Role of endothelial cells in pulmonary fibrosis via SREBP2 activation
Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease with limited treatment options. Despite endothelial cells (ECs) comprising 30% of the lung cellular composition, the role of EC dysfunction in pulmonary fibrosis (PF) remains unclear. We hypothesize that sterol regulatory element-bind...
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| creator | Martin, Marcy Zhang, Jiao Miao, Yifei He, Ming Kang, Jian Huang, Hsi-Yuan Chou, Chih-Hung Huang, Tse-Shun Hong, Hsiao-Chin Su, Shu-Han Wong, Simon S. Harper, Rebecca L. Wang, Lingli Bhattacharjee, Rakesh Huang, Hsien-Da Chen, Zhen Bouman Malhotra, Atul Rabinovitch, Marlene Hagood, James S. Shyy, John Y-J |
| description | Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease with limited treatment options. Despite endothelial cells (ECs) comprising 30% of the lung cellular composition, the role of EC dysfunction in pulmonary fibrosis (PF) remains unclear. We hypothesize that sterol regulatory element-binding protein 2 (SREBP2) plays a critical role in the pathogenesis of PF via EC phenotypic modifications. Transcriptome data demonstrate that SREBP2 overexpression in ECs led to the induction of the TGF, Wnt, and cytoskeleton remodeling gene ontology pathways and the increased expression of mesenchymal genes, such as snail family transcriptional repressor 1 (snai1), alpha-smooth muscle actin, vimentin, and neural cadherin. Furthermore, SREBP2 directly bound to the promoter regions and transactivated these mesenchymal genes. This transcriptomic change was associated with an epigenetic and phenotypic switch in ECs, leading to increased proliferation, stress fiber formation, and ECM deposition. Mice with endothelial-specific transgenic overexpression of SREBP2 (EC-SREBP2[N]-Tg mice) that were administered bleomycin to induce PF demonstrated exacerbated vascular remodeling and increased mesenchymal transition in the lung. SREBP2 was also found to be markedly increased in lung specimens from patients with IPF. These results suggest that SREBP2, induced by lung injury, can exacerbate PF in rodent models and in human patients with IPF. |
| doi_str_mv | 10.1172/jci.insight.125635 |
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Despite endothelial cells (ECs) comprising 30% of the lung cellular composition, the role of EC dysfunction in pulmonary fibrosis (PF) remains unclear. We hypothesize that sterol regulatory element-binding protein 2 (SREBP2) plays a critical role in the pathogenesis of PF via EC phenotypic modifications. Transcriptome data demonstrate that SREBP2 overexpression in ECs led to the induction of the TGF, Wnt, and cytoskeleton remodeling gene ontology pathways and the increased expression of mesenchymal genes, such as snail family transcriptional repressor 1 (snai1), alpha-smooth muscle actin, vimentin, and neural cadherin. Furthermore, SREBP2 directly bound to the promoter regions and transactivated these mesenchymal genes. This transcriptomic change was associated with an epigenetic and phenotypic switch in ECs, leading to increased proliferation, stress fiber formation, and ECM deposition. Mice with endothelial-specific transgenic overexpression of SREBP2 (EC-SREBP2[N]-Tg mice) that were administered bleomycin to induce PF demonstrated exacerbated vascular remodeling and increased mesenchymal transition in the lung. SREBP2 was also found to be markedly increased in lung specimens from patients with IPF. These results suggest that SREBP2, induced by lung injury, can exacerbate PF in rodent models and in human patients with IPF.</description><identifier>ISSN: 2379-3708</identifier><identifier>EISSN: 2379-3708</identifier><identifier>DOI: 10.1172/jci.insight.125635</identifier><identifier>PMID: 34806652</identifier><language>eng</language><publisher>ANN ARBOR: Amer Soc Clinical Investigation Inc</publisher><subject>Animals ; Endothelial Cells - metabolism ; Humans ; Life Sciences & Biomedicine ; Medicine, Research & Experimental ; Mice ; Pulmonary Fibrosis - genetics ; Pulmonology ; Research & Experimental Medicine ; Science & Technology ; Sterol Regulatory Element Binding Protein 2 - metabolism ; Vascular biology</subject><ispartof>JCI insight, 2021-11, Vol.6 (22), Article 125635</ispartof><rights>2021 Martin et al. 2021 Martin et al.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>27</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000721549800001</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c468t-2e48d9fdb9619e4e996e0c4da820f0663a02becfd156ef395021075338cfbfb3</citedby><cites>FETCH-LOGICAL-c468t-2e48d9fdb9619e4e996e0c4da820f0663a02becfd156ef395021075338cfbfb3</cites><orcidid>0000-0001-5714-1718 ; 0000-0003-0035-0185 ; 0000-0001-7886-7104 ; 0000-0003-3938-0330 ; 0000-0002-3291-1090 ; 0000-0002-5625-753X ; 0000-0003-4882-5629 ; 0000-0001-5871-9067</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8663776/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8663776/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,2103,2115,27929,27930,39263,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34806652$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Martin, Marcy</creatorcontrib><creatorcontrib>Zhang, Jiao</creatorcontrib><creatorcontrib>Miao, Yifei</creatorcontrib><creatorcontrib>He, Ming</creatorcontrib><creatorcontrib>Kang, Jian</creatorcontrib><creatorcontrib>Huang, Hsi-Yuan</creatorcontrib><creatorcontrib>Chou, Chih-Hung</creatorcontrib><creatorcontrib>Huang, Tse-Shun</creatorcontrib><creatorcontrib>Hong, Hsiao-Chin</creatorcontrib><creatorcontrib>Su, Shu-Han</creatorcontrib><creatorcontrib>Wong, Simon S.</creatorcontrib><creatorcontrib>Harper, Rebecca L.</creatorcontrib><creatorcontrib>Wang, Lingli</creatorcontrib><creatorcontrib>Bhattacharjee, Rakesh</creatorcontrib><creatorcontrib>Huang, Hsien-Da</creatorcontrib><creatorcontrib>Chen, Zhen Bouman</creatorcontrib><creatorcontrib>Malhotra, Atul</creatorcontrib><creatorcontrib>Rabinovitch, Marlene</creatorcontrib><creatorcontrib>Hagood, James S.</creatorcontrib><creatorcontrib>Shyy, John Y-J</creatorcontrib><title>Role of endothelial cells in pulmonary fibrosis via SREBP2 activation</title><title>JCI insight</title><addtitle>JCI INSIGHT</addtitle><addtitle>JCI Insight</addtitle><description>Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease with limited treatment options. Despite endothelial cells (ECs) comprising 30% of the lung cellular composition, the role of EC dysfunction in pulmonary fibrosis (PF) remains unclear. We hypothesize that sterol regulatory element-binding protein 2 (SREBP2) plays a critical role in the pathogenesis of PF via EC phenotypic modifications. Transcriptome data demonstrate that SREBP2 overexpression in ECs led to the induction of the TGF, Wnt, and cytoskeleton remodeling gene ontology pathways and the increased expression of mesenchymal genes, such as snail family transcriptional repressor 1 (snai1), alpha-smooth muscle actin, vimentin, and neural cadherin. Furthermore, SREBP2 directly bound to the promoter regions and transactivated these mesenchymal genes. This transcriptomic change was associated with an epigenetic and phenotypic switch in ECs, leading to increased proliferation, stress fiber formation, and ECM deposition. Mice with endothelial-specific transgenic overexpression of SREBP2 (EC-SREBP2[N]-Tg mice) that were administered bleomycin to induce PF demonstrated exacerbated vascular remodeling and increased mesenchymal transition in the lung. SREBP2 was also found to be markedly increased in lung specimens from patients with IPF. These results suggest that SREBP2, induced by lung injury, can exacerbate PF in rodent models and in human patients with IPF.</description><subject>Animals</subject><subject>Endothelial Cells - metabolism</subject><subject>Humans</subject><subject>Life Sciences & Biomedicine</subject><subject>Medicine, Research & Experimental</subject><subject>Mice</subject><subject>Pulmonary Fibrosis - genetics</subject><subject>Pulmonology</subject><subject>Research & Experimental Medicine</subject><subject>Science & Technology</subject><subject>Sterol Regulatory Element Binding Protein 2 - metabolism</subject><subject>Vascular biology</subject><issn>2379-3708</issn><issn>2379-3708</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>HGBXW</sourceid><sourceid>EIF</sourceid><sourceid>DOA</sourceid><recordid>eNqNkU1vEzEQhlcIRKvSP8AB7REJJfhj_XVBgijQSpVApXfL6x0njjZ2WHtT8e9xsmnU3jjZsp95ZzRPVb3HaI6xIJ831s99SH61znNMGKfsVXVJqFAzKpB8_ex-UV2ntEEIYdEQxOTb6oI2EnHOyGW1vI891NHVELqY19B709cW-j7VPtS7sd_GYIa_tfPtEJNP9d6b-vf98tsvUhub_d5kH8O76o0zfYLr03lVPXxfPixuZnc_f9wuvt7NbMNlnhFoZKdc1yqOFTSgFAdkm85IglwZiBpEWrCuw4yDo4ohgpFglErrWtfSq-p2iu2i2ejd4LdlNB2N18eHOKy0GbK3PWijpMBEONVYXhpYSVrETOtYA9goYkvWlylrN7Zb6CyEPJj-RejLn-DXehX3WpY5heAl4OMpYIh_RkhZb306bM4EiGPShCMkCUFHlEyoLTtMA7hzG4z0waYuNvXJpp5slqIPzwc8lzy5K8CnCXiENrpkPQQLZ6z4FgSzRkl0UF9o-f_0wuej10UcQ6b_AFj-v0M</recordid><startdate>20211122</startdate><enddate>20211122</enddate><creator>Martin, Marcy</creator><creator>Zhang, Jiao</creator><creator>Miao, Yifei</creator><creator>He, Ming</creator><creator>Kang, Jian</creator><creator>Huang, Hsi-Yuan</creator><creator>Chou, Chih-Hung</creator><creator>Huang, Tse-Shun</creator><creator>Hong, Hsiao-Chin</creator><creator>Su, Shu-Han</creator><creator>Wong, Simon S.</creator><creator>Harper, Rebecca L.</creator><creator>Wang, Lingli</creator><creator>Bhattacharjee, Rakesh</creator><creator>Huang, Hsien-Da</creator><creator>Chen, Zhen Bouman</creator><creator>Malhotra, Atul</creator><creator>Rabinovitch, Marlene</creator><creator>Hagood, James S.</creator><creator>Shyy, John Y-J</creator><general>Amer Soc Clinical Investigation Inc</general><general>American Society for Clinical Investigation</general><general>American Society for Clinical investigation</general><scope>BLEPL</scope><scope>DTL</scope><scope>HGBXW</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><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0001-5714-1718</orcidid><orcidid>https://orcid.org/0000-0003-0035-0185</orcidid><orcidid>https://orcid.org/0000-0001-7886-7104</orcidid><orcidid>https://orcid.org/0000-0003-3938-0330</orcidid><orcidid>https://orcid.org/0000-0002-3291-1090</orcidid><orcidid>https://orcid.org/0000-0002-5625-753X</orcidid><orcidid>https://orcid.org/0000-0003-4882-5629</orcidid><orcidid>https://orcid.org/0000-0001-5871-9067</orcidid></search><sort><creationdate>20211122</creationdate><title>Role of endothelial cells in pulmonary fibrosis via SREBP2 activation</title><author>Martin, Marcy ; Zhang, Jiao ; Miao, Yifei ; He, Ming ; Kang, Jian ; Huang, Hsi-Yuan ; Chou, Chih-Hung ; Huang, Tse-Shun ; Hong, Hsiao-Chin ; Su, Shu-Han ; Wong, Simon S. ; Harper, Rebecca L. ; Wang, Lingli ; Bhattacharjee, Rakesh ; Huang, Hsien-Da ; Chen, Zhen Bouman ; Malhotra, Atul ; Rabinovitch, Marlene ; Hagood, James S. ; Shyy, John Y-J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c468t-2e48d9fdb9619e4e996e0c4da820f0663a02becfd156ef395021075338cfbfb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>Endothelial Cells - metabolism</topic><topic>Humans</topic><topic>Life Sciences & Biomedicine</topic><topic>Medicine, Research & Experimental</topic><topic>Mice</topic><topic>Pulmonary Fibrosis - genetics</topic><topic>Pulmonology</topic><topic>Research & Experimental Medicine</topic><topic>Science & Technology</topic><topic>Sterol Regulatory Element Binding Protein 2 - metabolism</topic><topic>Vascular biology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Martin, Marcy</creatorcontrib><creatorcontrib>Zhang, Jiao</creatorcontrib><creatorcontrib>Miao, Yifei</creatorcontrib><creatorcontrib>He, Ming</creatorcontrib><creatorcontrib>Kang, Jian</creatorcontrib><creatorcontrib>Huang, Hsi-Yuan</creatorcontrib><creatorcontrib>Chou, Chih-Hung</creatorcontrib><creatorcontrib>Huang, Tse-Shun</creatorcontrib><creatorcontrib>Hong, Hsiao-Chin</creatorcontrib><creatorcontrib>Su, Shu-Han</creatorcontrib><creatorcontrib>Wong, Simon S.</creatorcontrib><creatorcontrib>Harper, Rebecca L.</creatorcontrib><creatorcontrib>Wang, Lingli</creatorcontrib><creatorcontrib>Bhattacharjee, Rakesh</creatorcontrib><creatorcontrib>Huang, Hsien-Da</creatorcontrib><creatorcontrib>Chen, Zhen Bouman</creatorcontrib><creatorcontrib>Malhotra, Atul</creatorcontrib><creatorcontrib>Rabinovitch, Marlene</creatorcontrib><creatorcontrib>Hagood, James S.</creatorcontrib><creatorcontrib>Shyy, John Y-J</creatorcontrib><collection>Web of Science Core Collection</collection><collection>Science Citation Index Expanded</collection><collection>Web of Science - Science Citation Index Expanded - 2021</collection><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><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>JCI insight</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Martin, Marcy</au><au>Zhang, Jiao</au><au>Miao, Yifei</au><au>He, Ming</au><au>Kang, Jian</au><au>Huang, Hsi-Yuan</au><au>Chou, Chih-Hung</au><au>Huang, Tse-Shun</au><au>Hong, Hsiao-Chin</au><au>Su, Shu-Han</au><au>Wong, Simon S.</au><au>Harper, Rebecca L.</au><au>Wang, Lingli</au><au>Bhattacharjee, Rakesh</au><au>Huang, Hsien-Da</au><au>Chen, Zhen Bouman</au><au>Malhotra, Atul</au><au>Rabinovitch, Marlene</au><au>Hagood, James S.</au><au>Shyy, John Y-J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of endothelial cells in pulmonary fibrosis via SREBP2 activation</atitle><jtitle>JCI insight</jtitle><stitle>JCI INSIGHT</stitle><addtitle>JCI Insight</addtitle><date>2021-11-22</date><risdate>2021</risdate><volume>6</volume><issue>22</issue><artnum>125635</artnum><issn>2379-3708</issn><eissn>2379-3708</eissn><abstract>Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease with limited treatment options. Despite endothelial cells (ECs) comprising 30% of the lung cellular composition, the role of EC dysfunction in pulmonary fibrosis (PF) remains unclear. We hypothesize that sterol regulatory element-binding protein 2 (SREBP2) plays a critical role in the pathogenesis of PF via EC phenotypic modifications. Transcriptome data demonstrate that SREBP2 overexpression in ECs led to the induction of the TGF, Wnt, and cytoskeleton remodeling gene ontology pathways and the increased expression of mesenchymal genes, such as snail family transcriptional repressor 1 (snai1), alpha-smooth muscle actin, vimentin, and neural cadherin. Furthermore, SREBP2 directly bound to the promoter regions and transactivated these mesenchymal genes. This transcriptomic change was associated with an epigenetic and phenotypic switch in ECs, leading to increased proliferation, stress fiber formation, and ECM deposition. Mice with endothelial-specific transgenic overexpression of SREBP2 (EC-SREBP2[N]-Tg mice) that were administered bleomycin to induce PF demonstrated exacerbated vascular remodeling and increased mesenchymal transition in the lung. SREBP2 was also found to be markedly increased in lung specimens from patients with IPF. These results suggest that SREBP2, induced by lung injury, can exacerbate PF in rodent models and in human patients with IPF.</abstract><cop>ANN ARBOR</cop><pub>Amer Soc Clinical Investigation Inc</pub><pmid>34806652</pmid><doi>10.1172/jci.insight.125635</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0001-5714-1718</orcidid><orcidid>https://orcid.org/0000-0003-0035-0185</orcidid><orcidid>https://orcid.org/0000-0001-7886-7104</orcidid><orcidid>https://orcid.org/0000-0003-3938-0330</orcidid><orcidid>https://orcid.org/0000-0002-3291-1090</orcidid><orcidid>https://orcid.org/0000-0002-5625-753X</orcidid><orcidid>https://orcid.org/0000-0003-4882-5629</orcidid><orcidid>https://orcid.org/0000-0001-5871-9067</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Endothelial Cells - metabolism Humans Life Sciences & Biomedicine Medicine, Research & Experimental Mice Pulmonary Fibrosis - genetics Pulmonology Research & Experimental Medicine Science & Technology Sterol Regulatory Element Binding Protein 2 - metabolism Vascular biology |
| title | Role of endothelial cells in pulmonary fibrosis via SREBP2 activation |
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