Oroxylin A prevents angiogenesis of LSECs in liver fibrosis via inhibition of YAP/HIF‐1α signaling
Angiogenesis of liver sinusoidal endothelial cells (LSECs) accompanies with hypoxia in liver fibrosis and they are of mutual promotion, which has raised wide concern. Here we established murine model of liver fibrosis and found that oroxylin A (40 mg/kg) could ameliorate angiogenesis in liver fibros...
Gespeichert in:
| Veröffentlicht in: | Journal of cellular biochemistry 2018-02, Vol.119 (2), p.2258-2268 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 2268 |
|---|---|
| container_issue | 2 |
| container_start_page | 2258 |
| container_title | Journal of cellular biochemistry |
| container_volume | 119 |
| creator | Zhang, Chenxi Bian, Mianli Chen, Xingran Jin, Huanhuan Zhao, Shifeng Yang, Xiang Shao, Jiangjuan Chen, Anping Guo, Qinglong Zhang, Feng Zheng, Shizhong |
| description | Angiogenesis of liver sinusoidal endothelial cells (LSECs) accompanies with hypoxia in liver fibrosis and they are of mutual promotion, which has raised wide concern. Here we established murine model of liver fibrosis and found that oroxylin A (40 mg/kg) could ameliorate angiogenesis in liver fibrosis may related to hypoxia inducible factor 1α (HIF‐1α). The underlying mechanism was further investigated by isolating and culturing murine primary LSECs. Hypoxia induced vascular endothelial growth factor A (VEGF‐A), angiopoietin 2 (Ang‐2), and platelet endothelial cell adhesion molecule‐1 (PECAM‐1/CD31) elevated in LSECs were reduced by oroxylin A or acriflavine (ACF, an HIF‐1α inhibitor), indicating HIF‐1α involved the angiogenesis of LSECs. Additionally, interference with Yes‐associated protein (YAP) significant downregulated the protein expression of HIF‐1α and VEGF‐A, while YAP plasmid exhibited an opposite effect. We next found that oroxylin A inhibited hypoxia‐induced nuclear translocation of YAP, which may influence the accumulation of HIF‐1α and subsequently decrease transcription of downstream target gene including VEGF‐A and Ang‐2, thereby exerting an anti‐angiogenic activity.
Oroxylin A inhibited hypoxia‐induced nuclear translocation of YAP, which may influence the accumulation of HIF‐1α and subsequently decrease transcription of downstream target gene including VEGF‐A and Ang‐2, thereby exerting an anti‐angiogenic activity. |
| doi_str_mv | 10.1002/jcb.26388 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_1979769349</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1979769349</sourcerecordid><originalsourceid>FETCH-LOGICAL-c2688-b8ef821065c791db1b5e7d381f69c469b0c469d4be0a14cf67edac32bfa3d4f23</originalsourceid><addsrcrecordid>eNp1kE1OwzAQRi0EoqWw4ALIEisWaf3XxF6WqKVFlYoELFhFcWIHVyUpdlvojiNwFS7CITgJDins2MxIM09PMx8Apxh1MUKkN89kl4SU8z3QxkhEAQsZ2wdtFFEUEIpJCxw5N0cICUHJIWgRzvsREawN1MxWr9uFKeEALq3aqHLlYFoWpipUqZxxsNJwejuMHfTMwmyUhdpIW9WrjUn99NFIszJVWZMPg5veeDL6envHnx_QmaJMvbs4Bgc6XTh1susdcD8a3sXjYDq7msSDaZCRkPNAcqU5wSjsZ5HAucSyr6KccqxDkbFQSFTXnEmFUswyHUYqTzNKpE5pzjShHXDeeJe2el4rt0rm1dr6G1yCRSSiUFAmPHXRUJl_w1mlk6U1T6ndJhgldaCJDzT5CdSzZzvjWj6p_I_8TdADvQZ4MQu1_d-UXMeXjfIbnH-Ayg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1979769349</pqid></control><display><type>article</type><title>Oroxylin A prevents angiogenesis of LSECs in liver fibrosis via inhibition of YAP/HIF‐1α signaling</title><source>MEDLINE</source><source>Wiley Online Library All Journals</source><creator>Zhang, Chenxi ; Bian, Mianli ; Chen, Xingran ; Jin, Huanhuan ; Zhao, Shifeng ; Yang, Xiang ; Shao, Jiangjuan ; Chen, Anping ; Guo, Qinglong ; Zhang, Feng ; Zheng, Shizhong</creator><creatorcontrib>Zhang, Chenxi ; Bian, Mianli ; Chen, Xingran ; Jin, Huanhuan ; Zhao, Shifeng ; Yang, Xiang ; Shao, Jiangjuan ; Chen, Anping ; Guo, Qinglong ; Zhang, Feng ; Zheng, Shizhong</creatorcontrib><description>Angiogenesis of liver sinusoidal endothelial cells (LSECs) accompanies with hypoxia in liver fibrosis and they are of mutual promotion, which has raised wide concern. Here we established murine model of liver fibrosis and found that oroxylin A (40 mg/kg) could ameliorate angiogenesis in liver fibrosis may related to hypoxia inducible factor 1α (HIF‐1α). The underlying mechanism was further investigated by isolating and culturing murine primary LSECs. Hypoxia induced vascular endothelial growth factor A (VEGF‐A), angiopoietin 2 (Ang‐2), and platelet endothelial cell adhesion molecule‐1 (PECAM‐1/CD31) elevated in LSECs were reduced by oroxylin A or acriflavine (ACF, an HIF‐1α inhibitor), indicating HIF‐1α involved the angiogenesis of LSECs. Additionally, interference with Yes‐associated protein (YAP) significant downregulated the protein expression of HIF‐1α and VEGF‐A, while YAP plasmid exhibited an opposite effect. We next found that oroxylin A inhibited hypoxia‐induced nuclear translocation of YAP, which may influence the accumulation of HIF‐1α and subsequently decrease transcription of downstream target gene including VEGF‐A and Ang‐2, thereby exerting an anti‐angiogenic activity.
Oroxylin A inhibited hypoxia‐induced nuclear translocation of YAP, which may influence the accumulation of HIF‐1α and subsequently decrease transcription of downstream target gene including VEGF‐A and Ang‐2, thereby exerting an anti‐angiogenic activity.</description><identifier>ISSN: 0730-2312</identifier><identifier>EISSN: 1097-4644</identifier><identifier>DOI: 10.1002/jcb.26388</identifier><identifier>PMID: 28857294</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Acriflavine ; Adaptor Proteins, Signal Transducing - metabolism ; Angiogenesis ; Angiopoietin ; Angiopoietin-2 - genetics ; Angiopoietin-2 - metabolism ; Animal models ; Animals ; Carbon Tetrachloride - toxicity ; CD31 antigen ; Cell adhesion ; Cell adhesion & migration ; Cell adhesion molecules ; Cell Cycle Proteins ; Cells, Cultured ; Disease Models, Animal ; Endothelial cells ; Endothelial Cells - cytology ; Endothelial Cells - drug effects ; Endothelial Cells - metabolism ; Fibrosis ; Flavonoids - administration & dosage ; Flavonoids - pharmacology ; Gene Expression Regulation - drug effects ; Hepatocytes ; HIF‐1α ; Hypoxia ; Hypoxia-inducible factor 1 ; Hypoxia-Inducible Factor 1, alpha Subunit - metabolism ; Hypoxia-inducible factor 1a ; Liver ; Liver Cirrhosis - chemically induced ; Liver Cirrhosis - drug therapy ; Liver Cirrhosis - genetics ; Liver Cirrhosis - metabolism ; liver fibrosis ; Male ; Mice ; Neovascularization, Pathologic - metabolism ; Neovascularization, Pathologic - prevention & control ; Nuclear transport ; oroxylin A ; Phosphoproteins - metabolism ; Signal Transduction - drug effects ; Signaling ; Transcription ; Translocation ; Vascular endothelial growth factor ; Vascular Endothelial Growth Factor A - genetics ; Vascular Endothelial Growth Factor A - metabolism ; YAP ; Yes-associated protein</subject><ispartof>Journal of cellular biochemistry, 2018-02, Vol.119 (2), p.2258-2268</ispartof><rights>2017 Wiley Periodicals, Inc.</rights><rights>2018 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c2688-b8ef821065c791db1b5e7d381f69c469b0c469d4be0a14cf67edac32bfa3d4f23</citedby><cites>FETCH-LOGICAL-c2688-b8ef821065c791db1b5e7d381f69c469b0c469d4be0a14cf67edac32bfa3d4f23</cites><orcidid>0000-0003-0676-0572</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.26388$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcb.26388$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1413,27906,27907,45556,45557</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28857294$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Chenxi</creatorcontrib><creatorcontrib>Bian, Mianli</creatorcontrib><creatorcontrib>Chen, Xingran</creatorcontrib><creatorcontrib>Jin, Huanhuan</creatorcontrib><creatorcontrib>Zhao, Shifeng</creatorcontrib><creatorcontrib>Yang, Xiang</creatorcontrib><creatorcontrib>Shao, Jiangjuan</creatorcontrib><creatorcontrib>Chen, Anping</creatorcontrib><creatorcontrib>Guo, Qinglong</creatorcontrib><creatorcontrib>Zhang, Feng</creatorcontrib><creatorcontrib>Zheng, Shizhong</creatorcontrib><title>Oroxylin A prevents angiogenesis of LSECs in liver fibrosis via inhibition of YAP/HIF‐1α signaling</title><title>Journal of cellular biochemistry</title><addtitle>J Cell Biochem</addtitle><description>Angiogenesis of liver sinusoidal endothelial cells (LSECs) accompanies with hypoxia in liver fibrosis and they are of mutual promotion, which has raised wide concern. Here we established murine model of liver fibrosis and found that oroxylin A (40 mg/kg) could ameliorate angiogenesis in liver fibrosis may related to hypoxia inducible factor 1α (HIF‐1α). The underlying mechanism was further investigated by isolating and culturing murine primary LSECs. Hypoxia induced vascular endothelial growth factor A (VEGF‐A), angiopoietin 2 (Ang‐2), and platelet endothelial cell adhesion molecule‐1 (PECAM‐1/CD31) elevated in LSECs were reduced by oroxylin A or acriflavine (ACF, an HIF‐1α inhibitor), indicating HIF‐1α involved the angiogenesis of LSECs. Additionally, interference with Yes‐associated protein (YAP) significant downregulated the protein expression of HIF‐1α and VEGF‐A, while YAP plasmid exhibited an opposite effect. We next found that oroxylin A inhibited hypoxia‐induced nuclear translocation of YAP, which may influence the accumulation of HIF‐1α and subsequently decrease transcription of downstream target gene including VEGF‐A and Ang‐2, thereby exerting an anti‐angiogenic activity.
Oroxylin A inhibited hypoxia‐induced nuclear translocation of YAP, which may influence the accumulation of HIF‐1α and subsequently decrease transcription of downstream target gene including VEGF‐A and Ang‐2, thereby exerting an anti‐angiogenic activity.</description><subject>Acriflavine</subject><subject>Adaptor Proteins, Signal Transducing - metabolism</subject><subject>Angiogenesis</subject><subject>Angiopoietin</subject><subject>Angiopoietin-2 - genetics</subject><subject>Angiopoietin-2 - metabolism</subject><subject>Animal models</subject><subject>Animals</subject><subject>Carbon Tetrachloride - toxicity</subject><subject>CD31 antigen</subject><subject>Cell adhesion</subject><subject>Cell adhesion & migration</subject><subject>Cell adhesion molecules</subject><subject>Cell Cycle Proteins</subject><subject>Cells, Cultured</subject><subject>Disease Models, Animal</subject><subject>Endothelial cells</subject><subject>Endothelial Cells - cytology</subject><subject>Endothelial Cells - drug effects</subject><subject>Endothelial Cells - metabolism</subject><subject>Fibrosis</subject><subject>Flavonoids - administration & dosage</subject><subject>Flavonoids - pharmacology</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Hepatocytes</subject><subject>HIF‐1α</subject><subject>Hypoxia</subject><subject>Hypoxia-inducible factor 1</subject><subject>Hypoxia-Inducible Factor 1, alpha Subunit - metabolism</subject><subject>Hypoxia-inducible factor 1a</subject><subject>Liver</subject><subject>Liver Cirrhosis - chemically induced</subject><subject>Liver Cirrhosis - drug therapy</subject><subject>Liver Cirrhosis - genetics</subject><subject>Liver Cirrhosis - metabolism</subject><subject>liver fibrosis</subject><subject>Male</subject><subject>Mice</subject><subject>Neovascularization, Pathologic - metabolism</subject><subject>Neovascularization, Pathologic - prevention & control</subject><subject>Nuclear transport</subject><subject>oroxylin A</subject><subject>Phosphoproteins - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Signaling</subject><subject>Transcription</subject><subject>Translocation</subject><subject>Vascular endothelial growth factor</subject><subject>Vascular Endothelial Growth Factor A - genetics</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><subject>YAP</subject><subject>Yes-associated protein</subject><issn>0730-2312</issn><issn>1097-4644</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kE1OwzAQRi0EoqWw4ALIEisWaf3XxF6WqKVFlYoELFhFcWIHVyUpdlvojiNwFS7CITgJDins2MxIM09PMx8Apxh1MUKkN89kl4SU8z3QxkhEAQsZ2wdtFFEUEIpJCxw5N0cICUHJIWgRzvsREawN1MxWr9uFKeEALq3aqHLlYFoWpipUqZxxsNJwejuMHfTMwmyUhdpIW9WrjUn99NFIszJVWZMPg5veeDL6envHnx_QmaJMvbs4Bgc6XTh1susdcD8a3sXjYDq7msSDaZCRkPNAcqU5wSjsZ5HAucSyr6KccqxDkbFQSFTXnEmFUswyHUYqTzNKpE5pzjShHXDeeJe2el4rt0rm1dr6G1yCRSSiUFAmPHXRUJl_w1mlk6U1T6ndJhgldaCJDzT5CdSzZzvjWj6p_I_8TdADvQZ4MQu1_d-UXMeXjfIbnH-Ayg</recordid><startdate>201802</startdate><enddate>201802</enddate><creator>Zhang, Chenxi</creator><creator>Bian, Mianli</creator><creator>Chen, Xingran</creator><creator>Jin, Huanhuan</creator><creator>Zhao, Shifeng</creator><creator>Yang, Xiang</creator><creator>Shao, Jiangjuan</creator><creator>Chen, Anping</creator><creator>Guo, Qinglong</creator><creator>Zhang, Feng</creator><creator>Zheng, Shizhong</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><orcidid>https://orcid.org/0000-0003-0676-0572</orcidid></search><sort><creationdate>201802</creationdate><title>Oroxylin A prevents angiogenesis of LSECs in liver fibrosis via inhibition of YAP/HIF‐1α signaling</title><author>Zhang, Chenxi ; Bian, Mianli ; Chen, Xingran ; Jin, Huanhuan ; Zhao, Shifeng ; Yang, Xiang ; Shao, Jiangjuan ; Chen, Anping ; Guo, Qinglong ; Zhang, Feng ; Zheng, Shizhong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2688-b8ef821065c791db1b5e7d381f69c469b0c469d4be0a14cf67edac32bfa3d4f23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Acriflavine</topic><topic>Adaptor Proteins, Signal Transducing - metabolism</topic><topic>Angiogenesis</topic><topic>Angiopoietin</topic><topic>Angiopoietin-2 - genetics</topic><topic>Angiopoietin-2 - metabolism</topic><topic>Animal models</topic><topic>Animals</topic><topic>Carbon Tetrachloride - toxicity</topic><topic>CD31 antigen</topic><topic>Cell adhesion</topic><topic>Cell adhesion & migration</topic><topic>Cell adhesion molecules</topic><topic>Cell Cycle Proteins</topic><topic>Cells, Cultured</topic><topic>Disease Models, Animal</topic><topic>Endothelial cells</topic><topic>Endothelial Cells - cytology</topic><topic>Endothelial Cells - drug effects</topic><topic>Endothelial Cells - metabolism</topic><topic>Fibrosis</topic><topic>Flavonoids - administration & dosage</topic><topic>Flavonoids - pharmacology</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Hepatocytes</topic><topic>HIF‐1α</topic><topic>Hypoxia</topic><topic>Hypoxia-inducible factor 1</topic><topic>Hypoxia-Inducible Factor 1, alpha Subunit - metabolism</topic><topic>Hypoxia-inducible factor 1a</topic><topic>Liver</topic><topic>Liver Cirrhosis - chemically induced</topic><topic>Liver Cirrhosis - drug therapy</topic><topic>Liver Cirrhosis - genetics</topic><topic>Liver Cirrhosis - metabolism</topic><topic>liver fibrosis</topic><topic>Male</topic><topic>Mice</topic><topic>Neovascularization, Pathologic - metabolism</topic><topic>Neovascularization, Pathologic - prevention & control</topic><topic>Nuclear transport</topic><topic>oroxylin A</topic><topic>Phosphoproteins - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Signaling</topic><topic>Transcription</topic><topic>Translocation</topic><topic>Vascular endothelial growth factor</topic><topic>Vascular Endothelial Growth Factor A - genetics</topic><topic>Vascular Endothelial Growth Factor A - metabolism</topic><topic>YAP</topic><topic>Yes-associated protein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Chenxi</creatorcontrib><creatorcontrib>Bian, Mianli</creatorcontrib><creatorcontrib>Chen, Xingran</creatorcontrib><creatorcontrib>Jin, Huanhuan</creatorcontrib><creatorcontrib>Zhao, Shifeng</creatorcontrib><creatorcontrib>Yang, Xiang</creatorcontrib><creatorcontrib>Shao, Jiangjuan</creatorcontrib><creatorcontrib>Chen, Anping</creatorcontrib><creatorcontrib>Guo, Qinglong</creatorcontrib><creatorcontrib>Zhang, Feng</creatorcontrib><creatorcontrib>Zheng, Shizhong</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><jtitle>Journal of cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Chenxi</au><au>Bian, Mianli</au><au>Chen, Xingran</au><au>Jin, Huanhuan</au><au>Zhao, Shifeng</au><au>Yang, Xiang</au><au>Shao, Jiangjuan</au><au>Chen, Anping</au><au>Guo, Qinglong</au><au>Zhang, Feng</au><au>Zheng, Shizhong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oroxylin A prevents angiogenesis of LSECs in liver fibrosis via inhibition of YAP/HIF‐1α signaling</atitle><jtitle>Journal of cellular biochemistry</jtitle><addtitle>J Cell Biochem</addtitle><date>2018-02</date><risdate>2018</risdate><volume>119</volume><issue>2</issue><spage>2258</spage><epage>2268</epage><pages>2258-2268</pages><issn>0730-2312</issn><eissn>1097-4644</eissn><abstract>Angiogenesis of liver sinusoidal endothelial cells (LSECs) accompanies with hypoxia in liver fibrosis and they are of mutual promotion, which has raised wide concern. Here we established murine model of liver fibrosis and found that oroxylin A (40 mg/kg) could ameliorate angiogenesis in liver fibrosis may related to hypoxia inducible factor 1α (HIF‐1α). The underlying mechanism was further investigated by isolating and culturing murine primary LSECs. Hypoxia induced vascular endothelial growth factor A (VEGF‐A), angiopoietin 2 (Ang‐2), and platelet endothelial cell adhesion molecule‐1 (PECAM‐1/CD31) elevated in LSECs were reduced by oroxylin A or acriflavine (ACF, an HIF‐1α inhibitor), indicating HIF‐1α involved the angiogenesis of LSECs. Additionally, interference with Yes‐associated protein (YAP) significant downregulated the protein expression of HIF‐1α and VEGF‐A, while YAP plasmid exhibited an opposite effect. We next found that oroxylin A inhibited hypoxia‐induced nuclear translocation of YAP, which may influence the accumulation of HIF‐1α and subsequently decrease transcription of downstream target gene including VEGF‐A and Ang‐2, thereby exerting an anti‐angiogenic activity.
Oroxylin A inhibited hypoxia‐induced nuclear translocation of YAP, which may influence the accumulation of HIF‐1α and subsequently decrease transcription of downstream target gene including VEGF‐A and Ang‐2, thereby exerting an anti‐angiogenic activity.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>28857294</pmid><doi>10.1002/jcb.26388</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0003-0676-0572</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0730-2312 |
| ispartof | Journal of cellular biochemistry, 2018-02, Vol.119 (2), p.2258-2268 |
| issn | 0730-2312 1097-4644 |
| language | eng |
| recordid | cdi_proquest_journals_1979769349 |
| source | MEDLINE; Wiley Online Library All Journals |
| subjects | Acriflavine Adaptor Proteins, Signal Transducing - metabolism Angiogenesis Angiopoietin Angiopoietin-2 - genetics Angiopoietin-2 - metabolism Animal models Animals Carbon Tetrachloride - toxicity CD31 antigen Cell adhesion Cell adhesion & migration Cell adhesion molecules Cell Cycle Proteins Cells, Cultured Disease Models, Animal Endothelial cells Endothelial Cells - cytology Endothelial Cells - drug effects Endothelial Cells - metabolism Fibrosis Flavonoids - administration & dosage Flavonoids - pharmacology Gene Expression Regulation - drug effects Hepatocytes HIF‐1α Hypoxia Hypoxia-inducible factor 1 Hypoxia-Inducible Factor 1, alpha Subunit - metabolism Hypoxia-inducible factor 1a Liver Liver Cirrhosis - chemically induced Liver Cirrhosis - drug therapy Liver Cirrhosis - genetics Liver Cirrhosis - metabolism liver fibrosis Male Mice Neovascularization, Pathologic - metabolism Neovascularization, Pathologic - prevention & control Nuclear transport oroxylin A Phosphoproteins - metabolism Signal Transduction - drug effects Signaling Transcription Translocation Vascular endothelial growth factor Vascular Endothelial Growth Factor A - genetics Vascular Endothelial Growth Factor A - metabolism YAP Yes-associated protein |
| title | Oroxylin A prevents angiogenesis of LSECs in liver fibrosis via inhibition of YAP/HIF‐1α signaling |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-17T10%3A56%3A21IST&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=Oroxylin%20A%20prevents%20angiogenesis%20of%20LSECs%20in%20liver%20fibrosis%20via%20inhibition%20of%20YAP/HIF%E2%80%901%CE%B1%20signaling&rft.jtitle=Journal%20of%20cellular%20biochemistry&rft.au=Zhang,%20Chenxi&rft.date=2018-02&rft.volume=119&rft.issue=2&rft.spage=2258&rft.epage=2268&rft.pages=2258-2268&rft.issn=0730-2312&rft.eissn=1097-4644&rft_id=info:doi/10.1002/jcb.26388&rft_dat=%3Cproquest_cross%3E1979769349%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=1979769349&rft_id=info:pmid/28857294&rfr_iscdi=true |