3 Tyr(705) phosphorylation in NRK-49F cells. These effects of LIF were not observed in Stat3(-/-) cells. Finally, LIF-Stat3 upregulated microRNA-29c expression, and the latter downregulated collagen type 1 and collagen type 3 expression in NRK-49F cells and in mice with unilateral ureteral obstruction. In conclusion, LIF played a role in antirenal fibrosis by competitively activating Stat3 Tyr(705) phosphorylation, which upregulated microRNA-29c to suppress collagen expression.</description><identifier>ISSN: 1931-857X</identifier><identifier>EISSN: 1522-1466</identifier><identifier>DOI: 10.1152/ajprenal.00634.2014</identifier><identifier>PMID: 26155847</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>Angiotensin II - pharmacology ; Animals ; Apoptosis ; Cells ; Cells, Cultured ; Collagen ; Collagen Type I - biosynthesis ; Collagen Type III - biosynthesis ; Computational Biology ; Extracellular Matrix Proteins - biosynthesis ; Fibrosis ; Gene Knockdown Techniques ; Interleukin-6 - metabolism ; Kidney - pathology ; Kidney Diseases - drug therapy ; Kidney Diseases - pathology ; Leukemia Inhibitory Factor - therapeutic use ; Mice ; MicroRNAs - genetics ; Nephritis, Interstitial - pathology ; Phosphorylation ; Rats ; Rodents ; STAT3 Transcription Factor - genetics ; Transfection ; Ureteral Obstruction - pathology</subject><ispartof>American journal of physiology. Renal physiology, 2015-10, Vol.309 (7), p.F595-F603</ispartof><rights>Copyright © 2015 the American Physiological Society.</rights><rights>Copyright American Physiological Society Oct 1, 2015</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c333t-8090d3629175b67adba297116583ff311e5d9e0bc40642e5641289efb6b479b03</citedby><cites>FETCH-LOGICAL-c333t-8090d3629175b67adba297116583ff311e5d9e0bc40642e5641289efb6b479b03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3026,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26155847$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yu, Ying</creatorcontrib><creatorcontrib>Wang, Yumei</creatorcontrib><creatorcontrib>Niu, Yangyang</creatorcontrib><creatorcontrib>Fu, Lanjun</creatorcontrib><creatorcontrib>Chin, Y Eugene</creatorcontrib><creatorcontrib>Yu, Chen</creatorcontrib><title>Leukemia inhibitory factor attenuates renal fibrosis through Stat3-miR-29c</title><title>American journal of physiology. Renal physiology</title><addtitle>Am J Physiol Renal Physiol</addtitle><description>Leukemia inhibitory factory (LIF), as a member of the IL-6 family, has been reported to ameliorate myocardial fibrosis and myocardial cell death. The purpose of the present study was to investigate the effect of LIF on renal fibrosis and its underlying mechanism. Our results showed, first, that LIF inhibited collagen type 1 and collagen type 3 expression induced by ANG II in NRK-49F (rat kidney fibroblast) cells and in mice with unilateral ureteral obstruction. Second, LIF induced Stat3 Tyr(705) phosphorylation and inhibited Stat3 Tyr(705) and Ser(727) phosphorylation induced by ANG II in NRK-49F cells. Third, LIF exerted an antirenal fibrosis effect mainly through activation of Stat3 Tyr(705) phosphorylation in NRK-49F cells. These effects of LIF were not observed in Stat3(-/-) cells. Finally, LIF-Stat3 upregulated microRNA-29c expression, and the latter downregulated collagen type 1 and collagen type 3 expression in NRK-49F cells and in mice with unilateral ureteral obstruction. In conclusion, LIF played a role in antirenal fibrosis by competitively activating Stat3 Tyr(705) phosphorylation, which upregulated microRNA-29c to suppress collagen expression.</description><subject>Angiotensin II - pharmacology</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Cells</subject><subject>Cells, Cultured</subject><subject>Collagen</subject><subject>Collagen Type I - biosynthesis</subject><subject>Collagen Type III - biosynthesis</subject><subject>Computational Biology</subject><subject>Extracellular Matrix Proteins - biosynthesis</subject><subject>Fibrosis</subject><subject>Gene Knockdown Techniques</subject><subject>Interleukin-6 - metabolism</subject><subject>Kidney - pathology</subject><subject>Kidney Diseases - drug therapy</subject><subject>Kidney Diseases - pathology</subject><subject>Leukemia Inhibitory Factor - therapeutic use</subject><subject>Mice</subject><subject>MicroRNAs - genetics</subject><subject>Nephritis, Interstitial - pathology</subject><subject>Phosphorylation</subject><subject>Rats</subject><subject>Rodents</subject><subject>STAT3 Transcription Factor - genetics</subject><subject>Transfection</subject><subject>Ureteral Obstruction - pathology</subject><issn>1931-857X</issn><issn>1522-1466</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkEtLAzEQx4MotlY_gSALXrxszeS1m6MUnxQEH-BtSXazNnUfNcke-u1NW-vB0wzMb2b4_xA6BzwF4ORaLVfOdKqZYiwomxIM7ACN44SkwIQ4jL2kkOY8-xihE--XGGMAAsdoRARwnrNsjJ7mZvgyrVWJ7RZW29C7dVKrMtZEhWC6QQXjk-2jpLba9d76JCxcP3wuktegAk1b-5ISWZ6io1o13pz91gl6v7t9mz2k8-f7x9nNPC0ppSHNscQVFURCxrXIVKUVkRmA4DmtawpgeCUN1iXDghHDBQOSS1NroVkmNaYTdLW7u3L992B8KFrrS9M0qjP94AvIIJeYM8EjevkPXfaDi1E2FMEsIxGNFN1RZUznnamLlbOtcusCcLFRXexVF1vVxUZ13Lr4vT3o1lR_O3u39AfDOHo4</recordid><startdate>20151001</startdate><enddate>20151001</enddate><creator>Yu, Ying</creator><creator>Wang, Yumei</creator><creator>Niu, Yangyang</creator><creator>Fu, Lanjun</creator><creator>Chin, Y Eugene</creator><creator>Yu, Chen</creator><general>American Physiological Society</general><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>20151001</creationdate><title>Leukemia inhibitory factor attenuates renal fibrosis through Stat3-miR-29c</title><author>Yu, Ying ; Wang, Yumei ; Niu, Yangyang ; Fu, Lanjun ; Chin, Y Eugene ; Yu, Chen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c333t-8090d3629175b67adba297116583ff311e5d9e0bc40642e5641289efb6b479b03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Angiotensin II - pharmacology</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Cells</topic><topic>Cells, Cultured</topic><topic>Collagen</topic><topic>Collagen Type I - biosynthesis</topic><topic>Collagen Type III - biosynthesis</topic><topic>Computational Biology</topic><topic>Extracellular Matrix Proteins - biosynthesis</topic><topic>Fibrosis</topic><topic>Gene Knockdown Techniques</topic><topic>Interleukin-6 - metabolism</topic><topic>Kidney - pathology</topic><topic>Kidney Diseases - drug therapy</topic><topic>Kidney Diseases - pathology</topic><topic>Leukemia Inhibitory Factor - therapeutic use</topic><topic>Mice</topic><topic>MicroRNAs - genetics</topic><topic>Nephritis, Interstitial - pathology</topic><topic>Phosphorylation</topic><topic>Rats</topic><topic>Rodents</topic><topic>STAT3 Transcription Factor - genetics</topic><topic>Transfection</topic><topic>Ureteral Obstruction - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yu, Ying</creatorcontrib><creatorcontrib>Wang, Yumei</creatorcontrib><creatorcontrib>Niu, Yangyang</creatorcontrib><creatorcontrib>Fu, Lanjun</creatorcontrib><creatorcontrib>Chin, Y Eugene</creatorcontrib><creatorcontrib>Yu, Chen</creatorcontrib><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>American journal of physiology. Renal physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yu, Ying</au><au>Wang, Yumei</au><au>Niu, Yangyang</au><au>Fu, Lanjun</au><au>Chin, Y Eugene</au><au>Yu, Chen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Leukemia inhibitory factor attenuates renal fibrosis through Stat3-miR-29c</atitle><jtitle>American journal of physiology. Renal physiology</jtitle><addtitle>Am J Physiol Renal Physiol</addtitle><date>2015-10-01</date><risdate>2015</risdate><volume>309</volume><issue>7</issue><spage>F595</spage><epage>F603</epage><pages>F595-F603</pages><issn>1931-857X</issn><eissn>1522-1466</eissn><abstract>Leukemia inhibitory factory (LIF), as a member of the IL-6 family, has been reported to ameliorate myocardial fibrosis and myocardial cell death. The purpose of the present study was to investigate the effect of LIF on renal fibrosis and its underlying mechanism. Our results showed, first, that LIF inhibited collagen type 1 and collagen type 3 expression induced by ANG II in NRK-49F (rat kidney fibroblast) cells and in mice with unilateral ureteral obstruction. Second, LIF induced Stat3 Tyr(705) phosphorylation and inhibited Stat3 Tyr(705) and Ser(727) phosphorylation induced by ANG II in NRK-49F cells. Third, LIF exerted an antirenal fibrosis effect mainly through activation of Stat3 Tyr(705) phosphorylation in NRK-49F cells. These effects of LIF were not observed in Stat3(-/-) cells. Finally, LIF-Stat3 upregulated microRNA-29c expression, and the latter downregulated collagen type 1 and collagen type 3 expression in NRK-49F cells and in mice with unilateral ureteral obstruction. In conclusion, LIF played a role in antirenal fibrosis by competitively activating Stat3 Tyr(705) phosphorylation, which upregulated microRNA-29c to suppress collagen expression.</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>26155847</pmid><doi>10.1152/ajprenal.00634.2014</doi></addata></record> |
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| source | MEDLINE; American Physiological Society; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Angiotensin II - pharmacology Animals Apoptosis Cells Cells, Cultured Collagen Collagen Type I - biosynthesis Collagen Type III - biosynthesis Computational Biology Extracellular Matrix Proteins - biosynthesis Fibrosis Gene Knockdown Techniques Interleukin-6 - metabolism Kidney - pathology Kidney Diseases - drug therapy Kidney Diseases - pathology Leukemia Inhibitory Factor - therapeutic use Mice MicroRNAs - genetics Nephritis, Interstitial - pathology Phosphorylation Rats Rodents STAT3 Transcription Factor - genetics Transfection Ureteral Obstruction - pathology |
| title | Leukemia inhibitory factor attenuates renal fibrosis through Stat3-miR-29c |
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