Pathologic Regulation of Collagen I by an Aberrant Protein Phosphatase 2A/Histone Deacetylase C4/MicroRNA-29 Signal Axis in Idiopathic Pulmonary Fibrosis Fibroblasts
Idiopathic pulmonary fibrosis (IPF) is characterized by the relentless expansion of fibroblasts depositing type I collagen within the alveolar wall and obliterating the alveolar airspace. MicroRNA (miR)-29 is a potent regulator of collagen expression. In IPF, miR-29 levels are low, whereas type I co...
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| Veröffentlicht in: | American journal of respiratory cell and molecular biology 2015-09, Vol.53 (3), p.391-399 |
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| creator | Khalil, Wajahat Xia, Hong Bodempudi, Vidya Kahm, Judy Hergert, Polla Smith, Karen Peterson, Mark Parker, Matthew Herrera, Jeremy Bitterman, Peter B Henke, Craig A |
| description | Idiopathic pulmonary fibrosis (IPF) is characterized by the relentless expansion of fibroblasts depositing type I collagen within the alveolar wall and obliterating the alveolar airspace. MicroRNA (miR)-29 is a potent regulator of collagen expression. In IPF, miR-29 levels are low, whereas type I collagen expression is high. However, the mechanism for suppression of miR-29 and increased type I collagen expression in IPF remains unclear. Here we show that when IPF fibroblasts are seeded on polymerized type I collagen, miR-29c levels are suppressed and type I collagen expression is high. In contrast, miR-29c is high and type I collagen expression is low in control fibroblasts. We demonstrate that the mechanism for suppression of miR-29 during IPF fibroblast interaction with polymerized collagen involves inappropriately low protein phosphatase (PP) 2A function, leading to histone deacetylase (HDA) C4 phosphorylation and decreased nuclear translocation of HDAC4. We demonstrate that overexpression of HDAC4 in IPF fibroblasts restored miR-29c levels and decreased type I collagen expression, whereas knocking down HDAC4 in control fibroblasts suppressed miR-29c levels and increased type I collagen expression. Our data indicate that IPF fibroblast interaction with polymerized type I collagen results in an aberrant PP2A/HDAC4 axis, which suppresses miR-29, causing a pathologic increase in type I collagen expression. |
| doi_str_mv | 10.1165/rcmb.2014-0150oc |
| format | Article |
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MicroRNA (miR)-29 is a potent regulator of collagen expression. In IPF, miR-29 levels are low, whereas type I collagen expression is high. However, the mechanism for suppression of miR-29 and increased type I collagen expression in IPF remains unclear. Here we show that when IPF fibroblasts are seeded on polymerized type I collagen, miR-29c levels are suppressed and type I collagen expression is high. In contrast, miR-29c is high and type I collagen expression is low in control fibroblasts. We demonstrate that the mechanism for suppression of miR-29 during IPF fibroblast interaction with polymerized collagen involves inappropriately low protein phosphatase (PP) 2A function, leading to histone deacetylase (HDA) C4 phosphorylation and decreased nuclear translocation of HDAC4. We demonstrate that overexpression of HDAC4 in IPF fibroblasts restored miR-29c levels and decreased type I collagen expression, whereas knocking down HDAC4 in control fibroblasts suppressed miR-29c levels and increased type I collagen expression. Our data indicate that IPF fibroblast interaction with polymerized type I collagen results in an aberrant PP2A/HDAC4 axis, which suppresses miR-29, causing a pathologic increase in type I collagen expression.</description><identifier>ISSN: 1044-1549</identifier><identifier>EISSN: 1535-4989</identifier><identifier>DOI: 10.1165/rcmb.2014-0150oc</identifier><identifier>PMID: 25612003</identifier><language>eng</language><publisher>United States: American Thoracic Society</publisher><subject>Acquisitions & mergers ; Cell Nucleus - enzymology ; Cells, Cultured ; Collagen ; Collagen Type I - metabolism ; Epigenesis, Genetic ; Fibroblasts ; Fibroblasts - enzymology ; Gene expression ; Genotype & phenotype ; Histone Deacetylases - metabolism ; Humans ; Idiopathic Pulmonary Fibrosis - metabolism ; Immunoglobulins ; MicroRNAs ; MicroRNAs - metabolism ; Original Research ; Patients ; Phosphatase ; Phosphoprotein Phosphatases - metabolism ; Phosphorylation ; Protein Phosphatase 2C ; Protein Processing, Post-Translational ; Protein Transport ; Proteins ; Pulmonary fibrosis ; Repressor Proteins - metabolism ; Rodents ; Signal Transduction ; Studies ; Transcription factors</subject><ispartof>American journal of respiratory cell and molecular biology, 2015-09, Vol.53 (3), p.391-399</ispartof><rights>Copyright American Thoracic Society Sep 2015</rights><rights>Copyright © 2015 by the American Thoracic Society 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c523t-696843d62eb2fd94d36a3ae1f4482d6dfb124e19b25790b8f50e9cb718eac1e23</citedby><cites>FETCH-LOGICAL-c523t-696843d62eb2fd94d36a3ae1f4482d6dfb124e19b25790b8f50e9cb718eac1e23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25612003$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Khalil, Wajahat</creatorcontrib><creatorcontrib>Xia, Hong</creatorcontrib><creatorcontrib>Bodempudi, Vidya</creatorcontrib><creatorcontrib>Kahm, Judy</creatorcontrib><creatorcontrib>Hergert, Polla</creatorcontrib><creatorcontrib>Smith, Karen</creatorcontrib><creatorcontrib>Peterson, Mark</creatorcontrib><creatorcontrib>Parker, Matthew</creatorcontrib><creatorcontrib>Herrera, Jeremy</creatorcontrib><creatorcontrib>Bitterman, Peter B</creatorcontrib><creatorcontrib>Henke, Craig A</creatorcontrib><title>Pathologic Regulation of Collagen I by an Aberrant Protein Phosphatase 2A/Histone Deacetylase C4/MicroRNA-29 Signal Axis in Idiopathic Pulmonary Fibrosis Fibroblasts</title><title>American journal of respiratory cell and molecular biology</title><addtitle>Am J Respir Cell Mol Biol</addtitle><description>Idiopathic pulmonary fibrosis (IPF) is characterized by the relentless expansion of fibroblasts depositing type I collagen within the alveolar wall and obliterating the alveolar airspace. MicroRNA (miR)-29 is a potent regulator of collagen expression. In IPF, miR-29 levels are low, whereas type I collagen expression is high. However, the mechanism for suppression of miR-29 and increased type I collagen expression in IPF remains unclear. Here we show that when IPF fibroblasts are seeded on polymerized type I collagen, miR-29c levels are suppressed and type I collagen expression is high. In contrast, miR-29c is high and type I collagen expression is low in control fibroblasts. We demonstrate that the mechanism for suppression of miR-29 during IPF fibroblast interaction with polymerized collagen involves inappropriately low protein phosphatase (PP) 2A function, leading to histone deacetylase (HDA) C4 phosphorylation and decreased nuclear translocation of HDAC4. We demonstrate that overexpression of HDAC4 in IPF fibroblasts restored miR-29c levels and decreased type I collagen expression, whereas knocking down HDAC4 in control fibroblasts suppressed miR-29c levels and increased type I collagen expression. Our data indicate that IPF fibroblast interaction with polymerized type I collagen results in an aberrant PP2A/HDAC4 axis, which suppresses miR-29, causing a pathologic increase in type I collagen expression.</description><subject>Acquisitions & mergers</subject><subject>Cell Nucleus - enzymology</subject><subject>Cells, Cultured</subject><subject>Collagen</subject><subject>Collagen Type I - metabolism</subject><subject>Epigenesis, Genetic</subject><subject>Fibroblasts</subject><subject>Fibroblasts - enzymology</subject><subject>Gene expression</subject><subject>Genotype & phenotype</subject><subject>Histone Deacetylases - metabolism</subject><subject>Humans</subject><subject>Idiopathic Pulmonary Fibrosis - metabolism</subject><subject>Immunoglobulins</subject><subject>MicroRNAs</subject><subject>MicroRNAs - metabolism</subject><subject>Original Research</subject><subject>Patients</subject><subject>Phosphatase</subject><subject>Phosphoprotein Phosphatases - metabolism</subject><subject>Phosphorylation</subject><subject>Protein Phosphatase 2C</subject><subject>Protein Processing, Post-Translational</subject><subject>Protein Transport</subject><subject>Proteins</subject><subject>Pulmonary fibrosis</subject><subject>Repressor Proteins - metabolism</subject><subject>Rodents</subject><subject>Signal Transduction</subject><subject>Studies</subject><subject>Transcription factors</subject><issn>1044-1549</issn><issn>1535-4989</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkk1v1DAQhiMEoh9w54QsceGSrsexvfEFaRUoXanQVYGzZSdO1lXW3toO6v4g_icOLRVw4mB5NH7mnfHoLYpXgM8AOFuEdqfPCAZaYmDYt0-KY2AVK6moxdMcY0pLYFQcFScx3mAMpAZ4XhwRxoFgXB0XPzYqbf3oB9uiazNMo0rWO-R71PhxVINxaI30ASmHVtqEoFxCm-CTsQ5ttj7utyqpaBBZLS5sTN4Z9N6o1qTDOKcbuvhk2-CvP69KItAXOzg1otWdjSgLrDvr97l_7r2Zxp13KhzQudXBxwz8CnSWSfFF8axXYzQvH-7T4tv5h6_NRXl59XHdrC7LlpEqlVzwmlYdJ0aTvhO0q7iqlIGe0pp0vOs1EGpAaMKWAuu6Z9iIVi-hziODIdVp8e5edz_pnela41JQo9wHu8ujSa-s_PvF2a0c_HdJGeeYQxZ4-yAQ_O1kYpI7G1uTN-mMn6KEJSH5gGD_gWJRCc4Ezuibf9AbP4W8yZnKRgBWC5EpfE_lfccYTP84N2A520XOdpGzXeRsl6sml7z-87-PBb_9Uf0EJKS91Q</recordid><startdate>201509</startdate><enddate>201509</enddate><creator>Khalil, Wajahat</creator><creator>Xia, Hong</creator><creator>Bodempudi, Vidya</creator><creator>Kahm, Judy</creator><creator>Hergert, Polla</creator><creator>Smith, Karen</creator><creator>Peterson, Mark</creator><creator>Parker, Matthew</creator><creator>Herrera, Jeremy</creator><creator>Bitterman, Peter B</creator><creator>Henke, Craig A</creator><general>American Thoracic 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>3V.</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>S0X</scope><scope>7X8</scope><scope>7U7</scope><scope>C1K</scope><scope>5PM</scope></search><sort><creationdate>201509</creationdate><title>Pathologic Regulation of Collagen I by an Aberrant Protein Phosphatase 2A/Histone Deacetylase C4/MicroRNA-29 Signal Axis in Idiopathic Pulmonary Fibrosis Fibroblasts</title><author>Khalil, Wajahat ; Xia, Hong ; Bodempudi, Vidya ; Kahm, Judy ; Hergert, Polla ; Smith, Karen ; Peterson, Mark ; Parker, Matthew ; Herrera, Jeremy ; Bitterman, Peter B ; Henke, Craig A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c523t-696843d62eb2fd94d36a3ae1f4482d6dfb124e19b25790b8f50e9cb718eac1e23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Acquisitions & mergers</topic><topic>Cell Nucleus - 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Academic</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>American journal of respiratory cell and molecular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Khalil, Wajahat</au><au>Xia, Hong</au><au>Bodempudi, Vidya</au><au>Kahm, Judy</au><au>Hergert, Polla</au><au>Smith, Karen</au><au>Peterson, Mark</au><au>Parker, Matthew</au><au>Herrera, Jeremy</au><au>Bitterman, Peter B</au><au>Henke, Craig A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pathologic Regulation of Collagen I by an Aberrant Protein Phosphatase 2A/Histone Deacetylase C4/MicroRNA-29 Signal Axis in Idiopathic Pulmonary Fibrosis Fibroblasts</atitle><jtitle>American journal of respiratory cell and molecular biology</jtitle><addtitle>Am J Respir Cell Mol Biol</addtitle><date>2015-09</date><risdate>2015</risdate><volume>53</volume><issue>3</issue><spage>391</spage><epage>399</epage><pages>391-399</pages><issn>1044-1549</issn><eissn>1535-4989</eissn><abstract>Idiopathic pulmonary fibrosis (IPF) is characterized by the relentless expansion of fibroblasts depositing type I collagen within the alveolar wall and obliterating the alveolar airspace. MicroRNA (miR)-29 is a potent regulator of collagen expression. In IPF, miR-29 levels are low, whereas type I collagen expression is high. However, the mechanism for suppression of miR-29 and increased type I collagen expression in IPF remains unclear. Here we show that when IPF fibroblasts are seeded on polymerized type I collagen, miR-29c levels are suppressed and type I collagen expression is high. In contrast, miR-29c is high and type I collagen expression is low in control fibroblasts. We demonstrate that the mechanism for suppression of miR-29 during IPF fibroblast interaction with polymerized collagen involves inappropriately low protein phosphatase (PP) 2A function, leading to histone deacetylase (HDA) C4 phosphorylation and decreased nuclear translocation of HDAC4. We demonstrate that overexpression of HDAC4 in IPF fibroblasts restored miR-29c levels and decreased type I collagen expression, whereas knocking down HDAC4 in control fibroblasts suppressed miR-29c levels and increased type I collagen expression. Our data indicate that IPF fibroblast interaction with polymerized type I collagen results in an aberrant PP2A/HDAC4 axis, which suppresses miR-29, causing a pathologic increase in type I collagen expression.</abstract><cop>United States</cop><pub>American Thoracic Society</pub><pmid>25612003</pmid><doi>10.1165/rcmb.2014-0150oc</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acquisitions & mergers Cell Nucleus - enzymology Cells, Cultured Collagen Collagen Type I - metabolism Epigenesis, Genetic Fibroblasts Fibroblasts - enzymology Gene expression Genotype & phenotype Histone Deacetylases - metabolism Humans Idiopathic Pulmonary Fibrosis - metabolism Immunoglobulins MicroRNAs MicroRNAs - metabolism Original Research Patients Phosphatase Phosphoprotein Phosphatases - metabolism Phosphorylation Protein Phosphatase 2C Protein Processing, Post-Translational Protein Transport Proteins Pulmonary fibrosis Repressor Proteins - metabolism Rodents Signal Transduction Studies Transcription factors |
| title | Pathologic Regulation of Collagen I by an Aberrant Protein Phosphatase 2A/Histone Deacetylase C4/MicroRNA-29 Signal Axis in Idiopathic Pulmonary Fibrosis Fibroblasts |
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