Potential role of the Jagged1/Notch1 signaling pathway in the endothelial‐myofibroblast transition during BLM‐induced pulmonary fibrosis
Endothelial cell myofibroblast transition (EndoMT) is found during the process of bleomycin (BLM)‐induced pulmonary fibrosis in rats, and plays a very important role in sustaining inflammation and collagen secretion. Moreover, some studies have suggested that the Notch1 signaling pathway may be invo...
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| Veröffentlicht in: | Journal of cellular physiology 2018-03, Vol.233 (3), p.2451-2463 |
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| description | Endothelial cell myofibroblast transition (EndoMT) is found during the process of bleomycin (BLM)‐induced pulmonary fibrosis in rats, and plays a very important role in sustaining inflammation and collagen secretion. Moreover, some studies have suggested that the Notch1 signaling pathway may be involved in the expression of α‐smooth muscle actin (α‐SMA) in pulmonary microvascular endothelial cells (PMVECs), a protein marker of EndoMT. Therefore, we aimed to investigate the expression level of α‐SMA and Notch1‐related signaling molecules in PMVECs from BLM‐induced rats and determine the relationship between the Notch1 signaling pathway and the expression of α‐SMA in PMVECs. We found that the expression levels of α‐SMA, Notch1, and Jagged1 were upregulated, while the expression levels of Dll4 were downregulated. Furthermore, there was a positive correlation between the expression of Jagged1 and the α‐SMA proteins in PMVECs, and NF‐κB was downregulated by decreasing the expression of Jagged1. In conclusion, the Jagged1/Notch1 signaling pathway is activated in PMVECs during the pathogenesis of BLM‐induced pulmonary fibrosis in rats, and it may induce α‐SMA expression via a non‐canonical pathway involving NF‐κB as the target molecule. The precise mechanism and the molecules involved in this signaling pathway need to be further elucidated.
The Jagged1/Notch1 signaling pathway is activated in PMVECs during the pathogenesis of BLM‐induced pulmonary fibrosis in rats, and it may induce α‐SMA expression via a non‐canonical pathway involving NF‐κB as the target molecule. |
| doi_str_mv | 10.1002/jcp.26122 |
| format | Article |
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The Jagged1/Notch1 signaling pathway is activated in PMVECs during the pathogenesis of BLM‐induced pulmonary fibrosis in rats, and it may induce α‐SMA expression via a non‐canonical pathway involving NF‐κB as the target molecule.</description><identifier>ISSN: 0021-9541</identifier><identifier>EISSN: 1097-4652</identifier><identifier>DOI: 10.1002/jcp.26122</identifier><identifier>PMID: 28776666</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Actin ; Actins - genetics ; Actins - metabolism ; Animals ; Bleomycin ; Cell Transdifferentiation ; Cells, Cultured ; Collagen ; Disease Models, Animal ; EndoMT ; Endothelial cells ; Endothelial Cells - metabolism ; Endothelial Cells - pathology ; Epithelial-Mesenchymal Transition ; Fibrosis ; Intracellular Signaling Peptides and Proteins - genetics ; Intracellular Signaling Peptides and Proteins - metabolism ; Jagged-1 Protein - genetics ; Jagged-1 Protein - metabolism ; Jagged1 ; Jagged1 protein ; Kinases ; Lung - blood supply ; Lung - metabolism ; Lung - pathology ; Lung diseases ; Male ; Membrane Proteins - genetics ; Membrane Proteins - metabolism ; Microvasculature ; Microvessels - metabolism ; Microvessels - pathology ; Muscles ; Myofibroblasts - metabolism ; Myofibroblasts - pathology ; NF-kappa B - metabolism ; NF-κB protein ; Nitric oxide ; Notch1 ; Notch1 protein ; Pathogenesis ; Proteins ; Pulmonary fibrosis ; Pulmonary Fibrosis - chemically induced ; Pulmonary Fibrosis - genetics ; Pulmonary Fibrosis - metabolism ; Pulmonary Fibrosis - pathology ; pulmonary microvascular endothelial cells ; Rats ; Rats, Sprague-Dawley ; Receptor, Notch1 - genetics ; Receptor, Notch1 - metabolism ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Rodents ; Secretion ; Signal Transduction ; Signaling ; Smooth muscle ; Up-Regulation</subject><ispartof>Journal of cellular physiology, 2018-03, Vol.233 (3), p.2451-2463</ispartof><rights>2017 Wiley Periodicals, Inc.</rights><rights>2018 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3532-ea96dc03f69b43cef4ea654beb3e59b4314cdfbbc98e9ae2cfdddad61e8d43823</citedby><cites>FETCH-LOGICAL-c3532-ea96dc03f69b43cef4ea654beb3e59b4314cdfbbc98e9ae2cfdddad61e8d43823</cites><orcidid>0000-0002-9971-5692</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%2Fjcp.26122$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcp.26122$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,781,785,1418,27929,27930,45579,45580</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28776666$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yin, Qian</creatorcontrib><creatorcontrib>Wang, Weihua</creatorcontrib><creatorcontrib>Cui, Guangbin</creatorcontrib><creatorcontrib>Yan, Linfeng</creatorcontrib><creatorcontrib>Zhang, Song</creatorcontrib><title>Potential role of the Jagged1/Notch1 signaling pathway in the endothelial‐myofibroblast transition during BLM‐induced pulmonary fibrosis</title><title>Journal of cellular physiology</title><addtitle>J Cell Physiol</addtitle><description>Endothelial cell myofibroblast transition (EndoMT) is found during the process of bleomycin (BLM)‐induced pulmonary fibrosis in rats, and plays a very important role in sustaining inflammation and collagen secretion. Moreover, some studies have suggested that the Notch1 signaling pathway may be involved in the expression of α‐smooth muscle actin (α‐SMA) in pulmonary microvascular endothelial cells (PMVECs), a protein marker of EndoMT. Therefore, we aimed to investigate the expression level of α‐SMA and Notch1‐related signaling molecules in PMVECs from BLM‐induced rats and determine the relationship between the Notch1 signaling pathway and the expression of α‐SMA in PMVECs. We found that the expression levels of α‐SMA, Notch1, and Jagged1 were upregulated, while the expression levels of Dll4 were downregulated. Furthermore, there was a positive correlation between the expression of Jagged1 and the α‐SMA proteins in PMVECs, and NF‐κB was downregulated by decreasing the expression of Jagged1. In conclusion, the Jagged1/Notch1 signaling pathway is activated in PMVECs during the pathogenesis of BLM‐induced pulmonary fibrosis in rats, and it may induce α‐SMA expression via a non‐canonical pathway involving NF‐κB as the target molecule. The precise mechanism and the molecules involved in this signaling pathway need to be further elucidated.
The Jagged1/Notch1 signaling pathway is activated in PMVECs during the pathogenesis of BLM‐induced pulmonary fibrosis in rats, and it may induce α‐SMA expression via a non‐canonical pathway involving NF‐κB as the target molecule.</description><subject>Actin</subject><subject>Actins - genetics</subject><subject>Actins - metabolism</subject><subject>Animals</subject><subject>Bleomycin</subject><subject>Cell Transdifferentiation</subject><subject>Cells, Cultured</subject><subject>Collagen</subject><subject>Disease Models, Animal</subject><subject>EndoMT</subject><subject>Endothelial cells</subject><subject>Endothelial Cells - metabolism</subject><subject>Endothelial Cells - pathology</subject><subject>Epithelial-Mesenchymal Transition</subject><subject>Fibrosis</subject><subject>Intracellular Signaling Peptides and Proteins - genetics</subject><subject>Intracellular Signaling Peptides and Proteins - metabolism</subject><subject>Jagged-1 Protein - genetics</subject><subject>Jagged-1 Protein - metabolism</subject><subject>Jagged1</subject><subject>Jagged1 protein</subject><subject>Kinases</subject><subject>Lung - blood supply</subject><subject>Lung - metabolism</subject><subject>Lung - pathology</subject><subject>Lung diseases</subject><subject>Male</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - metabolism</subject><subject>Microvasculature</subject><subject>Microvessels - metabolism</subject><subject>Microvessels - pathology</subject><subject>Muscles</subject><subject>Myofibroblasts - metabolism</subject><subject>Myofibroblasts - pathology</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB protein</subject><subject>Nitric oxide</subject><subject>Notch1</subject><subject>Notch1 protein</subject><subject>Pathogenesis</subject><subject>Proteins</subject><subject>Pulmonary fibrosis</subject><subject>Pulmonary Fibrosis - chemically induced</subject><subject>Pulmonary Fibrosis - genetics</subject><subject>Pulmonary Fibrosis - metabolism</subject><subject>Pulmonary Fibrosis - pathology</subject><subject>pulmonary microvascular endothelial cells</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptor, Notch1 - genetics</subject><subject>Receptor, Notch1 - metabolism</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Rodents</subject><subject>Secretion</subject><subject>Signal Transduction</subject><subject>Signaling</subject><subject>Smooth muscle</subject><subject>Up-Regulation</subject><issn>0021-9541</issn><issn>1097-4652</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kM9OGzEQxi3UqgTogRdAlnrqYYn_7DrrI0QtLUqBQ3teee3ZxNHGXmyvUG59AA48Y58EJ6G9dS4jzfy-TzMfQueUXFJC2HSth0smKGNHaEKJnBWlqNg7NMk7WsiqpMfoJMY1IURKzj-gY1bPZiLXBD0_-AQuWdXj4HvAvsNpBfhWLZdg6PTOJ72iONqlU711SzyotHpSW2zdngNnfO591v_5_bLZ-s62wbe9igmnoFy0yXqHzRh24uvFj0xZZ0YNBg9jv_FOhS3ei6KNZ-h9p_oIH9_6Kfr19cvP-bdicX_zfX61KDSvOCtASWE04Z2Qbck1dCUoUZUttByq3YiW2nRtq2UNUgHTnTFGGUGhNiWvGT9Fnw6-Q_CPI8TUrP0Y8oexoVLUVHAqd9TnA6XzcTFA1wzBbvK9DSXNLvcm597sc8_sxZvj2G7A_CP_Bp2B6QF4sj1s_-_U3M4fDpavPJ-SjQ</recordid><startdate>201803</startdate><enddate>201803</enddate><creator>Yin, Qian</creator><creator>Wang, Weihua</creator><creator>Cui, Guangbin</creator><creator>Yan, Linfeng</creator><creator>Zhang, Song</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>7TK</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><orcidid>https://orcid.org/0000-0002-9971-5692</orcidid></search><sort><creationdate>201803</creationdate><title>Potential role of the Jagged1/Notch1 signaling pathway in the endothelial‐myofibroblast transition during BLM‐induced pulmonary fibrosis</title><author>Yin, Qian ; Wang, Weihua ; Cui, Guangbin ; Yan, Linfeng ; Zhang, Song</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3532-ea96dc03f69b43cef4ea654beb3e59b4314cdfbbc98e9ae2cfdddad61e8d43823</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Actin</topic><topic>Actins - genetics</topic><topic>Actins - metabolism</topic><topic>Animals</topic><topic>Bleomycin</topic><topic>Cell Transdifferentiation</topic><topic>Cells, Cultured</topic><topic>Collagen</topic><topic>Disease Models, Animal</topic><topic>EndoMT</topic><topic>Endothelial cells</topic><topic>Endothelial Cells - metabolism</topic><topic>Endothelial Cells - pathology</topic><topic>Epithelial-Mesenchymal Transition</topic><topic>Fibrosis</topic><topic>Intracellular Signaling Peptides and Proteins - genetics</topic><topic>Intracellular Signaling Peptides and Proteins - metabolism</topic><topic>Jagged-1 Protein - genetics</topic><topic>Jagged-1 Protein - metabolism</topic><topic>Jagged1</topic><topic>Jagged1 protein</topic><topic>Kinases</topic><topic>Lung - blood supply</topic><topic>Lung - metabolism</topic><topic>Lung - pathology</topic><topic>Lung diseases</topic><topic>Male</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - metabolism</topic><topic>Microvasculature</topic><topic>Microvessels - metabolism</topic><topic>Microvessels - pathology</topic><topic>Muscles</topic><topic>Myofibroblasts - metabolism</topic><topic>Myofibroblasts - pathology</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB protein</topic><topic>Nitric oxide</topic><topic>Notch1</topic><topic>Notch1 protein</topic><topic>Pathogenesis</topic><topic>Proteins</topic><topic>Pulmonary fibrosis</topic><topic>Pulmonary Fibrosis - chemically induced</topic><topic>Pulmonary Fibrosis - genetics</topic><topic>Pulmonary Fibrosis - metabolism</topic><topic>Pulmonary Fibrosis - pathology</topic><topic>pulmonary microvascular endothelial cells</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptor, Notch1 - genetics</topic><topic>Receptor, Notch1 - metabolism</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Rodents</topic><topic>Secretion</topic><topic>Signal Transduction</topic><topic>Signaling</topic><topic>Smooth muscle</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yin, Qian</creatorcontrib><creatorcontrib>Wang, Weihua</creatorcontrib><creatorcontrib>Cui, Guangbin</creatorcontrib><creatorcontrib>Yan, Linfeng</creatorcontrib><creatorcontrib>Zhang, Song</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Journal of cellular physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yin, Qian</au><au>Wang, Weihua</au><au>Cui, Guangbin</au><au>Yan, Linfeng</au><au>Zhang, Song</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Potential role of the Jagged1/Notch1 signaling pathway in the endothelial‐myofibroblast transition during BLM‐induced pulmonary fibrosis</atitle><jtitle>Journal of cellular physiology</jtitle><addtitle>J Cell Physiol</addtitle><date>2018-03</date><risdate>2018</risdate><volume>233</volume><issue>3</issue><spage>2451</spage><epage>2463</epage><pages>2451-2463</pages><issn>0021-9541</issn><eissn>1097-4652</eissn><abstract>Endothelial cell myofibroblast transition (EndoMT) is found during the process of bleomycin (BLM)‐induced pulmonary fibrosis in rats, and plays a very important role in sustaining inflammation and collagen secretion. Moreover, some studies have suggested that the Notch1 signaling pathway may be involved in the expression of α‐smooth muscle actin (α‐SMA) in pulmonary microvascular endothelial cells (PMVECs), a protein marker of EndoMT. Therefore, we aimed to investigate the expression level of α‐SMA and Notch1‐related signaling molecules in PMVECs from BLM‐induced rats and determine the relationship between the Notch1 signaling pathway and the expression of α‐SMA in PMVECs. We found that the expression levels of α‐SMA, Notch1, and Jagged1 were upregulated, while the expression levels of Dll4 were downregulated. Furthermore, there was a positive correlation between the expression of Jagged1 and the α‐SMA proteins in PMVECs, and NF‐κB was downregulated by decreasing the expression of Jagged1. In conclusion, the Jagged1/Notch1 signaling pathway is activated in PMVECs during the pathogenesis of BLM‐induced pulmonary fibrosis in rats, and it may induce α‐SMA expression via a non‐canonical pathway involving NF‐κB as the target molecule. The precise mechanism and the molecules involved in this signaling pathway need to be further elucidated.
The Jagged1/Notch1 signaling pathway is activated in PMVECs during the pathogenesis of BLM‐induced pulmonary fibrosis in rats, and it may induce α‐SMA expression via a non‐canonical pathway involving NF‐κB as the target molecule.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>28776666</pmid><doi>10.1002/jcp.26122</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-9971-5692</orcidid></addata></record> |
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| subjects | Actin Actins - genetics Actins - metabolism Animals Bleomycin Cell Transdifferentiation Cells, Cultured Collagen Disease Models, Animal EndoMT Endothelial cells Endothelial Cells - metabolism Endothelial Cells - pathology Epithelial-Mesenchymal Transition Fibrosis Intracellular Signaling Peptides and Proteins - genetics Intracellular Signaling Peptides and Proteins - metabolism Jagged-1 Protein - genetics Jagged-1 Protein - metabolism Jagged1 Jagged1 protein Kinases Lung - blood supply Lung - metabolism Lung - pathology Lung diseases Male Membrane Proteins - genetics Membrane Proteins - metabolism Microvasculature Microvessels - metabolism Microvessels - pathology Muscles Myofibroblasts - metabolism Myofibroblasts - pathology NF-kappa B - metabolism NF-κB protein Nitric oxide Notch1 Notch1 protein Pathogenesis Proteins Pulmonary fibrosis Pulmonary Fibrosis - chemically induced Pulmonary Fibrosis - genetics Pulmonary Fibrosis - metabolism Pulmonary Fibrosis - pathology pulmonary microvascular endothelial cells Rats Rats, Sprague-Dawley Receptor, Notch1 - genetics Receptor, Notch1 - metabolism RNA, Messenger - genetics RNA, Messenger - metabolism Rodents Secretion Signal Transduction Signaling Smooth muscle Up-Regulation |
| title | Potential role of the Jagged1/Notch1 signaling pathway in the endothelial‐myofibroblast transition during BLM‐induced pulmonary fibrosis |
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