A microRNA circuit mediates transforming growth factor-β1 autoregulation in renal glomerular mesangial cells
Enhanced transforming growth factor-β1 (TGF-β1) expression in renal cells promotes fibrosis and hypertrophy during the progression of diabetic nephropathy. The TGF-β1 promoter is positively controlled by the E-box regulators, upstream stimulatory factors (USFs), in response to diabetic (high glucose...
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| Veröffentlicht in: | Kidney international 2011-08, Vol.80 (4), p.358-368 |
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| creator | Kato, Mitsuo Arce, Laura Wang, Mei Putta, Sumanth Lanting, Linda Natarajan, Rama |
| description | Enhanced transforming growth factor-β1 (TGF-β1) expression in renal cells promotes fibrosis and hypertrophy during the progression of diabetic nephropathy. The TGF-β1 promoter is positively controlled by the E-box regulators, upstream stimulatory factors (USFs), in response to diabetic (high glucose) conditions; however, it is not clear whether TGF-β1 is autoregulated by itself. As changes in microRNAs (miRNAs) have been implicated in kidney disease, we tested their involvement in this process. TGF-β1 levels were found to be upregulated by microRNA-192 (miR-192) or miR-200b/c in mouse mesangial cells. Amounts of miR-200b/c were increased in glomeruli from type 1 (streptozotocin) and type 2 (db/db) diabetic mice, and in mouse mesangial cells treated with TGF-β1 in vitro. Levels of miR-200b/c were also upregulated by miR-192 in the mesangial cells, suggesting that miR-200b/c are downstream of miR-192. Activity of the TGF-β1 promoter was upregulated by TGF-β1 or miR-192, demonstrating that the miR-192-miR-200 cascade induces TGF-β1 expression. TGF-β1 increased the occupancy of activators USF1 and Tfe3, and decreased that of the repressor Zeb1 on the TGF-β1 promoter E-box binding sites. Inhibitors of miR-192 decreased the expression of miR-200b/c, Col1a2, Col4a1, and TGF-β1 in mouse mesangial cells, and in mouse kidney cortex. Thus, miRNA-regulated circuits may amplify TGF-β1 signaling, accelerating chronic fibrotic diseases such as diabetic nephropathy. |
| doi_str_mv | 10.1038/ki.2011.43 |
| format | Article |
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The TGF-β1 promoter is positively controlled by the E-box regulators, upstream stimulatory factors (USFs), in response to diabetic (high glucose) conditions; however, it is not clear whether TGF-β1 is autoregulated by itself. As changes in microRNAs (miRNAs) have been implicated in kidney disease, we tested their involvement in this process. TGF-β1 levels were found to be upregulated by microRNA-192 (miR-192) or miR-200b/c in mouse mesangial cells. Amounts of miR-200b/c were increased in glomeruli from type 1 (streptozotocin) and type 2 (db/db) diabetic mice, and in mouse mesangial cells treated with TGF-β1 in vitro. Levels of miR-200b/c were also upregulated by miR-192 in the mesangial cells, suggesting that miR-200b/c are downstream of miR-192. Activity of the TGF-β1 promoter was upregulated by TGF-β1 or miR-192, demonstrating that the miR-192-miR-200 cascade induces TGF-β1 expression. TGF-β1 increased the occupancy of activators USF1 and Tfe3, and decreased that of the repressor Zeb1 on the TGF-β1 promoter E-box binding sites. Inhibitors of miR-192 decreased the expression of miR-200b/c, Col1a2, Col4a1, and TGF-β1 in mouse mesangial cells, and in mouse kidney cortex. Thus, miRNA-regulated circuits may amplify TGF-β1 signaling, accelerating chronic fibrotic diseases such as diabetic nephropathy.</description><identifier>ISSN: 0085-2538</identifier><identifier>EISSN: 1523-1755</identifier><identifier>DOI: 10.1038/ki.2011.43</identifier><identifier>PMID: 21389977</identifier><identifier>CODEN: KDYIA5</identifier><language>eng</language><publisher>Basingstoke: Elsevier Inc</publisher><subject>3' Untranslated Regions ; Animals ; Associated diseases and complications ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - metabolism ; Binding Sites ; Biological and medical sciences ; cell signaling ; Cells, Cultured ; Collagen Type I - metabolism ; Collagen Type IV - metabolism ; Diabetes Mellitus, Experimental - chemically induced ; Diabetes Mellitus, Experimental - genetics ; Diabetes Mellitus, Experimental - metabolism ; Diabetes Mellitus, Experimental - pathology ; Diabetes Mellitus, Type 1 - chemically induced ; Diabetes Mellitus, Type 1 - genetics ; Diabetes Mellitus, Type 1 - metabolism ; Diabetes Mellitus, Type 1 - pathology ; Diabetes Mellitus, Type 2 - genetics ; Diabetes Mellitus, Type 2 - metabolism ; Diabetes Mellitus, Type 2 - pathology ; Diabetes. Impaired glucose tolerance ; Diabetic Nephropathies - genetics ; Diabetic Nephropathies - metabolism ; Diabetic Nephropathies - pathology ; diabetic nephropathy ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Fibrosis ; gene expression ; Homeodomain Proteins - metabolism ; Homeostasis ; Kidneys ; Kruppel-Like Transcription Factors - metabolism ; Medical sciences ; Mesangial Cells - metabolism ; Mice ; MicroRNAs - metabolism ; Mutation ; Nephrology. Urinary tract diseases ; Oligonucleotides - metabolism ; Promoter Regions, Genetic ; TGF-β ; Time Factors ; Transfection ; Transforming Growth Factor beta1 - genetics ; Transforming Growth Factor beta1 - metabolism ; Up-Regulation ; Upstream Stimulatory Factors - metabolism ; Urinary system involvement in other diseases. Miscellaneous ; Zinc Finger E-box-Binding Homeobox 1</subject><ispartof>Kidney international, 2011-08, Vol.80 (4), p.358-368</ispartof><rights>2011 International Society of Nephrology</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4013-3cdfb611571bef965d4880085d0c3b45bd927cfdb9117303e1dcf141e64266ae3</citedby><cites>FETCH-LOGICAL-c4013-3cdfb611571bef965d4880085d0c3b45bd927cfdb9117303e1dcf141e64266ae3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24366354$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21389977$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kato, Mitsuo</creatorcontrib><creatorcontrib>Arce, Laura</creatorcontrib><creatorcontrib>Wang, Mei</creatorcontrib><creatorcontrib>Putta, Sumanth</creatorcontrib><creatorcontrib>Lanting, Linda</creatorcontrib><creatorcontrib>Natarajan, Rama</creatorcontrib><title>A microRNA circuit mediates transforming growth factor-β1 autoregulation in renal glomerular mesangial cells</title><title>Kidney international</title><addtitle>Kidney Int</addtitle><description>Enhanced transforming growth factor-β1 (TGF-β1) expression in renal cells promotes fibrosis and hypertrophy during the progression of diabetic nephropathy. The TGF-β1 promoter is positively controlled by the E-box regulators, upstream stimulatory factors (USFs), in response to diabetic (high glucose) conditions; however, it is not clear whether TGF-β1 is autoregulated by itself. As changes in microRNAs (miRNAs) have been implicated in kidney disease, we tested their involvement in this process. TGF-β1 levels were found to be upregulated by microRNA-192 (miR-192) or miR-200b/c in mouse mesangial cells. Amounts of miR-200b/c were increased in glomeruli from type 1 (streptozotocin) and type 2 (db/db) diabetic mice, and in mouse mesangial cells treated with TGF-β1 in vitro. Levels of miR-200b/c were also upregulated by miR-192 in the mesangial cells, suggesting that miR-200b/c are downstream of miR-192. Activity of the TGF-β1 promoter was upregulated by TGF-β1 or miR-192, demonstrating that the miR-192-miR-200 cascade induces TGF-β1 expression. TGF-β1 increased the occupancy of activators USF1 and Tfe3, and decreased that of the repressor Zeb1 on the TGF-β1 promoter E-box binding sites. Inhibitors of miR-192 decreased the expression of miR-200b/c, Col1a2, Col4a1, and TGF-β1 in mouse mesangial cells, and in mouse kidney cortex. Thus, miRNA-regulated circuits may amplify TGF-β1 signaling, accelerating chronic fibrotic diseases such as diabetic nephropathy.</description><subject>3' Untranslated Regions</subject><subject>Animals</subject><subject>Associated diseases and complications</subject><subject>Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - metabolism</subject><subject>Binding Sites</subject><subject>Biological and medical sciences</subject><subject>cell signaling</subject><subject>Cells, Cultured</subject><subject>Collagen Type I - metabolism</subject><subject>Collagen Type IV - metabolism</subject><subject>Diabetes Mellitus, Experimental - chemically induced</subject><subject>Diabetes Mellitus, Experimental - genetics</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>Diabetes Mellitus, Experimental - pathology</subject><subject>Diabetes Mellitus, Type 1 - chemically induced</subject><subject>Diabetes Mellitus, Type 1 - genetics</subject><subject>Diabetes Mellitus, Type 1 - metabolism</subject><subject>Diabetes Mellitus, Type 1 - pathology</subject><subject>Diabetes Mellitus, Type 2 - genetics</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Diabetes Mellitus, Type 2 - pathology</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Diabetic Nephropathies - genetics</subject><subject>Diabetic Nephropathies - metabolism</subject><subject>Diabetic Nephropathies - pathology</subject><subject>diabetic nephropathy</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Fibrosis</subject><subject>gene expression</subject><subject>Homeodomain Proteins - metabolism</subject><subject>Homeostasis</subject><subject>Kidneys</subject><subject>Kruppel-Like Transcription Factors - metabolism</subject><subject>Medical sciences</subject><subject>Mesangial Cells - metabolism</subject><subject>Mice</subject><subject>MicroRNAs - metabolism</subject><subject>Mutation</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Oligonucleotides - metabolism</subject><subject>Promoter Regions, Genetic</subject><subject>TGF-β</subject><subject>Time Factors</subject><subject>Transfection</subject><subject>Transforming Growth Factor beta1 - genetics</subject><subject>Transforming Growth Factor beta1 - metabolism</subject><subject>Up-Regulation</subject><subject>Upstream Stimulatory Factors - metabolism</subject><subject>Urinary system involvement in other diseases. Miscellaneous</subject><subject>Zinc Finger E-box-Binding Homeobox 1</subject><issn>0085-2538</issn><issn>1523-1755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptkMtKxDAUhoMoOl42PoBk40bomNMkvSwH8QaDgui6pOlJjdOLJK3ia_kgPpMZZ3Q2rpIcPv6T_yPkGNgUGM_OF3YaM4Cp4FtkAjLmEaRSbpMJY5mMYsmzPbLv_QsL75yzXbIXA8_yPE0npJ3R1mrXP9zNqLZOj3agLVZWDejp4FTnTe9a29W0dv378EyN0kPvoq9PoGoMN6zHRg2276jtqMNONbRu-hZdGLsQ5VVX2zDU2DT-kOwY1Xg8Wp8H5Onq8vHiJprfX99ezOaRFgx4xHVlygRAplCiyRNZiSxblqmY5qWQZZXHqTZVmQOknHGEShsQgImIk0QhPyBnq9zQzHuHpnh1tlXuowBWLJ0VC1ssnRWCB_hkBb-OZaj-h_5KCsDpGlBeq8YEK9r6DSd4knApNkGdGkaHf8DCLlf9bBIrAEP3N4uu8Npip4Nvh3ooqt7-98FvXjaSTg</recordid><startdate>201108</startdate><enddate>201108</enddate><creator>Kato, Mitsuo</creator><creator>Arce, Laura</creator><creator>Wang, Mei</creator><creator>Putta, Sumanth</creator><creator>Lanting, Linda</creator><creator>Natarajan, Rama</creator><general>Elsevier Inc</general><general>Nature Publishing Group</general><scope>6I.</scope><scope>AAFTH</scope><scope>IQODW</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></search><sort><creationdate>201108</creationdate><title>A microRNA circuit mediates transforming growth factor-β1 autoregulation in renal glomerular mesangial cells</title><author>Kato, Mitsuo ; Arce, Laura ; Wang, Mei ; Putta, Sumanth ; Lanting, Linda ; Natarajan, Rama</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4013-3cdfb611571bef965d4880085d0c3b45bd927cfdb9117303e1dcf141e64266ae3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>3' Untranslated Regions</topic><topic>Animals</topic><topic>Associated diseases and complications</topic><topic>Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - metabolism</topic><topic>Binding Sites</topic><topic>Biological and medical sciences</topic><topic>cell signaling</topic><topic>Cells, Cultured</topic><topic>Collagen Type I - metabolism</topic><topic>Collagen Type IV - metabolism</topic><topic>Diabetes Mellitus, Experimental - chemically induced</topic><topic>Diabetes Mellitus, Experimental - genetics</topic><topic>Diabetes Mellitus, Experimental - metabolism</topic><topic>Diabetes Mellitus, Experimental - pathology</topic><topic>Diabetes Mellitus, Type 1 - chemically induced</topic><topic>Diabetes Mellitus, Type 1 - genetics</topic><topic>Diabetes Mellitus, Type 1 - metabolism</topic><topic>Diabetes Mellitus, Type 1 - pathology</topic><topic>Diabetes Mellitus, Type 2 - genetics</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Diabetes Mellitus, Type 2 - pathology</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Diabetic Nephropathies - genetics</topic><topic>Diabetic Nephropathies - metabolism</topic><topic>Diabetic Nephropathies - pathology</topic><topic>diabetic nephropathy</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Fibrosis</topic><topic>gene expression</topic><topic>Homeodomain Proteins - metabolism</topic><topic>Homeostasis</topic><topic>Kidneys</topic><topic>Kruppel-Like Transcription Factors - metabolism</topic><topic>Medical sciences</topic><topic>Mesangial Cells - metabolism</topic><topic>Mice</topic><topic>MicroRNAs - metabolism</topic><topic>Mutation</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Oligonucleotides - metabolism</topic><topic>Promoter Regions, Genetic</topic><topic>TGF-β</topic><topic>Time Factors</topic><topic>Transfection</topic><topic>Transforming Growth Factor beta1 - genetics</topic><topic>Transforming Growth Factor beta1 - metabolism</topic><topic>Up-Regulation</topic><topic>Upstream Stimulatory Factors - metabolism</topic><topic>Urinary system involvement in other diseases. Miscellaneous</topic><topic>Zinc Finger E-box-Binding Homeobox 1</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kato, Mitsuo</creatorcontrib><creatorcontrib>Arce, Laura</creatorcontrib><creatorcontrib>Wang, Mei</creatorcontrib><creatorcontrib>Putta, Sumanth</creatorcontrib><creatorcontrib>Lanting, Linda</creatorcontrib><creatorcontrib>Natarajan, Rama</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Kidney international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kato, Mitsuo</au><au>Arce, Laura</au><au>Wang, Mei</au><au>Putta, Sumanth</au><au>Lanting, Linda</au><au>Natarajan, Rama</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A microRNA circuit mediates transforming growth factor-β1 autoregulation in renal glomerular mesangial cells</atitle><jtitle>Kidney international</jtitle><addtitle>Kidney Int</addtitle><date>2011-08</date><risdate>2011</risdate><volume>80</volume><issue>4</issue><spage>358</spage><epage>368</epage><pages>358-368</pages><issn>0085-2538</issn><eissn>1523-1755</eissn><coden>KDYIA5</coden><abstract>Enhanced transforming growth factor-β1 (TGF-β1) expression in renal cells promotes fibrosis and hypertrophy during the progression of diabetic nephropathy. The TGF-β1 promoter is positively controlled by the E-box regulators, upstream stimulatory factors (USFs), in response to diabetic (high glucose) conditions; however, it is not clear whether TGF-β1 is autoregulated by itself. As changes in microRNAs (miRNAs) have been implicated in kidney disease, we tested their involvement in this process. TGF-β1 levels were found to be upregulated by microRNA-192 (miR-192) or miR-200b/c in mouse mesangial cells. Amounts of miR-200b/c were increased in glomeruli from type 1 (streptozotocin) and type 2 (db/db) diabetic mice, and in mouse mesangial cells treated with TGF-β1 in vitro. Levels of miR-200b/c were also upregulated by miR-192 in the mesangial cells, suggesting that miR-200b/c are downstream of miR-192. Activity of the TGF-β1 promoter was upregulated by TGF-β1 or miR-192, demonstrating that the miR-192-miR-200 cascade induces TGF-β1 expression. TGF-β1 increased the occupancy of activators USF1 and Tfe3, and decreased that of the repressor Zeb1 on the TGF-β1 promoter E-box binding sites. Inhibitors of miR-192 decreased the expression of miR-200b/c, Col1a2, Col4a1, and TGF-β1 in mouse mesangial cells, and in mouse kidney cortex. Thus, miRNA-regulated circuits may amplify TGF-β1 signaling, accelerating chronic fibrotic diseases such as diabetic nephropathy.</abstract><cop>Basingstoke</cop><pub>Elsevier Inc</pub><pmid>21389977</pmid><doi>10.1038/ki.2011.43</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Kidney international, 2011-08, Vol.80 (4), p.358-368 |
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| subjects | 3' Untranslated Regions Animals Associated diseases and complications Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - metabolism Binding Sites Biological and medical sciences cell signaling Cells, Cultured Collagen Type I - metabolism Collagen Type IV - metabolism Diabetes Mellitus, Experimental - chemically induced Diabetes Mellitus, Experimental - genetics Diabetes Mellitus, Experimental - metabolism Diabetes Mellitus, Experimental - pathology Diabetes Mellitus, Type 1 - chemically induced Diabetes Mellitus, Type 1 - genetics Diabetes Mellitus, Type 1 - metabolism Diabetes Mellitus, Type 1 - pathology Diabetes Mellitus, Type 2 - genetics Diabetes Mellitus, Type 2 - metabolism Diabetes Mellitus, Type 2 - pathology Diabetes. Impaired glucose tolerance Diabetic Nephropathies - genetics Diabetic Nephropathies - metabolism Diabetic Nephropathies - pathology diabetic nephropathy Endocrine pancreas. Apud cells (diseases) Endocrinopathies Fibrosis gene expression Homeodomain Proteins - metabolism Homeostasis Kidneys Kruppel-Like Transcription Factors - metabolism Medical sciences Mesangial Cells - metabolism Mice MicroRNAs - metabolism Mutation Nephrology. Urinary tract diseases Oligonucleotides - metabolism Promoter Regions, Genetic TGF-β Time Factors Transfection Transforming Growth Factor beta1 - genetics Transforming Growth Factor beta1 - metabolism Up-Regulation Upstream Stimulatory Factors - metabolism Urinary system involvement in other diseases. Miscellaneous Zinc Finger E-box-Binding Homeobox 1 |
| title | A microRNA circuit mediates transforming growth factor-β1 autoregulation in renal glomerular mesangial cells |
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