TLR4-Myd88 pathway upregulated caveolin-1 expression contributes to coronary artery spasm
To study the role of toll-like receptors 4-myeloid differentiation factor 88 (TLR4-Myd88) dependent caveolin-1 (Cav-1) expression modulation in coronary artery spasm (CAS) and explore the underlying pathogenic mechanisms. Lipopolysaccharide (LPS) and acetylcholine (Ach) were used to develop the in v...
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| Veröffentlicht in: | Vascular pharmacology 2022-02, Vol.142, p.106947-106947, Article 106947 |
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| container_title | Vascular pharmacology |
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| creator | Zhao, Xin Tian, Jinfan Liu, Yue Ye, Zhishuai Xu, Mingyue Huang, Rongchong Song, Xiantao |
| description | To study the role of toll-like receptors 4-myeloid differentiation factor 88 (TLR4-Myd88) dependent caveolin-1 (Cav-1) expression modulation in coronary artery spasm (CAS) and explore the underlying pathogenic mechanisms.
Lipopolysaccharide (LPS) and acetylcholine (Ach) were used to develop the in vitro and in vivo models mimicking the physiological CAS microenvironment. LPS-induced upregulation of Cav-1 expression in mouse coronary and aorta endothelial cells was shown by western blot and immunofluorescence (IF) staining (p |
| doi_str_mv | 10.1016/j.vph.2021.106947 |
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Lipopolysaccharide (LPS) and acetylcholine (Ach) were used to develop the in vitro and in vivo models mimicking the physiological CAS microenvironment. LPS-induced upregulation of Cav-1 expression in mouse coronary and aorta endothelial cells was shown by western blot and immunofluorescence (IF) staining (p < 0.01). Caveolin-1-knockout (Cav-1−/−) mice had reduced aortic inflammation after LPS challenge, and fewer ST segment changes were observed through electrocardiogram (ECG) monitoring compared to wild type mice after LPS and ACh administration. In vitro, pretreating human umbilical vein endothelial cells (HUVECs) with siCav-1 to knock down Cav-1 expression reduced the endothelial inflammation following LPS challenge. SiCav-1 also partially reversed the attenuated Ca2+ concentration after LPS and ACh administration compared to the control group, which was evaluated by fluorescent molecular probing for Ca2+ alternation monitoring (p < 0.05). TLR4 and Myd88 downregulation by siRNA partially blocked the increased Cav-1 mRNA and protein expressions following LPS treatment, as well as partially reversed the decreased NO production evaluated by nitrate reductase method and the impaired Ca2+ concentration of endothelial cells induced by LPS and ACh.
These findings suggested that Cav-1, which was upregulated by TLR4-Myd88, served as an important modulator of CAS microenvironment establishment in vivo and in vitro, making it a potential pharmacologic target for the treatment of vasospasm via reduced endothelial cell inflammation.
[Display omitted]</description><identifier>ISSN: 1537-1891</identifier><identifier>EISSN: 1879-3649</identifier><identifier>DOI: 10.1016/j.vph.2021.106947</identifier><identifier>PMID: 34822994</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Aorta ; Calcium ; Calcium ions ; Caveolin ; Caveolin 1 - genetics ; Caveolin 1 - metabolism ; Caveolin-1 ; Coronary artery ; Coronary artery spasm ; Coronary vessels ; Coronary Vessels - metabolism ; Coronary Vessels - physiopathology ; EKG ; Electrocardiography ; Endothelial cells ; Endothelial dysfunction ; Fluorescence ; Human Umbilical Vein Endothelial Cells - metabolism ; Humans ; Immunofluorescence ; Inflammation ; Lipopolysaccharides ; Lipopolysaccharides - pharmacology ; Mice ; Microenvironments ; Mimicry ; Monitoring ; mRNA ; MyD88 protein ; Myeloid Differentiation Factor 88 - genetics ; Myeloid Differentiation Factor 88 - metabolism ; Nitrate reductase ; Reductases ; siRNA ; Spasm ; Telemedicine ; TLR4 protein ; Toll-Like Receptor 4 - genetics ; Toll-Like Receptor 4 - metabolism ; Toll-like receptors ; Umbilical vein</subject><ispartof>Vascular pharmacology, 2022-02, Vol.142, p.106947-106947, Article 106947</ispartof><rights>2021</rights><rights>Copyright © 2021. Published by Elsevier Inc.</rights><rights>Copyright Elsevier Science Ltd. Feb 2022</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c381t-9e4ce0f5db95fcd3e117f03db7dad6d4f751ecb9e9da722df24e465a9074e9583</citedby><cites>FETCH-LOGICAL-c381t-9e4ce0f5db95fcd3e117f03db7dad6d4f751ecb9e9da722df24e465a9074e9583</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.vph.2021.106947$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,778,782,3539,27911,27912,45982</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34822994$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhao, Xin</creatorcontrib><creatorcontrib>Tian, Jinfan</creatorcontrib><creatorcontrib>Liu, Yue</creatorcontrib><creatorcontrib>Ye, Zhishuai</creatorcontrib><creatorcontrib>Xu, Mingyue</creatorcontrib><creatorcontrib>Huang, Rongchong</creatorcontrib><creatorcontrib>Song, Xiantao</creatorcontrib><title>TLR4-Myd88 pathway upregulated caveolin-1 expression contributes to coronary artery spasm</title><title>Vascular pharmacology</title><addtitle>Vascul Pharmacol</addtitle><description>To study the role of toll-like receptors 4-myeloid differentiation factor 88 (TLR4-Myd88) dependent caveolin-1 (Cav-1) expression modulation in coronary artery spasm (CAS) and explore the underlying pathogenic mechanisms.
Lipopolysaccharide (LPS) and acetylcholine (Ach) were used to develop the in vitro and in vivo models mimicking the physiological CAS microenvironment. LPS-induced upregulation of Cav-1 expression in mouse coronary and aorta endothelial cells was shown by western blot and immunofluorescence (IF) staining (p < 0.01). Caveolin-1-knockout (Cav-1−/−) mice had reduced aortic inflammation after LPS challenge, and fewer ST segment changes were observed through electrocardiogram (ECG) monitoring compared to wild type mice after LPS and ACh administration. In vitro, pretreating human umbilical vein endothelial cells (HUVECs) with siCav-1 to knock down Cav-1 expression reduced the endothelial inflammation following LPS challenge. SiCav-1 also partially reversed the attenuated Ca2+ concentration after LPS and ACh administration compared to the control group, which was evaluated by fluorescent molecular probing for Ca2+ alternation monitoring (p < 0.05). TLR4 and Myd88 downregulation by siRNA partially blocked the increased Cav-1 mRNA and protein expressions following LPS treatment, as well as partially reversed the decreased NO production evaluated by nitrate reductase method and the impaired Ca2+ concentration of endothelial cells induced by LPS and ACh.
These findings suggested that Cav-1, which was upregulated by TLR4-Myd88, served as an important modulator of CAS microenvironment establishment in vivo and in vitro, making it a potential pharmacologic target for the treatment of vasospasm via reduced endothelial cell inflammation.
[Display omitted]</description><subject>Animals</subject><subject>Aorta</subject><subject>Calcium</subject><subject>Calcium ions</subject><subject>Caveolin</subject><subject>Caveolin 1 - genetics</subject><subject>Caveolin 1 - metabolism</subject><subject>Caveolin-1</subject><subject>Coronary artery</subject><subject>Coronary artery spasm</subject><subject>Coronary vessels</subject><subject>Coronary Vessels - metabolism</subject><subject>Coronary Vessels - physiopathology</subject><subject>EKG</subject><subject>Electrocardiography</subject><subject>Endothelial cells</subject><subject>Endothelial dysfunction</subject><subject>Fluorescence</subject><subject>Human Umbilical Vein Endothelial Cells - metabolism</subject><subject>Humans</subject><subject>Immunofluorescence</subject><subject>Inflammation</subject><subject>Lipopolysaccharides</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Mice</subject><subject>Microenvironments</subject><subject>Mimicry</subject><subject>Monitoring</subject><subject>mRNA</subject><subject>MyD88 protein</subject><subject>Myeloid Differentiation Factor 88 - genetics</subject><subject>Myeloid Differentiation Factor 88 - metabolism</subject><subject>Nitrate reductase</subject><subject>Reductases</subject><subject>siRNA</subject><subject>Spasm</subject><subject>Telemedicine</subject><subject>TLR4 protein</subject><subject>Toll-Like Receptor 4 - genetics</subject><subject>Toll-Like Receptor 4 - metabolism</subject><subject>Toll-like receptors</subject><subject>Umbilical vein</subject><issn>1537-1891</issn><issn>1879-3649</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kEuPFCEURonROA_9AW5MJW7cVMsFqoC4MpPRMWljYsaFK0LBLYdOdVEC1dr_XiY9unDh6j5y7hc4hLwAugEK_Zvd5rDcbRhlUOdeC_mInIOSuuW90I9r33HZgtJwRi5y3lEKSvX6KTnjQjGmtTgn3263X0T76eiVahZb7n7aY7MuCb-vky3oG2cPGKcwt9Dgr7rPOcS5cXEuKQxrwdyUWMcUZ5uOjU0Fa8mLzftn5Mlop4zPH-ol-fr--vbqpt1-_vDx6t22dVxBaTUKh3Ts_KC70XmOAHKk3A_SW997McoO0A0atbeSMT8ygaLvrKZSoO4UvySvT7lLij9WzMXsQ3Y4TXbGuGbDeiqqLOC0oq_-QXdxTXN9XaW4lgxYxyoFJ8qlmHPC0Swp7Ov3DFBz793sTPVu7r2bk_d68_IheR326P9e_BFdgbcnAKuKQ8Bksgs4O_QhoSvGx_Cf-N-ITJOo</recordid><startdate>202202</startdate><enddate>202202</enddate><creator>Zhao, Xin</creator><creator>Tian, Jinfan</creator><creator>Liu, Yue</creator><creator>Ye, Zhishuai</creator><creator>Xu, Mingyue</creator><creator>Huang, Rongchong</creator><creator>Song, Xiantao</creator><general>Elsevier Inc</general><general>Elsevier Science Ltd</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>7T5</scope><scope>7U7</scope><scope>C1K</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>202202</creationdate><title>TLR4-Myd88 pathway upregulated caveolin-1 expression contributes to coronary artery spasm</title><author>Zhao, Xin ; Tian, Jinfan ; Liu, Yue ; Ye, Zhishuai ; Xu, Mingyue ; Huang, Rongchong ; Song, Xiantao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c381t-9e4ce0f5db95fcd3e117f03db7dad6d4f751ecb9e9da722df24e465a9074e9583</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Animals</topic><topic>Aorta</topic><topic>Calcium</topic><topic>Calcium ions</topic><topic>Caveolin</topic><topic>Caveolin 1 - genetics</topic><topic>Caveolin 1 - metabolism</topic><topic>Caveolin-1</topic><topic>Coronary artery</topic><topic>Coronary artery spasm</topic><topic>Coronary vessels</topic><topic>Coronary Vessels - metabolism</topic><topic>Coronary Vessels - physiopathology</topic><topic>EKG</topic><topic>Electrocardiography</topic><topic>Endothelial cells</topic><topic>Endothelial dysfunction</topic><topic>Fluorescence</topic><topic>Human Umbilical Vein Endothelial Cells - metabolism</topic><topic>Humans</topic><topic>Immunofluorescence</topic><topic>Inflammation</topic><topic>Lipopolysaccharides</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Mice</topic><topic>Microenvironments</topic><topic>Mimicry</topic><topic>Monitoring</topic><topic>mRNA</topic><topic>MyD88 protein</topic><topic>Myeloid Differentiation Factor 88 - genetics</topic><topic>Myeloid Differentiation Factor 88 - metabolism</topic><topic>Nitrate reductase</topic><topic>Reductases</topic><topic>siRNA</topic><topic>Spasm</topic><topic>Telemedicine</topic><topic>TLR4 protein</topic><topic>Toll-Like Receptor 4 - genetics</topic><topic>Toll-Like Receptor 4 - metabolism</topic><topic>Toll-like receptors</topic><topic>Umbilical vein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhao, Xin</creatorcontrib><creatorcontrib>Tian, Jinfan</creatorcontrib><creatorcontrib>Liu, Yue</creatorcontrib><creatorcontrib>Ye, Zhishuai</creatorcontrib><creatorcontrib>Xu, Mingyue</creatorcontrib><creatorcontrib>Huang, Rongchong</creatorcontrib><creatorcontrib>Song, Xiantao</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Vascular pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhao, Xin</au><au>Tian, Jinfan</au><au>Liu, Yue</au><au>Ye, Zhishuai</au><au>Xu, Mingyue</au><au>Huang, Rongchong</au><au>Song, Xiantao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TLR4-Myd88 pathway upregulated caveolin-1 expression contributes to coronary artery spasm</atitle><jtitle>Vascular pharmacology</jtitle><addtitle>Vascul Pharmacol</addtitle><date>2022-02</date><risdate>2022</risdate><volume>142</volume><spage>106947</spage><epage>106947</epage><pages>106947-106947</pages><artnum>106947</artnum><issn>1537-1891</issn><eissn>1879-3649</eissn><abstract>To study the role of toll-like receptors 4-myeloid differentiation factor 88 (TLR4-Myd88) dependent caveolin-1 (Cav-1) expression modulation in coronary artery spasm (CAS) and explore the underlying pathogenic mechanisms.
Lipopolysaccharide (LPS) and acetylcholine (Ach) were used to develop the in vitro and in vivo models mimicking the physiological CAS microenvironment. LPS-induced upregulation of Cav-1 expression in mouse coronary and aorta endothelial cells was shown by western blot and immunofluorescence (IF) staining (p < 0.01). Caveolin-1-knockout (Cav-1−/−) mice had reduced aortic inflammation after LPS challenge, and fewer ST segment changes were observed through electrocardiogram (ECG) monitoring compared to wild type mice after LPS and ACh administration. In vitro, pretreating human umbilical vein endothelial cells (HUVECs) with siCav-1 to knock down Cav-1 expression reduced the endothelial inflammation following LPS challenge. SiCav-1 also partially reversed the attenuated Ca2+ concentration after LPS and ACh administration compared to the control group, which was evaluated by fluorescent molecular probing for Ca2+ alternation monitoring (p < 0.05). TLR4 and Myd88 downregulation by siRNA partially blocked the increased Cav-1 mRNA and protein expressions following LPS treatment, as well as partially reversed the decreased NO production evaluated by nitrate reductase method and the impaired Ca2+ concentration of endothelial cells induced by LPS and ACh.
These findings suggested that Cav-1, which was upregulated by TLR4-Myd88, served as an important modulator of CAS microenvironment establishment in vivo and in vitro, making it a potential pharmacologic target for the treatment of vasospasm via reduced endothelial cell inflammation.
[Display omitted]</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>34822994</pmid><doi>10.1016/j.vph.2021.106947</doi><tpages>1</tpages></addata></record> |
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| subjects | Animals Aorta Calcium Calcium ions Caveolin Caveolin 1 - genetics Caveolin 1 - metabolism Caveolin-1 Coronary artery Coronary artery spasm Coronary vessels Coronary Vessels - metabolism Coronary Vessels - physiopathology EKG Electrocardiography Endothelial cells Endothelial dysfunction Fluorescence Human Umbilical Vein Endothelial Cells - metabolism Humans Immunofluorescence Inflammation Lipopolysaccharides Lipopolysaccharides - pharmacology Mice Microenvironments Mimicry Monitoring mRNA MyD88 protein Myeloid Differentiation Factor 88 - genetics Myeloid Differentiation Factor 88 - metabolism Nitrate reductase Reductases siRNA Spasm Telemedicine TLR4 protein Toll-Like Receptor 4 - genetics Toll-Like Receptor 4 - metabolism Toll-like receptors Umbilical vein |
| title | TLR4-Myd88 pathway upregulated caveolin-1 expression contributes to coronary artery spasm |
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