Identification of RUNX1 as a Mediator of Aberrant Retinal Angiogenesis
Proliferative diabetic retinopathy (PDR) is a common cause of blindness in the developed world's working adult population and affects those with type 1 and type 2 diabetes. We identified Runt-related transcription factor 1 (RUNX1) as a gene upregulated in CD31 vascular endothelial cells obtaine...
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| Veröffentlicht in: | Diabetes (New York, N.Y.) N.Y.), 2017-07, Vol.66 (7), p.1950-1956 |
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| container_title | Diabetes (New York, N.Y.) |
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| creator | Lam, Jonathan D Oh, Daniel J Wong, Lindsay L Amarnani, Dhanesh Park-Windhol, Cindy Sanchez, Angie V Cardona-Velez, Jonathan McGuone, Declan Stemmer-Rachamimov, Anat O Eliott, Dean Bielenberg, Diane R van Zyl, Tave Shen, Lishuang Gai, Xiaowu D'Amore, Patricia A Kim, Leo A Arboleda-Velasquez, Joseph F |
| description | Proliferative diabetic retinopathy (PDR) is a common cause of blindness in the developed world's working adult population and affects those with type 1 and type 2 diabetes. We identified Runt-related transcription factor 1 (RUNX1) as a gene upregulated in CD31
vascular endothelial cells obtained from human PDR fibrovascular membranes (FVMs) via transcriptomic analysis. In vitro studies using human retinal microvascular endothelial cells (HRMECs) showed increased RUNX1 RNA and protein expression in response to high glucose, whereas RUNX1 inhibition reduced HRMEC migration, proliferation, and tube formation. Immunohistochemical staining for RUNX1 showed reactivity in vessels of patient-derived FVMs and angiogenic tufts in the retina of mice with oxygen-induced retinopathy, suggesting that RUNX1 upregulation is a hallmark of aberrant retinal angiogenesis. Inhibition of RUNX1 activity with the Ro5-3335 small molecule resulted in a significant reduction of neovascular tufts in oxygen-induced retinopathy, supporting the feasibility of targeting RUNX1 in aberrant retinal angiogenesis. |
| doi_str_mv | 10.2337/db16-1035 |
| format | Article |
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vascular endothelial cells obtained from human PDR fibrovascular membranes (FVMs) via transcriptomic analysis. In vitro studies using human retinal microvascular endothelial cells (HRMECs) showed increased RUNX1 RNA and protein expression in response to high glucose, whereas RUNX1 inhibition reduced HRMEC migration, proliferation, and tube formation. Immunohistochemical staining for RUNX1 showed reactivity in vessels of patient-derived FVMs and angiogenic tufts in the retina of mice with oxygen-induced retinopathy, suggesting that RUNX1 upregulation is a hallmark of aberrant retinal angiogenesis. Inhibition of RUNX1 activity with the Ro5-3335 small molecule resulted in a significant reduction of neovascular tufts in oxygen-induced retinopathy, supporting the feasibility of targeting RUNX1 in aberrant retinal angiogenesis.</description><identifier>ISSN: 0012-1797</identifier><identifier>EISSN: 1939-327X</identifier><identifier>DOI: 10.2337/db16-1035</identifier><identifier>PMID: 28400392</identifier><language>eng</language><publisher>United States: American Diabetes Association</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Angiogenesis ; Animals ; Blindness ; Cell Movement - drug effects ; Cell Proliferation - drug effects ; Cells ; Core Binding Factor Alpha 2 Subunit - antagonists & inhibitors ; Core Binding Factor Alpha 2 Subunit - genetics ; Core Binding Factor Alpha 2 Subunit - metabolism ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Type 1 - complications ; Diabetes Mellitus, Type 1 - metabolism ; Diabetes Mellitus, Type 2 - complications ; Diabetes Mellitus, Type 2 - metabolism ; Diabetic retinopathy ; Diabetic Retinopathy - etiology ; Diabetic Retinopathy - genetics ; Diabetic Retinopathy - metabolism ; Disease Models, Animal ; Endothelial cells ; Endothelial Cells - drug effects ; Endothelial Cells - metabolism ; Female ; Glucose ; Glucose - pharmacology ; Humans ; Immunohistochemistry ; Male ; Mice ; Microvasculature ; Middle Aged ; Molecules ; Oxygen ; Oxygen - adverse effects ; Pathophysiology ; Protein expression ; Retina ; Retina - metabolism ; Retinal Neovascularization - genetics ; Retinal Neovascularization - metabolism ; Retinopathy ; Ribonucleic acid ; RNA ; RNA, Messenger - metabolism ; Runx1 protein</subject><ispartof>Diabetes (New York, N.Y.), 2017-07, Vol.66 (7), p.1950-1956</ispartof><rights>2017 by the American Diabetes Association.</rights><rights>Copyright American Diabetes Association Jul 1, 2017</rights><rights>2017 by the American Diabetes Association. 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c469t-332ffe80846e51805d955fc2e9147fb2b948d2ce514021b5addaf7b97d5b5c2c3</citedby><cites>FETCH-LOGICAL-c469t-332ffe80846e51805d955fc2e9147fb2b948d2ce514021b5addaf7b97d5b5c2c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5482092/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5482092/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28400392$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lam, Jonathan D</creatorcontrib><creatorcontrib>Oh, Daniel J</creatorcontrib><creatorcontrib>Wong, Lindsay L</creatorcontrib><creatorcontrib>Amarnani, Dhanesh</creatorcontrib><creatorcontrib>Park-Windhol, Cindy</creatorcontrib><creatorcontrib>Sanchez, Angie V</creatorcontrib><creatorcontrib>Cardona-Velez, Jonathan</creatorcontrib><creatorcontrib>McGuone, Declan</creatorcontrib><creatorcontrib>Stemmer-Rachamimov, Anat O</creatorcontrib><creatorcontrib>Eliott, Dean</creatorcontrib><creatorcontrib>Bielenberg, Diane R</creatorcontrib><creatorcontrib>van Zyl, Tave</creatorcontrib><creatorcontrib>Shen, Lishuang</creatorcontrib><creatorcontrib>Gai, Xiaowu</creatorcontrib><creatorcontrib>D'Amore, Patricia A</creatorcontrib><creatorcontrib>Kim, Leo A</creatorcontrib><creatorcontrib>Arboleda-Velasquez, Joseph F</creatorcontrib><title>Identification of RUNX1 as a Mediator of Aberrant Retinal Angiogenesis</title><title>Diabetes (New York, N.Y.)</title><addtitle>Diabetes</addtitle><description>Proliferative diabetic retinopathy (PDR) is a common cause of blindness in the developed world's working adult population and affects those with type 1 and type 2 diabetes. We identified Runt-related transcription factor 1 (RUNX1) as a gene upregulated in CD31
vascular endothelial cells obtained from human PDR fibrovascular membranes (FVMs) via transcriptomic analysis. In vitro studies using human retinal microvascular endothelial cells (HRMECs) showed increased RUNX1 RNA and protein expression in response to high glucose, whereas RUNX1 inhibition reduced HRMEC migration, proliferation, and tube formation. Immunohistochemical staining for RUNX1 showed reactivity in vessels of patient-derived FVMs and angiogenic tufts in the retina of mice with oxygen-induced retinopathy, suggesting that RUNX1 upregulation is a hallmark of aberrant retinal angiogenesis. Inhibition of RUNX1 activity with the Ro5-3335 small molecule resulted in a significant reduction of neovascular tufts in oxygen-induced retinopathy, supporting the feasibility of targeting RUNX1 in aberrant retinal angiogenesis.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Angiogenesis</subject><subject>Animals</subject><subject>Blindness</subject><subject>Cell Movement - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>Cells</subject><subject>Core Binding Factor Alpha 2 Subunit - antagonists & inhibitors</subject><subject>Core Binding Factor Alpha 2 Subunit - genetics</subject><subject>Core Binding Factor Alpha 2 Subunit - metabolism</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Type 1 - complications</subject><subject>Diabetes Mellitus, Type 1 - metabolism</subject><subject>Diabetes Mellitus, Type 2 - complications</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Diabetic retinopathy</subject><subject>Diabetic Retinopathy - etiology</subject><subject>Diabetic Retinopathy - genetics</subject><subject>Diabetic Retinopathy - metabolism</subject><subject>Disease Models, Animal</subject><subject>Endothelial cells</subject><subject>Endothelial Cells - drug effects</subject><subject>Endothelial Cells - metabolism</subject><subject>Female</subject><subject>Glucose</subject><subject>Glucose - pharmacology</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Male</subject><subject>Mice</subject><subject>Microvasculature</subject><subject>Middle Aged</subject><subject>Molecules</subject><subject>Oxygen</subject><subject>Oxygen - adverse effects</subject><subject>Pathophysiology</subject><subject>Protein expression</subject><subject>Retina</subject><subject>Retina - metabolism</subject><subject>Retinal Neovascularization - genetics</subject><subject>Retinal Neovascularization - metabolism</subject><subject>Retinopathy</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA, Messenger - metabolism</subject><subject>Runx1 protein</subject><issn>0012-1797</issn><issn>1939-327X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkUtLAzEUhYMotj4W_gEZcKOL0dw8OpONUIpVwQeIQnchk0eNTCeaTAX_vSlWUbmLC_d8HM7lIHQA-JRQWp2ZBkYlYMo30BAEFSUl1WwTDTEGUkIlqgHaSekFYzzKs40GpGYYU0GGaHptbNd757XqfeiK4IqHp7sZFCoVqri1xqs-xNV53NgYVdcXD7b3nWqLcTf3YW47m3zaQ1tOtcnur_cueppePE6uypv7y-vJ-KbUbCT6klLinK1xzUaWQ425EZw7TawAVrmGNILVhuisMUyg4coY5apGVIY3XBNNd9H5l-_rsllYo3P2qFr5Gv1CxQ8ZlJd_lc4_y3l4l5zVBAuSDY7XBjG8LW3q5cInbdtWdTYsk4S6rjAHYCKjR__Ql7CM-fNMCQoEQDCaqZMvSseQUrTuJwxguWpHrtqRq3Yye_g7_Q_5XQf9BBJYiWI</recordid><startdate>20170701</startdate><enddate>20170701</enddate><creator>Lam, Jonathan D</creator><creator>Oh, Daniel J</creator><creator>Wong, Lindsay L</creator><creator>Amarnani, Dhanesh</creator><creator>Park-Windhol, Cindy</creator><creator>Sanchez, Angie V</creator><creator>Cardona-Velez, Jonathan</creator><creator>McGuone, Declan</creator><creator>Stemmer-Rachamimov, Anat O</creator><creator>Eliott, Dean</creator><creator>Bielenberg, Diane R</creator><creator>van Zyl, Tave</creator><creator>Shen, Lishuang</creator><creator>Gai, Xiaowu</creator><creator>D'Amore, Patricia A</creator><creator>Kim, Leo A</creator><creator>Arboleda-Velasquez, Joseph F</creator><general>American Diabetes Association</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>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20170701</creationdate><title>Identification of RUNX1 as a Mediator of Aberrant Retinal Angiogenesis</title><author>Lam, Jonathan D ; Oh, Daniel J ; Wong, Lindsay L ; Amarnani, Dhanesh ; Park-Windhol, Cindy ; Sanchez, Angie V ; Cardona-Velez, Jonathan ; McGuone, Declan ; Stemmer-Rachamimov, Anat O ; Eliott, Dean ; Bielenberg, Diane R ; van Zyl, Tave ; Shen, Lishuang ; Gai, Xiaowu ; D'Amore, Patricia A ; Kim, Leo A ; Arboleda-Velasquez, Joseph F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c469t-332ffe80846e51805d955fc2e9147fb2b948d2ce514021b5addaf7b97d5b5c2c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Angiogenesis</topic><topic>Animals</topic><topic>Blindness</topic><topic>Cell Movement - drug effects</topic><topic>Cell Proliferation - drug effects</topic><topic>Cells</topic><topic>Core Binding Factor Alpha 2 Subunit - antagonists & inhibitors</topic><topic>Core Binding Factor Alpha 2 Subunit - genetics</topic><topic>Core Binding Factor Alpha 2 Subunit - metabolism</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes Mellitus, Type 1 - complications</topic><topic>Diabetes Mellitus, Type 1 - metabolism</topic><topic>Diabetes Mellitus, Type 2 - complications</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Diabetic retinopathy</topic><topic>Diabetic Retinopathy - etiology</topic><topic>Diabetic Retinopathy - genetics</topic><topic>Diabetic Retinopathy - metabolism</topic><topic>Disease Models, Animal</topic><topic>Endothelial cells</topic><topic>Endothelial Cells - drug effects</topic><topic>Endothelial Cells - metabolism</topic><topic>Female</topic><topic>Glucose</topic><topic>Glucose - pharmacology</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Male</topic><topic>Mice</topic><topic>Microvasculature</topic><topic>Middle Aged</topic><topic>Molecules</topic><topic>Oxygen</topic><topic>Oxygen - adverse effects</topic><topic>Pathophysiology</topic><topic>Protein expression</topic><topic>Retina</topic><topic>Retina - metabolism</topic><topic>Retinal Neovascularization - genetics</topic><topic>Retinal Neovascularization - metabolism</topic><topic>Retinopathy</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>RNA, Messenger - metabolism</topic><topic>Runx1 protein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lam, Jonathan D</creatorcontrib><creatorcontrib>Oh, Daniel J</creatorcontrib><creatorcontrib>Wong, Lindsay L</creatorcontrib><creatorcontrib>Amarnani, Dhanesh</creatorcontrib><creatorcontrib>Park-Windhol, Cindy</creatorcontrib><creatorcontrib>Sanchez, Angie V</creatorcontrib><creatorcontrib>Cardona-Velez, Jonathan</creatorcontrib><creatorcontrib>McGuone, Declan</creatorcontrib><creatorcontrib>Stemmer-Rachamimov, Anat O</creatorcontrib><creatorcontrib>Eliott, Dean</creatorcontrib><creatorcontrib>Bielenberg, Diane R</creatorcontrib><creatorcontrib>van Zyl, Tave</creatorcontrib><creatorcontrib>Shen, Lishuang</creatorcontrib><creatorcontrib>Gai, Xiaowu</creatorcontrib><creatorcontrib>D'Amore, Patricia A</creatorcontrib><creatorcontrib>Kim, Leo A</creatorcontrib><creatorcontrib>Arboleda-Velasquez, Joseph F</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Diabetes (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lam, Jonathan D</au><au>Oh, Daniel J</au><au>Wong, Lindsay L</au><au>Amarnani, Dhanesh</au><au>Park-Windhol, Cindy</au><au>Sanchez, Angie V</au><au>Cardona-Velez, Jonathan</au><au>McGuone, Declan</au><au>Stemmer-Rachamimov, Anat O</au><au>Eliott, Dean</au><au>Bielenberg, Diane R</au><au>van Zyl, Tave</au><au>Shen, Lishuang</au><au>Gai, Xiaowu</au><au>D'Amore, Patricia A</au><au>Kim, Leo A</au><au>Arboleda-Velasquez, Joseph F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Identification of RUNX1 as a Mediator of Aberrant Retinal Angiogenesis</atitle><jtitle>Diabetes (New York, N.Y.)</jtitle><addtitle>Diabetes</addtitle><date>2017-07-01</date><risdate>2017</risdate><volume>66</volume><issue>7</issue><spage>1950</spage><epage>1956</epage><pages>1950-1956</pages><issn>0012-1797</issn><eissn>1939-327X</eissn><abstract>Proliferative diabetic retinopathy (PDR) is a common cause of blindness in the developed world's working adult population and affects those with type 1 and type 2 diabetes. We identified Runt-related transcription factor 1 (RUNX1) as a gene upregulated in CD31
vascular endothelial cells obtained from human PDR fibrovascular membranes (FVMs) via transcriptomic analysis. In vitro studies using human retinal microvascular endothelial cells (HRMECs) showed increased RUNX1 RNA and protein expression in response to high glucose, whereas RUNX1 inhibition reduced HRMEC migration, proliferation, and tube formation. Immunohistochemical staining for RUNX1 showed reactivity in vessels of patient-derived FVMs and angiogenic tufts in the retina of mice with oxygen-induced retinopathy, suggesting that RUNX1 upregulation is a hallmark of aberrant retinal angiogenesis. Inhibition of RUNX1 activity with the Ro5-3335 small molecule resulted in a significant reduction of neovascular tufts in oxygen-induced retinopathy, supporting the feasibility of targeting RUNX1 in aberrant retinal angiogenesis.</abstract><cop>United States</cop><pub>American Diabetes Association</pub><pmid>28400392</pmid><doi>10.2337/db16-1035</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Aged Aged, 80 and over Angiogenesis Animals Blindness Cell Movement - drug effects Cell Proliferation - drug effects Cells Core Binding Factor Alpha 2 Subunit - antagonists & inhibitors Core Binding Factor Alpha 2 Subunit - genetics Core Binding Factor Alpha 2 Subunit - metabolism Diabetes Diabetes mellitus Diabetes Mellitus, Type 1 - complications Diabetes Mellitus, Type 1 - metabolism Diabetes Mellitus, Type 2 - complications Diabetes Mellitus, Type 2 - metabolism Diabetic retinopathy Diabetic Retinopathy - etiology Diabetic Retinopathy - genetics Diabetic Retinopathy - metabolism Disease Models, Animal Endothelial cells Endothelial Cells - drug effects Endothelial Cells - metabolism Female Glucose Glucose - pharmacology Humans Immunohistochemistry Male Mice Microvasculature Middle Aged Molecules Oxygen Oxygen - adverse effects Pathophysiology Protein expression Retina Retina - metabolism Retinal Neovascularization - genetics Retinal Neovascularization - metabolism Retinopathy Ribonucleic acid RNA RNA, Messenger - metabolism Runx1 protein |
| title | Identification of RUNX1 as a Mediator of Aberrant Retinal Angiogenesis |
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