CXCR4 down-regulation by small interfering RNA inhibits invasion and tubule formation of human retinal microvascular endothelial cells
The progressive alterations to the retinal microvasculature in diabetic retinopathy are known to cause vision loss. Chemokines are characterized by their ability to induce cell invasion, adhesion and migration. In this study, we used double siRNA transfection to transiently and selectively decrease...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2007-07, Vol.358 (4), p.990-996 |
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| container_title | Biochemical and biophysical research communications |
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| creator | Yu, Keming Zhuang, Jing Kaminski, Joseph M. Ambati, Bala Gao, Qianying Ma, Ping Liao, Dongjiang Li, Fan Liu, Xuan Ge, Jian |
| description | The progressive alterations to the retinal microvasculature in diabetic retinopathy are known to cause vision loss. Chemokines are characterized by their ability to induce cell invasion, adhesion and migration. In this study, we used double siRNA transfection to transiently and selectively decrease the level of the endogenous CXCR4 in human retinal microvascular endothelial cells (HRMECs). The functional consequences of silencing CXCR4 expression in HRMECs were investigated using an endothelial cell migration assay and tubule formation in Matrigel. When CXCR4 expression was decreased with siRNA, HRMECs were less invasive and also resulted in markedly diminished vascular networks on Matrigel as compared to the controls. Additionally, hypoxia and VEGF, the factors affecting microvascular, regulate the expression level of CXCR4 in HRMECs, respectively, which have synergistic, additive effect in the HRMECs. As such, CXCR4 antagonists may become a therapeutic target for the treatment of retinal angiopathies. |
| doi_str_mv | 10.1016/j.bbrc.2007.05.004 |
| format | Article |
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Chemokines are characterized by their ability to induce cell invasion, adhesion and migration. In this study, we used double siRNA transfection to transiently and selectively decrease the level of the endogenous CXCR4 in human retinal microvascular endothelial cells (HRMECs). The functional consequences of silencing CXCR4 expression in HRMECs were investigated using an endothelial cell migration assay and tubule formation in Matrigel. When CXCR4 expression was decreased with siRNA, HRMECs were less invasive and also resulted in markedly diminished vascular networks on Matrigel as compared to the controls. Additionally, hypoxia and VEGF, the factors affecting microvascular, regulate the expression level of CXCR4 in HRMECs, respectively, which have synergistic, additive effect in the HRMECs. As such, CXCR4 antagonists may become a therapeutic target for the treatment of retinal angiopathies.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2007.05.004</identifier><identifier>PMID: 17521613</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Blood Vessels - cytology ; Blood Vessels - growth & development ; Blood Vessels - metabolism ; Cells, Cultured ; CXCR4 ; Down-Regulation ; Endothelial Cells - cytology ; Endothelial Cells - physiology ; Gene Silencing - physiology ; Human retinal microvascular endothelial cells ; Humans ; Hypoxia ; Neovascularization, Physiologic - physiology ; Receptors, CXCR4 - genetics ; Receptors, CXCR4 - metabolism ; Retinal Vessels - cytology ; Retinal Vessels - metabolism ; RNA, Small Interfering - genetics ; siRNA ; VEGF</subject><ispartof>Biochemical and biophysical research communications, 2007-07, Vol.358 (4), p.990-996</ispartof><rights>2007</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c451t-b96e68e62e71a2a9142be403f88b9077026dcbc93624f8f260c1522327112abd3</citedby><cites>FETCH-LOGICAL-c451t-b96e68e62e71a2a9142be403f88b9077026dcbc93624f8f260c1522327112abd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0006291X07009461$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17521613$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yu, Keming</creatorcontrib><creatorcontrib>Zhuang, Jing</creatorcontrib><creatorcontrib>Kaminski, Joseph M.</creatorcontrib><creatorcontrib>Ambati, Bala</creatorcontrib><creatorcontrib>Gao, Qianying</creatorcontrib><creatorcontrib>Ma, Ping</creatorcontrib><creatorcontrib>Liao, Dongjiang</creatorcontrib><creatorcontrib>Li, Fan</creatorcontrib><creatorcontrib>Liu, Xuan</creatorcontrib><creatorcontrib>Ge, Jian</creatorcontrib><title>CXCR4 down-regulation by small interfering RNA inhibits invasion and tubule formation of human retinal microvascular endothelial cells</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>The progressive alterations to the retinal microvasculature in diabetic retinopathy are known to cause vision loss. Chemokines are characterized by their ability to induce cell invasion, adhesion and migration. In this study, we used double siRNA transfection to transiently and selectively decrease the level of the endogenous CXCR4 in human retinal microvascular endothelial cells (HRMECs). The functional consequences of silencing CXCR4 expression in HRMECs were investigated using an endothelial cell migration assay and tubule formation in Matrigel. When CXCR4 expression was decreased with siRNA, HRMECs were less invasive and also resulted in markedly diminished vascular networks on Matrigel as compared to the controls. Additionally, hypoxia and VEGF, the factors affecting microvascular, regulate the expression level of CXCR4 in HRMECs, respectively, which have synergistic, additive effect in the HRMECs. As such, CXCR4 antagonists may become a therapeutic target for the treatment of retinal angiopathies.</description><subject>Blood Vessels - cytology</subject><subject>Blood Vessels - growth & development</subject><subject>Blood Vessels - metabolism</subject><subject>Cells, Cultured</subject><subject>CXCR4</subject><subject>Down-Regulation</subject><subject>Endothelial Cells - cytology</subject><subject>Endothelial Cells - physiology</subject><subject>Gene Silencing - physiology</subject><subject>Human retinal microvascular endothelial cells</subject><subject>Humans</subject><subject>Hypoxia</subject><subject>Neovascularization, Physiologic - physiology</subject><subject>Receptors, CXCR4 - genetics</subject><subject>Receptors, CXCR4 - metabolism</subject><subject>Retinal Vessels - cytology</subject><subject>Retinal Vessels - metabolism</subject><subject>RNA, Small Interfering - genetics</subject><subject>siRNA</subject><subject>VEGF</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1q3DAURkVpaSaTvkAXRavu7N4r27IN3YShbQohhdBAdkKSrzMabDmV7JS8QJ67MjPQXbuShM736ecw9h4hR0D56ZAbE2wuAOocqhygfMU2CC1kAqF8zTYAIDPR4v0ZO4_xAIBYyvYtO8O6Eiix2LCX3f3utuTd9NtngR6WQc9u8tw88zjqYeDOzxR6Cs4_8Nuby7TeO-PmmCZPOq6o9h2fF7MMxPspjMf81PP9MmrPA83O64GPzoYpJWw6IXDy3TTvaXBpx9IwxAv2ptdDpHenccvuvn75ubvKrn98-767vM5sWeGcmVaSbEgKqlEL3WIpDJVQ9E1jWqhrELKzxraFFGXf9EKCxUqIQtSIQpuu2LKPx97HMP1aKM5qdHG9gfY0LVHVUMm6geq_ILayLkWq3jJxBNP7YgzUq8fgRh2eFYJaNamDWjWpVZOCSiVNKfTh1L6Ykbq_kZOXBHw-ApQ-48lRUNE68pY6F8jOqpvcv_r_AII0pQw</recordid><startdate>20070713</startdate><enddate>20070713</enddate><creator>Yu, Keming</creator><creator>Zhuang, Jing</creator><creator>Kaminski, Joseph M.</creator><creator>Ambati, Bala</creator><creator>Gao, Qianying</creator><creator>Ma, Ping</creator><creator>Liao, Dongjiang</creator><creator>Li, Fan</creator><creator>Liu, Xuan</creator><creator>Ge, Jian</creator><general>Elsevier 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>7TM</scope><scope>7X8</scope></search><sort><creationdate>20070713</creationdate><title>CXCR4 down-regulation by small interfering RNA inhibits invasion and tubule formation of human retinal microvascular endothelial cells</title><author>Yu, Keming ; Zhuang, Jing ; Kaminski, Joseph M. ; Ambati, Bala ; Gao, Qianying ; Ma, Ping ; Liao, Dongjiang ; Li, Fan ; Liu, Xuan ; Ge, Jian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c451t-b96e68e62e71a2a9142be403f88b9077026dcbc93624f8f260c1522327112abd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Blood Vessels - cytology</topic><topic>Blood Vessels - growth & development</topic><topic>Blood Vessels - metabolism</topic><topic>Cells, Cultured</topic><topic>CXCR4</topic><topic>Down-Regulation</topic><topic>Endothelial Cells - cytology</topic><topic>Endothelial Cells - physiology</topic><topic>Gene Silencing - physiology</topic><topic>Human retinal microvascular endothelial cells</topic><topic>Humans</topic><topic>Hypoxia</topic><topic>Neovascularization, Physiologic - physiology</topic><topic>Receptors, CXCR4 - genetics</topic><topic>Receptors, CXCR4 - metabolism</topic><topic>Retinal Vessels - cytology</topic><topic>Retinal Vessels - metabolism</topic><topic>RNA, Small Interfering - genetics</topic><topic>siRNA</topic><topic>VEGF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yu, Keming</creatorcontrib><creatorcontrib>Zhuang, Jing</creatorcontrib><creatorcontrib>Kaminski, Joseph M.</creatorcontrib><creatorcontrib>Ambati, Bala</creatorcontrib><creatorcontrib>Gao, Qianying</creatorcontrib><creatorcontrib>Ma, Ping</creatorcontrib><creatorcontrib>Liao, Dongjiang</creatorcontrib><creatorcontrib>Li, Fan</creatorcontrib><creatorcontrib>Liu, Xuan</creatorcontrib><creatorcontrib>Ge, Jian</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Nucleic Acids Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yu, Keming</au><au>Zhuang, Jing</au><au>Kaminski, Joseph M.</au><au>Ambati, Bala</au><au>Gao, Qianying</au><au>Ma, Ping</au><au>Liao, Dongjiang</au><au>Li, Fan</au><au>Liu, Xuan</au><au>Ge, Jian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CXCR4 down-regulation by small interfering RNA inhibits invasion and tubule formation of human retinal microvascular endothelial cells</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2007-07-13</date><risdate>2007</risdate><volume>358</volume><issue>4</issue><spage>990</spage><epage>996</epage><pages>990-996</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>The progressive alterations to the retinal microvasculature in diabetic retinopathy are known to cause vision loss. Chemokines are characterized by their ability to induce cell invasion, adhesion and migration. In this study, we used double siRNA transfection to transiently and selectively decrease the level of the endogenous CXCR4 in human retinal microvascular endothelial cells (HRMECs). The functional consequences of silencing CXCR4 expression in HRMECs were investigated using an endothelial cell migration assay and tubule formation in Matrigel. When CXCR4 expression was decreased with siRNA, HRMECs were less invasive and also resulted in markedly diminished vascular networks on Matrigel as compared to the controls. Additionally, hypoxia and VEGF, the factors affecting microvascular, regulate the expression level of CXCR4 in HRMECs, respectively, which have synergistic, additive effect in the HRMECs. 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| subjects | Blood Vessels - cytology Blood Vessels - growth & development Blood Vessels - metabolism Cells, Cultured CXCR4 Down-Regulation Endothelial Cells - cytology Endothelial Cells - physiology Gene Silencing - physiology Human retinal microvascular endothelial cells Humans Hypoxia Neovascularization, Physiologic - physiology Receptors, CXCR4 - genetics Receptors, CXCR4 - metabolism Retinal Vessels - cytology Retinal Vessels - metabolism RNA, Small Interfering - genetics siRNA VEGF |
| title | CXCR4 down-regulation by small interfering RNA inhibits invasion and tubule formation of human retinal microvascular endothelial cells |
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