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The Effect of Interleukin 38 on Angiogenesis in a Model of Oxygen-induced Retinopathy
Interleukin 38 (IL-38) is a novel identified cytokine of IL-1 family in which some members are important in inflammation and angiogenesis. However, the role of IL-38 in regulating angiogenesis is unknown. The aim of the present study is to explore the effect of IL-38 on angiogenesis. Oxygen-induced...
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Published in: | Scientific reports 2017-06, Vol.7 (1), p.2756-9, Article 2756 |
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description | Interleukin 38 (IL-38) is a novel identified cytokine of IL-1 family in which some members are important in inflammation and angiogenesis. However, the role of IL-38 in regulating angiogenesis is unknown. The aim of the present study is to explore the effect of IL-38 on angiogenesis. Oxygen-induced retinopathy (OIR) of C57BL/6 J mice was induced by exposure of hyperoxia (75% oxygen) from postnatal day 7 (P7) to P12 and then returned to room air. The mice were injected with IL-38. At P17, neovascular region (tufts) and avascular area of the retinas were analyzed. The data showed that administration of IL-38
in vivo
inhibited retinal angiogenesis significantly. Furthermore, the addition of IL-38 to the cell cultures attenuated the proliferation, scratch wound healing and tube formation of vascular endothelial cells induced by VEGF significantly. Our findings suggest that IL-38 is an antiangiogenic cytokine in pathophysiological settings and may have therapeutic potential for angiogenesis related diseases. |
doi_str_mv | 10.1038/s41598-017-03079-z |
format | article |
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in vivo
inhibited retinal angiogenesis significantly. Furthermore, the addition of IL-38 to the cell cultures attenuated the proliferation, scratch wound healing and tube formation of vascular endothelial cells induced by VEGF significantly. Our findings suggest that IL-38 is an antiangiogenic cytokine in pathophysiological settings and may have therapeutic potential for angiogenesis related diseases.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-017-03079-z</identifier><identifier>PMID: 28584235</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/21 ; 13/51 ; 631/250/127/1213 ; 64/60 ; 692/699/249/2510 ; Angiogenesis ; Angiogenesis Inhibitors - pharmacology ; Animals ; Animals, Newborn ; Cell Movement - drug effects ; Cell proliferation ; Cell Proliferation - drug effects ; Cytokines ; Data processing ; Disease Models, Animal ; Endothelial cells ; Endothelial Cells - drug effects ; Endothelial Cells - metabolism ; Human Umbilical Vein Endothelial Cells ; Humanities and Social Sciences ; Humans ; Hyperoxia ; Interleukin 1 ; Interleukins - pharmacology ; Mice ; multidisciplinary ; Oxygen ; Oxygen - adverse effects ; Retina ; Retinal Diseases - etiology ; Retinal Diseases - metabolism ; Retinal Diseases - pathology ; Retinal Neovascularization - etiology ; Retinal Neovascularization - metabolism ; Retinal Neovascularization - pathology ; Retinopathy ; Rodents ; Science ; Science (multidisciplinary) ; Vascular endothelial growth factor ; Wound healing</subject><ispartof>Scientific reports, 2017-06, Vol.7 (1), p.2756-9, Article 2756</ispartof><rights>The Author(s) 2017</rights><rights>Copyright Nature Publishing Group Jun 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c540t-7ff65417127050bd4b87a227c1b97034753be4a4f6e289429514433705385aad3</citedby><cites>FETCH-LOGICAL-c540t-7ff65417127050bd4b87a227c1b97034753be4a4f6e289429514433705385aad3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/1955526517/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1955526517?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,25731,27901,27902,36989,36990,44566,53766,53768,74869</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28584235$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Jing</creatorcontrib><creatorcontrib>Zhao, Ruijuan</creatorcontrib><creatorcontrib>Chen, Jianping</creatorcontrib><creatorcontrib>Jin, Jiayi</creatorcontrib><creatorcontrib>Yu, Ying</creatorcontrib><creatorcontrib>Tian, Yunzhe</creatorcontrib><creatorcontrib>Li, Weihua</creatorcontrib><creatorcontrib>Wang, Wencong</creatorcontrib><creatorcontrib>Zhou, Hongyan</creatorcontrib><creatorcontrib>Bo Su, Shao</creatorcontrib><title>The Effect of Interleukin 38 on Angiogenesis in a Model of Oxygen-induced Retinopathy</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Interleukin 38 (IL-38) is a novel identified cytokine of IL-1 family in which some members are important in inflammation and angiogenesis. However, the role of IL-38 in regulating angiogenesis is unknown. The aim of the present study is to explore the effect of IL-38 on angiogenesis. Oxygen-induced retinopathy (OIR) of C57BL/6 J mice was induced by exposure of hyperoxia (75% oxygen) from postnatal day 7 (P7) to P12 and then returned to room air. The mice were injected with IL-38. At P17, neovascular region (tufts) and avascular area of the retinas were analyzed. The data showed that administration of IL-38
in vivo
inhibited retinal angiogenesis significantly. Furthermore, the addition of IL-38 to the cell cultures attenuated the proliferation, scratch wound healing and tube formation of vascular endothelial cells induced by VEGF significantly. Our findings suggest that IL-38 is an antiangiogenic cytokine in pathophysiological settings and may have therapeutic potential for angiogenesis related diseases.</description><subject>13/21</subject><subject>13/51</subject><subject>631/250/127/1213</subject><subject>64/60</subject><subject>692/699/249/2510</subject><subject>Angiogenesis</subject><subject>Angiogenesis Inhibitors - pharmacology</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Cell Movement - drug effects</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - drug effects</subject><subject>Cytokines</subject><subject>Data processing</subject><subject>Disease Models, Animal</subject><subject>Endothelial cells</subject><subject>Endothelial Cells - drug effects</subject><subject>Endothelial Cells - metabolism</subject><subject>Human Umbilical Vein Endothelial Cells</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Hyperoxia</subject><subject>Interleukin 1</subject><subject>Interleukins - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Jing</au><au>Zhao, Ruijuan</au><au>Chen, Jianping</au><au>Jin, Jiayi</au><au>Yu, Ying</au><au>Tian, Yunzhe</au><au>Li, Weihua</au><au>Wang, Wencong</au><au>Zhou, Hongyan</au><au>Bo Su, Shao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Effect of Interleukin 38 on Angiogenesis in a Model of Oxygen-induced Retinopathy</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2017-06-05</date><risdate>2017</risdate><volume>7</volume><issue>1</issue><spage>2756</spage><epage>9</epage><pages>2756-9</pages><artnum>2756</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Interleukin 38 (IL-38) is a novel identified cytokine of IL-1 family in which some members are important in inflammation and angiogenesis. However, the role of IL-38 in regulating angiogenesis is unknown. The aim of the present study is to explore the effect of IL-38 on angiogenesis. Oxygen-induced retinopathy (OIR) of C57BL/6 J mice was induced by exposure of hyperoxia (75% oxygen) from postnatal day 7 (P7) to P12 and then returned to room air. The mice were injected with IL-38. At P17, neovascular region (tufts) and avascular area of the retinas were analyzed. The data showed that administration of IL-38
in vivo
inhibited retinal angiogenesis significantly. Furthermore, the addition of IL-38 to the cell cultures attenuated the proliferation, scratch wound healing and tube formation of vascular endothelial cells induced by VEGF significantly. Our findings suggest that IL-38 is an antiangiogenic cytokine in pathophysiological settings and may have therapeutic potential for angiogenesis related diseases.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>28584235</pmid><doi>10.1038/s41598-017-03079-z</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 13/21 13/51 631/250/127/1213 64/60 692/699/249/2510 Angiogenesis Angiogenesis Inhibitors - pharmacology Animals Animals, Newborn Cell Movement - drug effects Cell proliferation Cell Proliferation - drug effects Cytokines Data processing Disease Models, Animal Endothelial cells Endothelial Cells - drug effects Endothelial Cells - metabolism Human Umbilical Vein Endothelial Cells Humanities and Social Sciences Humans Hyperoxia Interleukin 1 Interleukins - pharmacology Mice multidisciplinary Oxygen Oxygen - adverse effects Retina Retinal Diseases - etiology Retinal Diseases - metabolism Retinal Diseases - pathology Retinal Neovascularization - etiology Retinal Neovascularization - metabolism Retinal Neovascularization - pathology Retinopathy Rodents Science Science (multidisciplinary) Vascular endothelial growth factor Wound healing |
title | The Effect of Interleukin 38 on Angiogenesis in a Model of Oxygen-induced Retinopathy |
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