Sirtuin 6 inhibits myofibroblast differentiation via inactivating transforming growth factor‐β1/Smad2 and nuclear factor‐κB signaling pathways in human fetal lung fibroblasts
Fibroblast‐to‐myofibroblast differentiation, which is characterized by increased expression of α‐smooth muscle actin, is known to be involved in the pathogenesis of idiopathic pulmonary fibrosis. Sirtuin 6 (SIRT6), a member of the sirtuin family, has been proved to inhibit epithelial‐to‐mesenchymal...
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| Veröffentlicht in: | Journal of cellular biochemistry 2019-01, Vol.120 (1), p.93-104 |
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| creator | Zhang, Qian Tu, Wei Tian, Kunming Han, Lianyong Wang, Qin Chen, Panpan Zhou, Xue |
| description | Fibroblast‐to‐myofibroblast differentiation, which is characterized by increased expression of α‐smooth muscle actin, is known to be involved in the pathogenesis of idiopathic pulmonary fibrosis. Sirtuin 6 (SIRT6), a member of the sirtuin family, has been proved to inhibit epithelial‐to‐mesenchymal transition during idiopathic pulmonary fibrosis. However, the function of SIRT6 in lung myofibroblast differentiation is still obscure. Transforming growth factor‐β1 (TGF‐β1) is one of the main factors that can powerfully promote myofibroblast differentiation. In the current study, we aimed to explore the role of SIRT6 in the cellular model of fibroblast‐to‐myofibroblast differentiation induced by TGF‐β1 using human fetal lung fibroblasts (HFL1). We demonstrated that the SIRT6 protein level is upregulated by TGF‐β1 in HFL1 cells. Overexpression of SIRT6 significantly suppresses TGF‐β1‐induced myofibroblast differentiation in HFL1 cells. Mechanistically, SIRT6 decreases phosphorylation and nuclear translocation of Smad2 under TGF‐β1 stimulation. Nevertheless, mutant SIRT6 (H133Y) without histone deacetylase activity fails to inhibit phosphorylation and nuclear translocation of Smad2. Meanwhile, SIRT6 interacts with the nuclear factor‐κB (NF‐κB) subunit p65 and represses TGF‐β1‐induced NF‐κB‐dependent transcriptional activity, which is also dependent on its deacetylase activity. Overexpression of wild‐type SIRT6 but not the H133Y mutant inhibits the expression of NF‐κB‐dependent genes including interleukin (IL)‐1β, IL‐6 and matrix metalloproteinase‐9 (MMP‐9) induced by TGF‐β1, all of which have been demonstrated to promote myofibroblast differentiation. Collectively, our study reveals that SIRT6 prevents TGF‐β1‐induced lung myofibroblast differentiation through inhibiting TGF‐β1/Smad2 and NF‐κB signaling pathways.
Sirtuin 6 (SIRT6) overexpression attenuates fibroblast‐to‐myofibroblast differentiation induced by transforming growth factor‐β1 (TGF‐β1) in human fetal lung fibroblasts. Mechanistically, wild‐type SIRT6, but not the H133Y mutant without deacetylase activity, decreases phosphorylation and nuclear translocation of Smad2 under TGF‐β1 stimulation. Meanwhile, SIRT6 interacted with the nuclear factor‐κB (NF‐κB) subunit p65 and repressed TGF‐β1‐induced NF‐κB‐dependent transcriptional activity and the expression of NF‐κB‐dependent genes including interleukin (IL)‐1β, IL‐6 and matrix metalloproteinase‐9 (MMP‐9), which is also dependent on its deacetylase activit |
| doi_str_mv | 10.1002/jcb.27128 |
| format | Article |
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Sirtuin 6 (SIRT6) overexpression attenuates fibroblast‐to‐myofibroblast differentiation induced by transforming growth factor‐β1 (TGF‐β1) in human fetal lung fibroblasts. Mechanistically, wild‐type SIRT6, but not the H133Y mutant without deacetylase activity, decreases phosphorylation and nuclear translocation of Smad2 under TGF‐β1 stimulation. Meanwhile, SIRT6 interacted with the nuclear factor‐κB (NF‐κB) subunit p65 and repressed TGF‐β1‐induced NF‐κB‐dependent transcriptional activity and the expression of NF‐κB‐dependent genes including interleukin (IL)‐1β, IL‐6 and matrix metalloproteinase‐9 (MMP‐9), which is also dependent on its deacetylase activity.</description><identifier>ISSN: 0730-2312</identifier><identifier>EISSN: 1097-4644</identifier><identifier>DOI: 10.1002/jcb.27128</identifier><identifier>PMID: 30230565</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Actin ; Cell Differentiation ; Cell Line ; Cell Proliferation - drug effects ; Cell Survival - drug effects ; Differentiation ; Fetuses ; Fibroblasts ; fibroblast‐to‐myofibroblast differentiation ; Fibrosis ; Gene expression ; Gene Expression Regulation ; Growth factors ; Histone deacetylase ; Humans ; idiopathic pulmonary fibrosis ; Idiopathic Pulmonary Fibrosis - metabolism ; Idiopathic Pulmonary Fibrosis - pathology ; Interleukin-1beta - genetics ; Interleukin-6 - genetics ; Interleukins ; Lung - cytology ; Lung - pathology ; Lung diseases ; Matrix metalloproteinase ; Matrix Metalloproteinase 9 - genetics ; Mesenchyme ; Metalloproteinase ; Muscles ; Myofibroblasts - metabolism ; NF-kappa B p50 Subunit - genetics ; NF-kappa B p50 Subunit - metabolism ; nuclear factor‐κB (NF‐κB) ; Nuclear transport ; Pathogenesis ; Phosphorylation ; Proteins ; Pulmonary fibrosis ; Reverse Transcriptase Polymerase Chain Reaction ; Signal transduction ; Signaling ; sirtuin 6 (SIRT6) ; Sirtuins - genetics ; Sirtuins - metabolism ; Smad2 protein ; Smad2 Protein - metabolism ; Smooth muscle ; Transcription ; Transcription, Genetic ; Transfection ; Transforming growth factor ; Transforming Growth Factor beta1 - metabolism ; Transforming Growth Factor beta1 - pharmacology ; Transforming growth factor-b1 ; transforming growth factor‐β1 (TGF‐β1)/Smad2 ; Translocation</subject><ispartof>Journal of cellular biochemistry, 2019-01, Vol.120 (1), p.93-104</ispartof><rights>2018 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3038-bf3384197865cc8a1e37aac0d320ac8910148d5fb8ce0bd039c16a36f2155b0b3</citedby><cites>FETCH-LOGICAL-c3038-bf3384197865cc8a1e37aac0d320ac8910148d5fb8ce0bd039c16a36f2155b0b3</cites><orcidid>0000-0002-8254-9341</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcb.27128$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcb.27128$$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/30230565$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Qian</creatorcontrib><creatorcontrib>Tu, Wei</creatorcontrib><creatorcontrib>Tian, Kunming</creatorcontrib><creatorcontrib>Han, Lianyong</creatorcontrib><creatorcontrib>Wang, Qin</creatorcontrib><creatorcontrib>Chen, Panpan</creatorcontrib><creatorcontrib>Zhou, Xue</creatorcontrib><title>Sirtuin 6 inhibits myofibroblast differentiation via inactivating transforming growth factor‐β1/Smad2 and nuclear factor‐κB signaling pathways in human fetal lung fibroblasts</title><title>Journal of cellular biochemistry</title><addtitle>J Cell Biochem</addtitle><description>Fibroblast‐to‐myofibroblast differentiation, which is characterized by increased expression of α‐smooth muscle actin, is known to be involved in the pathogenesis of idiopathic pulmonary fibrosis. Sirtuin 6 (SIRT6), a member of the sirtuin family, has been proved to inhibit epithelial‐to‐mesenchymal transition during idiopathic pulmonary fibrosis. However, the function of SIRT6 in lung myofibroblast differentiation is still obscure. Transforming growth factor‐β1 (TGF‐β1) is one of the main factors that can powerfully promote myofibroblast differentiation. In the current study, we aimed to explore the role of SIRT6 in the cellular model of fibroblast‐to‐myofibroblast differentiation induced by TGF‐β1 using human fetal lung fibroblasts (HFL1). We demonstrated that the SIRT6 protein level is upregulated by TGF‐β1 in HFL1 cells. Overexpression of SIRT6 significantly suppresses TGF‐β1‐induced myofibroblast differentiation in HFL1 cells. Mechanistically, SIRT6 decreases phosphorylation and nuclear translocation of Smad2 under TGF‐β1 stimulation. Nevertheless, mutant SIRT6 (H133Y) without histone deacetylase activity fails to inhibit phosphorylation and nuclear translocation of Smad2. Meanwhile, SIRT6 interacts with the nuclear factor‐κB (NF‐κB) subunit p65 and represses TGF‐β1‐induced NF‐κB‐dependent transcriptional activity, which is also dependent on its deacetylase activity. Overexpression of wild‐type SIRT6 but not the H133Y mutant inhibits the expression of NF‐κB‐dependent genes including interleukin (IL)‐1β, IL‐6 and matrix metalloproteinase‐9 (MMP‐9) induced by TGF‐β1, all of which have been demonstrated to promote myofibroblast differentiation. Collectively, our study reveals that SIRT6 prevents TGF‐β1‐induced lung myofibroblast differentiation through inhibiting TGF‐β1/Smad2 and NF‐κB signaling pathways.
Sirtuin 6 (SIRT6) overexpression attenuates fibroblast‐to‐myofibroblast differentiation induced by transforming growth factor‐β1 (TGF‐β1) in human fetal lung fibroblasts. Mechanistically, wild‐type SIRT6, but not the H133Y mutant without deacetylase activity, decreases phosphorylation and nuclear translocation of Smad2 under TGF‐β1 stimulation. Meanwhile, SIRT6 interacted with the nuclear factor‐κB (NF‐κB) subunit p65 and repressed TGF‐β1‐induced NF‐κB‐dependent transcriptional activity and the expression of NF‐κB‐dependent genes including interleukin (IL)‐1β, IL‐6 and matrix metalloproteinase‐9 (MMP‐9), which is also dependent on its deacetylase activity.</description><subject>Actin</subject><subject>Cell Differentiation</subject><subject>Cell Line</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Survival - drug effects</subject><subject>Differentiation</subject><subject>Fetuses</subject><subject>Fibroblasts</subject><subject>fibroblast‐to‐myofibroblast differentiation</subject><subject>Fibrosis</subject><subject>Gene expression</subject><subject>Gene Expression Regulation</subject><subject>Growth factors</subject><subject>Histone deacetylase</subject><subject>Humans</subject><subject>idiopathic pulmonary fibrosis</subject><subject>Idiopathic Pulmonary Fibrosis - metabolism</subject><subject>Idiopathic Pulmonary Fibrosis - pathology</subject><subject>Interleukin-1beta - genetics</subject><subject>Interleukin-6 - genetics</subject><subject>Interleukins</subject><subject>Lung - cytology</subject><subject>Lung - pathology</subject><subject>Lung diseases</subject><subject>Matrix metalloproteinase</subject><subject>Matrix Metalloproteinase 9 - genetics</subject><subject>Mesenchyme</subject><subject>Metalloproteinase</subject><subject>Muscles</subject><subject>Myofibroblasts - metabolism</subject><subject>NF-kappa B p50 Subunit - genetics</subject><subject>NF-kappa B p50 Subunit - metabolism</subject><subject>nuclear factor‐κB (NF‐κB)</subject><subject>Nuclear transport</subject><subject>Pathogenesis</subject><subject>Phosphorylation</subject><subject>Proteins</subject><subject>Pulmonary fibrosis</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Signal transduction</subject><subject>Signaling</subject><subject>sirtuin 6 (SIRT6)</subject><subject>Sirtuins - genetics</subject><subject>Sirtuins - metabolism</subject><subject>Smad2 protein</subject><subject>Smad2 Protein - metabolism</subject><subject>Smooth muscle</subject><subject>Transcription</subject><subject>Transcription, Genetic</subject><subject>Transfection</subject><subject>Transforming growth factor</subject><subject>Transforming Growth Factor beta1 - metabolism</subject><subject>Transforming Growth Factor beta1 - pharmacology</subject><subject>Transforming growth factor-b1</subject><subject>transforming growth factor‐β1 (TGF‐β1)/Smad2</subject><subject>Translocation</subject><issn>0730-2312</issn><issn>1097-4644</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kc2OUyEYhonROLW68AYMiRtddPoB53fpNP5mEhej65MPDrQ050AFzjTdeQlei3HlRXgRXonUjj8xcUEIvA9PgJeQhwzOGQBfbpU85zXjzS0yY9DWi6IqittkBrWABReMn5F7MW4BoG0Fv0vOBHABZVXOyJcrG9JkHa2odRsrbYp0PHhjZfBywJhob43RQbtkMVnv6LXFjKJK9jpvuDVNAV00PozHxTr4fdpQk3Mfvn_89O0zW16N2HOKrqduUoPG8Ff89YJGu3Y4HA_vMG32eIjZTzfTiI4anXCgw5TDP1eK98kdg0PUD27mOXn_4vm71avF5duXr1fPLhdKgGgW0gjRFKytm6pUqkGmRY2ooBccUDUtA1Y0fWlkozTIHkSrWIWiMpyVpQQp5uTJybsL_sOkY-pGG5UeBnTaT7HjrG7zqFmZ0cf_oFs_hfyuIyUqLooq__mcPD1RKvgYgzbdLtgRw6Fj0B2r7HKV3c8qM_voxjjJUfe_yV_dZWB5AvZ20If_m7o3q4uT8geOf67e</recordid><startdate>201901</startdate><enddate>201901</enddate><creator>Zhang, Qian</creator><creator>Tu, Wei</creator><creator>Tian, Kunming</creator><creator>Han, Lianyong</creator><creator>Wang, Qin</creator><creator>Chen, Panpan</creator><creator>Zhou, Xue</creator><general>Wiley Subscription Services, Inc</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>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-8254-9341</orcidid></search><sort><creationdate>201901</creationdate><title>Sirtuin 6 inhibits myofibroblast differentiation via inactivating transforming growth factor‐β1/Smad2 and nuclear factor‐κB signaling pathways in human fetal lung fibroblasts</title><author>Zhang, Qian ; Tu, Wei ; Tian, Kunming ; Han, Lianyong ; Wang, Qin ; Chen, Panpan ; Zhou, Xue</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3038-bf3384197865cc8a1e37aac0d320ac8910148d5fb8ce0bd039c16a36f2155b0b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Actin</topic><topic>Cell Differentiation</topic><topic>Cell Line</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Survival - drug effects</topic><topic>Differentiation</topic><topic>Fetuses</topic><topic>Fibroblasts</topic><topic>fibroblast‐to‐myofibroblast differentiation</topic><topic>Fibrosis</topic><topic>Gene expression</topic><topic>Gene Expression Regulation</topic><topic>Growth factors</topic><topic>Histone deacetylase</topic><topic>Humans</topic><topic>idiopathic pulmonary fibrosis</topic><topic>Idiopathic Pulmonary Fibrosis - metabolism</topic><topic>Idiopathic Pulmonary Fibrosis - pathology</topic><topic>Interleukin-1beta - genetics</topic><topic>Interleukin-6 - genetics</topic><topic>Interleukins</topic><topic>Lung - cytology</topic><topic>Lung - pathology</topic><topic>Lung diseases</topic><topic>Matrix metalloproteinase</topic><topic>Matrix Metalloproteinase 9 - genetics</topic><topic>Mesenchyme</topic><topic>Metalloproteinase</topic><topic>Muscles</topic><topic>Myofibroblasts - metabolism</topic><topic>NF-kappa B p50 Subunit - genetics</topic><topic>NF-kappa B p50 Subunit - metabolism</topic><topic>nuclear factor‐κB (NF‐κB)</topic><topic>Nuclear transport</topic><topic>Pathogenesis</topic><topic>Phosphorylation</topic><topic>Proteins</topic><topic>Pulmonary fibrosis</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Signal transduction</topic><topic>Signaling</topic><topic>sirtuin 6 (SIRT6)</topic><topic>Sirtuins - genetics</topic><topic>Sirtuins - metabolism</topic><topic>Smad2 protein</topic><topic>Smad2 Protein - metabolism</topic><topic>Smooth muscle</topic><topic>Transcription</topic><topic>Transcription, Genetic</topic><topic>Transfection</topic><topic>Transforming growth factor</topic><topic>Transforming Growth Factor beta1 - metabolism</topic><topic>Transforming Growth Factor beta1 - pharmacology</topic><topic>Transforming growth factor-b1</topic><topic>transforming growth factor‐β1 (TGF‐β1)/Smad2</topic><topic>Translocation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Qian</creatorcontrib><creatorcontrib>Tu, Wei</creatorcontrib><creatorcontrib>Tian, Kunming</creatorcontrib><creatorcontrib>Han, Lianyong</creatorcontrib><creatorcontrib>Wang, Qin</creatorcontrib><creatorcontrib>Chen, Panpan</creatorcontrib><creatorcontrib>Zhou, Xue</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Qian</au><au>Tu, Wei</au><au>Tian, Kunming</au><au>Han, Lianyong</au><au>Wang, Qin</au><au>Chen, Panpan</au><au>Zhou, Xue</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sirtuin 6 inhibits myofibroblast differentiation via inactivating transforming growth factor‐β1/Smad2 and nuclear factor‐κB signaling pathways in human fetal lung fibroblasts</atitle><jtitle>Journal of cellular biochemistry</jtitle><addtitle>J Cell Biochem</addtitle><date>2019-01</date><risdate>2019</risdate><volume>120</volume><issue>1</issue><spage>93</spage><epage>104</epage><pages>93-104</pages><issn>0730-2312</issn><eissn>1097-4644</eissn><abstract>Fibroblast‐to‐myofibroblast differentiation, which is characterized by increased expression of α‐smooth muscle actin, is known to be involved in the pathogenesis of idiopathic pulmonary fibrosis. Sirtuin 6 (SIRT6), a member of the sirtuin family, has been proved to inhibit epithelial‐to‐mesenchymal transition during idiopathic pulmonary fibrosis. However, the function of SIRT6 in lung myofibroblast differentiation is still obscure. Transforming growth factor‐β1 (TGF‐β1) is one of the main factors that can powerfully promote myofibroblast differentiation. In the current study, we aimed to explore the role of SIRT6 in the cellular model of fibroblast‐to‐myofibroblast differentiation induced by TGF‐β1 using human fetal lung fibroblasts (HFL1). We demonstrated that the SIRT6 protein level is upregulated by TGF‐β1 in HFL1 cells. Overexpression of SIRT6 significantly suppresses TGF‐β1‐induced myofibroblast differentiation in HFL1 cells. Mechanistically, SIRT6 decreases phosphorylation and nuclear translocation of Smad2 under TGF‐β1 stimulation. Nevertheless, mutant SIRT6 (H133Y) without histone deacetylase activity fails to inhibit phosphorylation and nuclear translocation of Smad2. Meanwhile, SIRT6 interacts with the nuclear factor‐κB (NF‐κB) subunit p65 and represses TGF‐β1‐induced NF‐κB‐dependent transcriptional activity, which is also dependent on its deacetylase activity. Overexpression of wild‐type SIRT6 but not the H133Y mutant inhibits the expression of NF‐κB‐dependent genes including interleukin (IL)‐1β, IL‐6 and matrix metalloproteinase‐9 (MMP‐9) induced by TGF‐β1, all of which have been demonstrated to promote myofibroblast differentiation. Collectively, our study reveals that SIRT6 prevents TGF‐β1‐induced lung myofibroblast differentiation through inhibiting TGF‐β1/Smad2 and NF‐κB signaling pathways.
Sirtuin 6 (SIRT6) overexpression attenuates fibroblast‐to‐myofibroblast differentiation induced by transforming growth factor‐β1 (TGF‐β1) in human fetal lung fibroblasts. Mechanistically, wild‐type SIRT6, but not the H133Y mutant without deacetylase activity, decreases phosphorylation and nuclear translocation of Smad2 under TGF‐β1 stimulation. Meanwhile, SIRT6 interacted with the nuclear factor‐κB (NF‐κB) subunit p65 and repressed TGF‐β1‐induced NF‐κB‐dependent transcriptional activity and the expression of NF‐κB‐dependent genes including interleukin (IL)‐1β, IL‐6 and matrix metalloproteinase‐9 (MMP‐9), which is also dependent on its deacetylase activity.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>30230565</pmid><doi>10.1002/jcb.27128</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-8254-9341</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Journal of cellular biochemistry, 2019-01, Vol.120 (1), p.93-104 |
| issn | 0730-2312 1097-4644 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2179217715 |
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| subjects | Actin Cell Differentiation Cell Line Cell Proliferation - drug effects Cell Survival - drug effects Differentiation Fetuses Fibroblasts fibroblast‐to‐myofibroblast differentiation Fibrosis Gene expression Gene Expression Regulation Growth factors Histone deacetylase Humans idiopathic pulmonary fibrosis Idiopathic Pulmonary Fibrosis - metabolism Idiopathic Pulmonary Fibrosis - pathology Interleukin-1beta - genetics Interleukin-6 - genetics Interleukins Lung - cytology Lung - pathology Lung diseases Matrix metalloproteinase Matrix Metalloproteinase 9 - genetics Mesenchyme Metalloproteinase Muscles Myofibroblasts - metabolism NF-kappa B p50 Subunit - genetics NF-kappa B p50 Subunit - metabolism nuclear factor‐κB (NF‐κB) Nuclear transport Pathogenesis Phosphorylation Proteins Pulmonary fibrosis Reverse Transcriptase Polymerase Chain Reaction Signal transduction Signaling sirtuin 6 (SIRT6) Sirtuins - genetics Sirtuins - metabolism Smad2 protein Smad2 Protein - metabolism Smooth muscle Transcription Transcription, Genetic Transfection Transforming growth factor Transforming Growth Factor beta1 - metabolism Transforming Growth Factor beta1 - pharmacology Transforming growth factor-b1 transforming growth factor‐β1 (TGF‐β1)/Smad2 Translocation |
| title | Sirtuin 6 inhibits myofibroblast differentiation via inactivating transforming growth factor‐β1/Smad2 and nuclear factor‐κB signaling pathways in human fetal lung fibroblasts |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-12T11%3A27%3A02IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Sirtuin%206%20inhibits%20myofibroblast%20differentiation%20via%20inactivating%20transforming%20growth%20factor%E2%80%90%CE%B21/Smad2%20and%20nuclear%20factor%E2%80%90%CE%BAB%20signaling%20pathways%20in%20human%20fetal%20lung%20fibroblasts&rft.jtitle=Journal%20of%20cellular%20biochemistry&rft.au=Zhang,%20Qian&rft.date=2019-01&rft.volume=120&rft.issue=1&rft.spage=93&rft.epage=104&rft.pages=93-104&rft.issn=0730-2312&rft.eissn=1097-4644&rft_id=info:doi/10.1002/jcb.27128&rft_dat=%3Cproquest_cross%3E2179217715%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2136234602&rft_id=info:pmid/30230565&rfr_iscdi=true |