Suppression of choroidal neovascularization by Endostar in rats

Choroidal neovascularization (CNV) is common in various retinal and choroidal diseases, and may result in severe and irreversible loss of vision. Our previous studies suggested that Endostar, a novel recombinant endostatin, is able to inhibit the proliferation and migration of choroid-retinal endoth...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Molecular medicine reports 2015-05, Vol.11 (5), p.3621-3625
Hauptverfasser: LIU, JIAN, YE, PANPAN, SU, ZHAOAN, LIN, KANA, HE, FENGYING, XU, WEN
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 3625
container_issue 5
container_start_page 3621
container_title Molecular medicine reports
container_volume 11
creator LIU, JIAN
YE, PANPAN
SU, ZHAOAN
LIN, KANA
HE, FENGYING
XU, WEN
description Choroidal neovascularization (CNV) is common in various retinal and choroidal diseases, and may result in severe and irreversible loss of vision. Our previous studies suggested that Endostar, a novel recombinant endostatin, is able to inhibit the proliferation and migration of choroid-retinal endothelial cells. To further evaluate the effect of Endostar on the formation of CNV in vivo, a rat model of laser-induced CNV was constructed and Endostar or phosphate-buffered saline treatment was administered intravitreally every other day. Using fluorescein angiography (FA), reduced CNV incidence and leakage grade was observed in the Endostar group. In addition, CNV area and maximal thickness were prominently reduced in the Endostar group measured by choroid flat mounts and sections. Furthermore, vascular endothelial growth factor (VEGF), hypoxia-inducible factor 1α and chemokine C-X-C motif ligand 1 were markedly reduced in the Endostar group as determined by quantitative polymerase chain reaction and downregulation of VEGF was also verified by western blot analysis at the protein level. This study demonstrates that Endostar suppressed CNV in a rat model, which may be largely mediated by the downregulation of VEGF and other angiogenic molecules.
doi_str_mv 10.3892/mmr.2014.3132
format Article
fullrecord <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_1658421112</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A420928652</galeid><sourcerecordid>A420928652</sourcerecordid><originalsourceid>FETCH-LOGICAL-c459t-a0710eb080eb88b4f2a6406e89375858a74d0681324de31dc39e4a38d72a747a3</originalsourceid><addsrcrecordid>eNptkctLxDAQxoMovo9epeBBL13zbJOTLOILBA_qOcw2qUbapiatoH-9KbsqigSSIfObL5P5EDogeMakoqdtG2YUEz5jhNE1tE1KRXKGMV9fxVSpcgvtxPiCcSGoUJtoiwrBOaZsG53dj30fbIzOd5mvs-rZB-8MNFln_RvEamwguA8YpvziPbvojI8DhMx1WYAh7qGNGppo91fnLnq8vHg4v85v765uzue3ecWFGnLAJcF2gWXapFzwmkLBcWGlYqWQQkLJDS5k-gI3lhFTMWU5MGlKmlIlsF10stTtg38dbRx062JlmwZSn2PUpBCSU0IITejRH_TFj6FL3Wmi0gNFybj4oZ6gsdp1tR8CVJOonnOKFZVpWIma_UOlZWzrKt_Z2qX7XwX5sqAKPsZga90H10J41wTryTCdDNOTYXoyLPGHq2bHRWvNN_3lUAKOl0DsoTMuTf-bSUo5ITkWOSsoYZ-BoZq6</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1932467345</pqid></control><display><type>article</type><title>Suppression of choroidal neovascularization by Endostar in rats</title><source>Spandidos Publications Journals</source><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>LIU, JIAN ; YE, PANPAN ; SU, ZHAOAN ; LIN, KANA ; HE, FENGYING ; XU, WEN</creator><creatorcontrib>LIU, JIAN ; YE, PANPAN ; SU, ZHAOAN ; LIN, KANA ; HE, FENGYING ; XU, WEN</creatorcontrib><description>Choroidal neovascularization (CNV) is common in various retinal and choroidal diseases, and may result in severe and irreversible loss of vision. Our previous studies suggested that Endostar, a novel recombinant endostatin, is able to inhibit the proliferation and migration of choroid-retinal endothelial cells. To further evaluate the effect of Endostar on the formation of CNV in vivo, a rat model of laser-induced CNV was constructed and Endostar or phosphate-buffered saline treatment was administered intravitreally every other day. Using fluorescein angiography (FA), reduced CNV incidence and leakage grade was observed in the Endostar group. In addition, CNV area and maximal thickness were prominently reduced in the Endostar group measured by choroid flat mounts and sections. Furthermore, vascular endothelial growth factor (VEGF), hypoxia-inducible factor 1α and chemokine C-X-C motif ligand 1 were markedly reduced in the Endostar group as determined by quantitative polymerase chain reaction and downregulation of VEGF was also verified by western blot analysis at the protein level. This study demonstrates that Endostar suppressed CNV in a rat model, which may be largely mediated by the downregulation of VEGF and other angiogenic molecules.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2014.3132</identifier><identifier>PMID: 25544023</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Angiogenesis ; Angiography ; Animals ; Cell proliferation ; choroidal neovascularization ; Choroidal Neovascularization - drug therapy ; Choroidal Neovascularization - etiology ; Choroidal Neovascularization - pathology ; Cybernetics ; Down-Regulation ; Drug dosages ; drug therapy ; Endostatin ; Endostatins - pharmacology ; Endothelial cells ; Fluorescein ; Fluorescein Angiography ; Gene Expression Profiling ; Gene Expression Regulation - drug effects ; Hypoxia-Inducible Factor 1, alpha Subunit - genetics ; Hypoxia-Inducible Factor 1, alpha Subunit - metabolism ; Hypoxia-inducible factors ; Leukocyte migration ; Male ; Neovascularization ; Neutrophils ; Patient outcomes ; Polymerase chain reaction ; Prevention ; Proteins ; Rats ; Recombinant molecules ; Retina ; Rodents ; Studies ; Vascular endothelial growth factor ; Vascular Endothelial Growth Factor A - genetics ; Vascular Endothelial Growth Factor A - metabolism ; Vascularization</subject><ispartof>Molecular medicine reports, 2015-05, Vol.11 (5), p.3621-3625</ispartof><rights>Copyright © 2015, Spandidos Publications</rights><rights>COPYRIGHT 2015 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c459t-a0710eb080eb88b4f2a6406e89375858a74d0681324de31dc39e4a38d72a747a3</citedby><cites>FETCH-LOGICAL-c459t-a0710eb080eb88b4f2a6406e89375858a74d0681324de31dc39e4a38d72a747a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,5556,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25544023$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>LIU, JIAN</creatorcontrib><creatorcontrib>YE, PANPAN</creatorcontrib><creatorcontrib>SU, ZHAOAN</creatorcontrib><creatorcontrib>LIN, KANA</creatorcontrib><creatorcontrib>HE, FENGYING</creatorcontrib><creatorcontrib>XU, WEN</creatorcontrib><title>Suppression of choroidal neovascularization by Endostar in rats</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Choroidal neovascularization (CNV) is common in various retinal and choroidal diseases, and may result in severe and irreversible loss of vision. Our previous studies suggested that Endostar, a novel recombinant endostatin, is able to inhibit the proliferation and migration of choroid-retinal endothelial cells. To further evaluate the effect of Endostar on the formation of CNV in vivo, a rat model of laser-induced CNV was constructed and Endostar or phosphate-buffered saline treatment was administered intravitreally every other day. Using fluorescein angiography (FA), reduced CNV incidence and leakage grade was observed in the Endostar group. In addition, CNV area and maximal thickness were prominently reduced in the Endostar group measured by choroid flat mounts and sections. Furthermore, vascular endothelial growth factor (VEGF), hypoxia-inducible factor 1α and chemokine C-X-C motif ligand 1 were markedly reduced in the Endostar group as determined by quantitative polymerase chain reaction and downregulation of VEGF was also verified by western blot analysis at the protein level. This study demonstrates that Endostar suppressed CNV in a rat model, which may be largely mediated by the downregulation of VEGF and other angiogenic molecules.</description><subject>Angiogenesis</subject><subject>Angiography</subject><subject>Animals</subject><subject>Cell proliferation</subject><subject>choroidal neovascularization</subject><subject>Choroidal Neovascularization - drug therapy</subject><subject>Choroidal Neovascularization - etiology</subject><subject>Choroidal Neovascularization - pathology</subject><subject>Cybernetics</subject><subject>Down-Regulation</subject><subject>Drug dosages</subject><subject>drug therapy</subject><subject>Endostatin</subject><subject>Endostatins - pharmacology</subject><subject>Endothelial cells</subject><subject>Fluorescein</subject><subject>Fluorescein Angiography</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Hypoxia-Inducible Factor 1, alpha Subunit - genetics</subject><subject>Hypoxia-Inducible Factor 1, alpha Subunit - metabolism</subject><subject>Hypoxia-inducible factors</subject><subject>Leukocyte migration</subject><subject>Male</subject><subject>Neovascularization</subject><subject>Neutrophils</subject><subject>Patient outcomes</subject><subject>Polymerase chain reaction</subject><subject>Prevention</subject><subject>Proteins</subject><subject>Rats</subject><subject>Recombinant molecules</subject><subject>Retina</subject><subject>Rodents</subject><subject>Studies</subject><subject>Vascular endothelial growth factor</subject><subject>Vascular Endothelial Growth Factor A - genetics</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><subject>Vascularization</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptkctLxDAQxoMovo9epeBBL13zbJOTLOILBA_qOcw2qUbapiatoH-9KbsqigSSIfObL5P5EDogeMakoqdtG2YUEz5jhNE1tE1KRXKGMV9fxVSpcgvtxPiCcSGoUJtoiwrBOaZsG53dj30fbIzOd5mvs-rZB-8MNFln_RvEamwguA8YpvziPbvojI8DhMx1WYAh7qGNGppo91fnLnq8vHg4v85v765uzue3ecWFGnLAJcF2gWXapFzwmkLBcWGlYqWQQkLJDS5k-gI3lhFTMWU5MGlKmlIlsF10stTtg38dbRx062JlmwZSn2PUpBCSU0IITejRH_TFj6FL3Wmi0gNFybj4oZ6gsdp1tR8CVJOonnOKFZVpWIma_UOlZWzrKt_Z2qX7XwX5sqAKPsZga90H10J41wTryTCdDNOTYXoyLPGHq2bHRWvNN_3lUAKOl0DsoTMuTf-bSUo5ITkWOSsoYZ-BoZq6</recordid><startdate>20150501</startdate><enddate>20150501</enddate><creator>LIU, JIAN</creator><creator>YE, PANPAN</creator><creator>SU, ZHAOAN</creator><creator>LIN, KANA</creator><creator>HE, FENGYING</creator><creator>XU, WEN</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK 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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20150501</creationdate><title>Suppression of choroidal neovascularization by Endostar in rats</title><author>LIU, JIAN ; YE, PANPAN ; SU, ZHAOAN ; LIN, KANA ; HE, FENGYING ; XU, WEN</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c459t-a0710eb080eb88b4f2a6406e89375858a74d0681324de31dc39e4a38d72a747a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Angiogenesis</topic><topic>Angiography</topic><topic>Animals</topic><topic>Cell proliferation</topic><topic>choroidal neovascularization</topic><topic>Choroidal Neovascularization - drug therapy</topic><topic>Choroidal Neovascularization - etiology</topic><topic>Choroidal Neovascularization - pathology</topic><topic>Cybernetics</topic><topic>Down-Regulation</topic><topic>Drug dosages</topic><topic>drug therapy</topic><topic>Endostatin</topic><topic>Endostatins - pharmacology</topic><topic>Endothelial cells</topic><topic>Fluorescein</topic><topic>Fluorescein Angiography</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Hypoxia-Inducible Factor 1, alpha Subunit - genetics</topic><topic>Hypoxia-Inducible Factor 1, alpha Subunit - metabolism</topic><topic>Hypoxia-inducible factors</topic><topic>Leukocyte migration</topic><topic>Male</topic><topic>Neovascularization</topic><topic>Neutrophils</topic><topic>Patient outcomes</topic><topic>Polymerase chain reaction</topic><topic>Prevention</topic><topic>Proteins</topic><topic>Rats</topic><topic>Recombinant molecules</topic><topic>Retina</topic><topic>Rodents</topic><topic>Studies</topic><topic>Vascular endothelial growth factor</topic><topic>Vascular Endothelial Growth Factor A - genetics</topic><topic>Vascular Endothelial Growth Factor A - metabolism</topic><topic>Vascularization</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>LIU, JIAN</creatorcontrib><creatorcontrib>YE, PANPAN</creatorcontrib><creatorcontrib>SU, ZHAOAN</creatorcontrib><creatorcontrib>LIN, KANA</creatorcontrib><creatorcontrib>HE, FENGYING</creatorcontrib><creatorcontrib>XU, WEN</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 Central (Corporate)</collection><collection>Health &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>LIU, JIAN</au><au>YE, PANPAN</au><au>SU, ZHAOAN</au><au>LIN, KANA</au><au>HE, FENGYING</au><au>XU, WEN</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Suppression of choroidal neovascularization by Endostar in rats</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2015-05-01</date><risdate>2015</risdate><volume>11</volume><issue>5</issue><spage>3621</spage><epage>3625</epage><pages>3621-3625</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Choroidal neovascularization (CNV) is common in various retinal and choroidal diseases, and may result in severe and irreversible loss of vision. Our previous studies suggested that Endostar, a novel recombinant endostatin, is able to inhibit the proliferation and migration of choroid-retinal endothelial cells. To further evaluate the effect of Endostar on the formation of CNV in vivo, a rat model of laser-induced CNV was constructed and Endostar or phosphate-buffered saline treatment was administered intravitreally every other day. Using fluorescein angiography (FA), reduced CNV incidence and leakage grade was observed in the Endostar group. In addition, CNV area and maximal thickness were prominently reduced in the Endostar group measured by choroid flat mounts and sections. Furthermore, vascular endothelial growth factor (VEGF), hypoxia-inducible factor 1α and chemokine C-X-C motif ligand 1 were markedly reduced in the Endostar group as determined by quantitative polymerase chain reaction and downregulation of VEGF was also verified by western blot analysis at the protein level. This study demonstrates that Endostar suppressed CNV in a rat model, which may be largely mediated by the downregulation of VEGF and other angiogenic molecules.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>25544023</pmid><doi>10.3892/mmr.2014.3132</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 1791-2997
ispartof Molecular medicine reports, 2015-05, Vol.11 (5), p.3621-3625
issn 1791-2997
1791-3004
language eng
recordid cdi_proquest_miscellaneous_1658421112
source Spandidos Publications Journals; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection
subjects Angiogenesis
Angiography
Animals
Cell proliferation
choroidal neovascularization
Choroidal Neovascularization - drug therapy
Choroidal Neovascularization - etiology
Choroidal Neovascularization - pathology
Cybernetics
Down-Regulation
Drug dosages
drug therapy
Endostatin
Endostatins - pharmacology
Endothelial cells
Fluorescein
Fluorescein Angiography
Gene Expression Profiling
Gene Expression Regulation - drug effects
Hypoxia-Inducible Factor 1, alpha Subunit - genetics
Hypoxia-Inducible Factor 1, alpha Subunit - metabolism
Hypoxia-inducible factors
Leukocyte migration
Male
Neovascularization
Neutrophils
Patient outcomes
Polymerase chain reaction
Prevention
Proteins
Rats
Recombinant molecules
Retina
Rodents
Studies
Vascular endothelial growth factor
Vascular Endothelial Growth Factor A - genetics
Vascular Endothelial Growth Factor A - metabolism
Vascularization
title Suppression of choroidal neovascularization by Endostar in rats
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-20T03%3A15%3A00IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Suppression%20of%20choroidal%20neovascularization%20by%20Endostar%20in%20rats&rft.jtitle=Molecular%20medicine%20reports&rft.au=LIU,%20JIAN&rft.date=2015-05-01&rft.volume=11&rft.issue=5&rft.spage=3621&rft.epage=3625&rft.pages=3621-3625&rft.issn=1791-2997&rft.eissn=1791-3004&rft_id=info:doi/10.3892/mmr.2014.3132&rft_dat=%3Cgale_proqu%3EA420928652%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1932467345&rft_id=info:pmid/25544023&rft_galeid=A420928652&rfr_iscdi=true