Weak UVB Irradiation Promotes Macrophage M2 Polarization and Stabilizes Atherosclerosis
Atherosclerosis (AS) is a chronic cardiovascular disease endangering human health and is one of the most common causes of myocardial infarction and stroke. Macrophage polarization plays a vital role in regulating plaque stability. As an important component of sunlight, ultraviolet B (UVB) has been p...
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| Veröffentlicht in: | Journal of cardiovascular translational research 2022-08, Vol.15 (4), p.855-864 |
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| container_title | Journal of cardiovascular translational research |
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| creator | Li, Xin-Yun Qin, Tao Zhang, Peng-Fei Yan, Wen-jiang Lei, Ling-Li Kuang, Jiang-Ying Li, Hao-Dong Zhang, Wen-Cheng Lu, Xiao-Ting Sun, Yuan-Yuan |
| description | Atherosclerosis (AS) is a chronic cardiovascular disease endangering human health and is one of the most common causes of myocardial infarction and stroke. Macrophage polarization plays a vital role in regulating plaque stability. As an important component of sunlight, ultraviolet B (UVB) has been proven to promote vitamin D and nitric oxide synthesis. This research used an AS model in ApoE
−/−
mice to study the effects of UVB on macrophage polarization and atherosclerotic plaque stability. In vitro, UVB irradiation increased arginase-I (Arg-I, M2 macrophage) and macrophage mannose receptor (CD206) expression, while the expression of inducible nitric oxide synthase (iNOS) (M1 macrophage) and CD86 was decreased. UVB promoted Akt phosphorylation in vitro. In vivo, UVB irradiation promoted the stabilization of atherosclerotic lesion plaques, while the phenotype of M2 macrophages increased. Our research provides new evidence for UVB in preventing and treating atherosclerosis. |
| doi_str_mv | 10.1007/s12265-021-10189-7 |
| format | Article |
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−/−
mice to study the effects of UVB on macrophage polarization and atherosclerotic plaque stability. In vitro, UVB irradiation increased arginase-I (Arg-I, M2 macrophage) and macrophage mannose receptor (CD206) expression, while the expression of inducible nitric oxide synthase (iNOS) (M1 macrophage) and CD86 was decreased. UVB promoted Akt phosphorylation in vitro. In vivo, UVB irradiation promoted the stabilization of atherosclerotic lesion plaques, while the phenotype of M2 macrophages increased. Our research provides new evidence for UVB in preventing and treating atherosclerosis.</description><identifier>ISSN: 1937-5387</identifier><identifier>EISSN: 1937-5395</identifier><identifier>DOI: 10.1007/s12265-021-10189-7</identifier><identifier>PMID: 34811697</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animals ; Atherosclerosis - metabolism ; Biomedical Engineering and Bioengineering ; Biomedicine ; Cardiology ; Human Genetics ; Humans ; Macrophage Activation ; Macrophages - pathology ; Medicine ; Medicine & Public Health ; Mice ; Original ; Original Article ; Phenotype ; Plaque, Atherosclerotic - pathology</subject><ispartof>Journal of cardiovascular translational research, 2022-08, Vol.15 (4), p.855-864</ispartof><rights>The Author(s) 2021</rights><rights>2021. The Author(s).</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c446t-174cfb740174aa49ec8fa88b14cd5a557fce20f85cd9634dd73dfef9b5f021763</citedby><cites>FETCH-LOGICAL-c446t-174cfb740174aa49ec8fa88b14cd5a557fce20f85cd9634dd73dfef9b5f021763</cites><orcidid>0000-0001-8671-5522</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12265-021-10189-7$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12265-021-10189-7$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34811697$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Xin-Yun</creatorcontrib><creatorcontrib>Qin, Tao</creatorcontrib><creatorcontrib>Zhang, Peng-Fei</creatorcontrib><creatorcontrib>Yan, Wen-jiang</creatorcontrib><creatorcontrib>Lei, Ling-Li</creatorcontrib><creatorcontrib>Kuang, Jiang-Ying</creatorcontrib><creatorcontrib>Li, Hao-Dong</creatorcontrib><creatorcontrib>Zhang, Wen-Cheng</creatorcontrib><creatorcontrib>Lu, Xiao-Ting</creatorcontrib><creatorcontrib>Sun, Yuan-Yuan</creatorcontrib><title>Weak UVB Irradiation Promotes Macrophage M2 Polarization and Stabilizes Atherosclerosis</title><title>Journal of cardiovascular translational research</title><addtitle>J. of Cardiovasc. Trans. Res</addtitle><addtitle>J Cardiovasc Transl Res</addtitle><description>Atherosclerosis (AS) is a chronic cardiovascular disease endangering human health and is one of the most common causes of myocardial infarction and stroke. Macrophage polarization plays a vital role in regulating plaque stability. As an important component of sunlight, ultraviolet B (UVB) has been proven to promote vitamin D and nitric oxide synthesis. This research used an AS model in ApoE
−/−
mice to study the effects of UVB on macrophage polarization and atherosclerotic plaque stability. In vitro, UVB irradiation increased arginase-I (Arg-I, M2 macrophage) and macrophage mannose receptor (CD206) expression, while the expression of inducible nitric oxide synthase (iNOS) (M1 macrophage) and CD86 was decreased. UVB promoted Akt phosphorylation in vitro. In vivo, UVB irradiation promoted the stabilization of atherosclerotic lesion plaques, while the phenotype of M2 macrophages increased. Our research provides new evidence for UVB in preventing and treating atherosclerosis.</description><subject>Animals</subject><subject>Atherosclerosis - metabolism</subject><subject>Biomedical Engineering and Bioengineering</subject><subject>Biomedicine</subject><subject>Cardiology</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Macrophage Activation</subject><subject>Macrophages - pathology</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice</subject><subject>Original</subject><subject>Original Article</subject><subject>Phenotype</subject><subject>Plaque, Atherosclerotic - pathology</subject><issn>1937-5387</issn><issn>1937-5395</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><recordid>eNp9kUtLxDAQx4Movr-AB-nRSzXPpr0IuvgCRcHXMUzTZDfabdakK-inN1pd9OJlZmB-889k_gjtELxPMJYHkVBaiBxTkhNMyiqXS2idVEzmglVieVGXcg1txPiEcUGxlKtojfGSkKKS6-jx0cBzdv9wnF2EAI2D3vkuuwl-6nsTsyvQwc8mMDbZFc1ufAvBvQ8MdE1220PtWveeyKN-YoKPuv2MLm6hFQttNNvfeRPdn57cjc7zy-uzi9HRZa45L_qcSK5tLTlOBQCvjC4tlGVNuG4ECCGtNhTbUuimKhhvGskaa2xVC5u-LQu2iQ4H3dm8nppGm64P0KpZcFMIb8qDU387nZuosX9VVUGpIDgJ7H0LBP8yN7FXUxe1aVvojJ9HRQtMeMkE4wmlA5puEmMwdvEMwerTETU4otJq6ssRJdPQ7u8FFyM_FiSADUBMrW5sgnry89Clo_0n-wEhpZjs</recordid><startdate>20220801</startdate><enddate>20220801</enddate><creator>Li, Xin-Yun</creator><creator>Qin, Tao</creator><creator>Zhang, Peng-Fei</creator><creator>Yan, Wen-jiang</creator><creator>Lei, Ling-Li</creator><creator>Kuang, Jiang-Ying</creator><creator>Li, Hao-Dong</creator><creator>Zhang, Wen-Cheng</creator><creator>Lu, Xiao-Ting</creator><creator>Sun, Yuan-Yuan</creator><general>Springer US</general><scope>C6C</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><orcidid>https://orcid.org/0000-0001-8671-5522</orcidid></search><sort><creationdate>20220801</creationdate><title>Weak UVB Irradiation Promotes Macrophage M2 Polarization and Stabilizes Atherosclerosis</title><author>Li, Xin-Yun ; Qin, Tao ; Zhang, Peng-Fei ; Yan, Wen-jiang ; Lei, Ling-Li ; Kuang, Jiang-Ying ; Li, Hao-Dong ; Zhang, Wen-Cheng ; Lu, Xiao-Ting ; Sun, Yuan-Yuan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c446t-174cfb740174aa49ec8fa88b14cd5a557fce20f85cd9634dd73dfef9b5f021763</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Animals</topic><topic>Atherosclerosis - metabolism</topic><topic>Biomedical Engineering and Bioengineering</topic><topic>Biomedicine</topic><topic>Cardiology</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Macrophage Activation</topic><topic>Macrophages - pathology</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mice</topic><topic>Original</topic><topic>Original Article</topic><topic>Phenotype</topic><topic>Plaque, Atherosclerotic - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Xin-Yun</creatorcontrib><creatorcontrib>Qin, Tao</creatorcontrib><creatorcontrib>Zhang, Peng-Fei</creatorcontrib><creatorcontrib>Yan, Wen-jiang</creatorcontrib><creatorcontrib>Lei, Ling-Li</creatorcontrib><creatorcontrib>Kuang, Jiang-Ying</creatorcontrib><creatorcontrib>Li, Hao-Dong</creatorcontrib><creatorcontrib>Zhang, Wen-Cheng</creatorcontrib><creatorcontrib>Lu, Xiao-Ting</creatorcontrib><creatorcontrib>Sun, Yuan-Yuan</creatorcontrib><collection>Springer Nature OA Free Journals</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><jtitle>Journal of cardiovascular translational research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Xin-Yun</au><au>Qin, Tao</au><au>Zhang, Peng-Fei</au><au>Yan, Wen-jiang</au><au>Lei, Ling-Li</au><au>Kuang, Jiang-Ying</au><au>Li, Hao-Dong</au><au>Zhang, Wen-Cheng</au><au>Lu, Xiao-Ting</au><au>Sun, Yuan-Yuan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Weak UVB Irradiation Promotes Macrophage M2 Polarization and Stabilizes Atherosclerosis</atitle><jtitle>Journal of cardiovascular translational research</jtitle><stitle>J. of Cardiovasc. Trans. Res</stitle><addtitle>J Cardiovasc Transl Res</addtitle><date>2022-08-01</date><risdate>2022</risdate><volume>15</volume><issue>4</issue><spage>855</spage><epage>864</epage><pages>855-864</pages><issn>1937-5387</issn><eissn>1937-5395</eissn><abstract>Atherosclerosis (AS) is a chronic cardiovascular disease endangering human health and is one of the most common causes of myocardial infarction and stroke. Macrophage polarization plays a vital role in regulating plaque stability. As an important component of sunlight, ultraviolet B (UVB) has been proven to promote vitamin D and nitric oxide synthesis. This research used an AS model in ApoE
−/−
mice to study the effects of UVB on macrophage polarization and atherosclerotic plaque stability. In vitro, UVB irradiation increased arginase-I (Arg-I, M2 macrophage) and macrophage mannose receptor (CD206) expression, while the expression of inducible nitric oxide synthase (iNOS) (M1 macrophage) and CD86 was decreased. UVB promoted Akt phosphorylation in vitro. In vivo, UVB irradiation promoted the stabilization of atherosclerotic lesion plaques, while the phenotype of M2 macrophages increased. Our research provides new evidence for UVB in preventing and treating atherosclerosis.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>34811697</pmid><doi>10.1007/s12265-021-10189-7</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0001-8671-5522</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Atherosclerosis - metabolism Biomedical Engineering and Bioengineering Biomedicine Cardiology Human Genetics Humans Macrophage Activation Macrophages - pathology Medicine Medicine & Public Health Mice Original Original Article Phenotype Plaque, Atherosclerotic - pathology |
| title | Weak UVB Irradiation Promotes Macrophage M2 Polarization and Stabilizes Atherosclerosis |
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