Antagonistic effects of endostatin-vascular endothelial growth inhibitor chimeric recombinant adenovirus on homocysteine-induced vascular endothelial cells injury in vitro and in vivo
The study is inclined to investigate the antagonistic effects of endostatin-vascular endothelial growth inhibitor chimeric recombinant adenovirus (Ad-hENDO-VEGI) on homocysteine (Hcy)-induced vascular endothelial cells (VECs) injury in vitro and in vivo. Human VECs cell line ECV304 was selected and...
Gespeichert in:
| Veröffentlicht in: | Medicine (Baltimore) 2016-11, Vol.95 (44), p.e5197-e5197 |
|---|---|
| Hauptverfasser: | , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | e5197 |
|---|---|
| container_issue | 44 |
| container_start_page | e5197 |
| container_title | Medicine (Baltimore) |
| container_volume | 95 |
| creator | Cui, Zhen-Tian Liu, Jian-Ping Yao, Jian-Min |
| description | The study is inclined to investigate the antagonistic effects of endostatin-vascular endothelial growth inhibitor chimeric recombinant adenovirus (Ad-hENDO-VEGI) on homocysteine (Hcy)-induced vascular endothelial cells (VECs) injury in vitro and in vivo.
Human VECs cell line ECV304 was selected and infected with Ad-hENDO-VEGI. The LDH leakage, SOD activity, and MDA levels were measured by the automatic biochemical analyzer. Cell survival rate was counted by Trypanblau dying. The TNF-α and MCP-1 protein expressions were detected by ELISA assay. The protein expressions of fusion protein of Ad-hENDO-VEGI, nuclear factor kappa B p65 (NF-kappa B p65), and NF-kappa B inhibitor alpha (I-kappa B-α) were detected by Western blotting. A rat model of hyper-homocysteinemia was constructed. Thirty-six Wistar rats were randomly divided into 3 groups: the control group, the model group, and the Ad-hENDO-VEGI group. Serum Hcy levels in rats were measured with enzymatic cycling method. Endothelial vasodilation function was evaluated with the treatment of sodium nitroprusside and acetylcholine.
After Ad-hENDO-VEGI infection, high expressions (41 kD) of fusion proteins in ECV304 cells were observed. The injury severity of Hcy on ECV304 cells had a dose-dependent manner, and the injury reached a steady stage at 1.0 mmol/L. Thus, 1.0 mmol/L Hcy was selected for further experiments. With an increase of Ad-hENDO-VEGI in ECV304 cells after Hcy treatment, LDH leakage, MDA, TNF-α, MCP-1, and nuclear NF-kappa B p65 protein expression were gradually decreased, and cell survival rate, SOD activity, and I-kappa B-α protein expression were gradually increased. Compared with the control group, the model group had a higher Hcy level and attenuated vasodilator response. The Ad-hENDO-VEGI group exhibited a lower Hcy level and enhanced vasodilator response than the model group.
These results indicated that Ad-hENDO-VEGI could down-regulate NF-kappa B p65 expression and suppress inflammatory response, thereby alleviating Hcy-induced VECs injury. |
| doi_str_mv | 10.1097/MD.0000000000005197 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5591108</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1841804560</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4505-f0821f5b6e67fd331faee2a6593422302229ddeac2b5b79d662ab2046f50e2873</originalsourceid><addsrcrecordid>eNptks9u1DAQxiMEokvhCZCQj1xSbCe2kwtS1fJPasUFzpZjjzcujl1sJ6t9Ml6PbLdUBeHLyJ5vfjPWN1X1muAzgnvx7vryDD86jPTiSbUhrOE163n7tNpgTFktetGeVC9yvsGYNIK2z6sTKjrWdRxvql_noahtDC4XpxFYC7pkFC2CYGIuqrhQLyrr2at091ZG8E55tE1xV0bkwugGV2JCenQTpBWSQMdpcEGFgpSBEBeX5pUZ0BinqPe5gAtQu2BmDQb9l67B-7zCb-a0XwNaXEkRqWCOlyW-rJ5Z5TO8uo-n1fePH75dfK6vvn76cnF-VeuWYVZb3FFi2cCBC2uahlgFQBVnfdNS2mBKaW8MKE0HNojecE7VQHHLLcNAO9GcVu-P3Nt5mMBoCCUpL2-Tm1Tay6ic_DsT3Ci3cZGM9YTgbgW8vQek-HOGXOTk8uF7KkCcsyRdSzrcMo5XaXOU6hRzTmAf2hAsD5bL60v5r-Vr1ZvHEz7U_PF4FbRHwS76Ain_8PMOkhxB-TLe8ZjoaU0x4evEBNf4sDfNb6KDvZc</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1841804560</pqid></control><display><type>article</type><title>Antagonistic effects of endostatin-vascular endothelial growth inhibitor chimeric recombinant adenovirus on homocysteine-induced vascular endothelial cells injury in vitro and in vivo</title><source>Wolters Kluwer Open Health</source><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>IngentaConnect Free/Open Access Journals</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><creator>Cui, Zhen-Tian ; Liu, Jian-Ping ; Yao, Jian-Min</creator><creatorcontrib>Cui, Zhen-Tian ; Liu, Jian-Ping ; Yao, Jian-Min</creatorcontrib><description>The study is inclined to investigate the antagonistic effects of endostatin-vascular endothelial growth inhibitor chimeric recombinant adenovirus (Ad-hENDO-VEGI) on homocysteine (Hcy)-induced vascular endothelial cells (VECs) injury in vitro and in vivo.
Human VECs cell line ECV304 was selected and infected with Ad-hENDO-VEGI. The LDH leakage, SOD activity, and MDA levels were measured by the automatic biochemical analyzer. Cell survival rate was counted by Trypanblau dying. The TNF-α and MCP-1 protein expressions were detected by ELISA assay. The protein expressions of fusion protein of Ad-hENDO-VEGI, nuclear factor kappa B p65 (NF-kappa B p65), and NF-kappa B inhibitor alpha (I-kappa B-α) were detected by Western blotting. A rat model of hyper-homocysteinemia was constructed. Thirty-six Wistar rats were randomly divided into 3 groups: the control group, the model group, and the Ad-hENDO-VEGI group. Serum Hcy levels in rats were measured with enzymatic cycling method. Endothelial vasodilation function was evaluated with the treatment of sodium nitroprusside and acetylcholine.
After Ad-hENDO-VEGI infection, high expressions (41 kD) of fusion proteins in ECV304 cells were observed. The injury severity of Hcy on ECV304 cells had a dose-dependent manner, and the injury reached a steady stage at 1.0 mmol/L. Thus, 1.0 mmol/L Hcy was selected for further experiments. With an increase of Ad-hENDO-VEGI in ECV304 cells after Hcy treatment, LDH leakage, MDA, TNF-α, MCP-1, and nuclear NF-kappa B p65 protein expression were gradually decreased, and cell survival rate, SOD activity, and I-kappa B-α protein expression were gradually increased. Compared with the control group, the model group had a higher Hcy level and attenuated vasodilator response. The Ad-hENDO-VEGI group exhibited a lower Hcy level and enhanced vasodilator response than the model group.
These results indicated that Ad-hENDO-VEGI could down-regulate NF-kappa B p65 expression and suppress inflammatory response, thereby alleviating Hcy-induced VECs injury.</description><identifier>ISSN: 0025-7974</identifier><identifier>EISSN: 1536-5964</identifier><identifier>DOI: 10.1097/MD.0000000000005197</identifier><identifier>PMID: 27858860</identifier><language>eng</language><publisher>United States: The Authors. Published by Wolters Kluwer Health, Inc. All rights reserved</publisher><subject>Adenoviridae ; Animals ; Cells, Cultured ; Chimera ; Clinical Trial/Experimental Study ; Endostatins ; Endothelial Cells - drug effects ; Endothelial Cells - virology ; Homocysteine - pharmacology ; Homocysteine - physiology ; Humans ; Male ; Rats ; Rats, Wistar ; Vascular Endothelial Growth Factors - antagonists & inhibitors</subject><ispartof>Medicine (Baltimore), 2016-11, Vol.95 (44), p.e5197-e5197</ispartof><rights>The Authors. Published by Wolters Kluwer Health, Inc. All rights reserved.</rights><rights>Copyright © 2016 the Author(s). Published by Wolters Kluwer Health, Inc. All rights reserved. 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4505-f0821f5b6e67fd331faee2a6593422302229ddeac2b5b79d662ab2046f50e2873</citedby><cites>FETCH-LOGICAL-c4505-f0821f5b6e67fd331faee2a6593422302229ddeac2b5b79d662ab2046f50e2873</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/PMC5591108/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5591108/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27858860$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cui, Zhen-Tian</creatorcontrib><creatorcontrib>Liu, Jian-Ping</creatorcontrib><creatorcontrib>Yao, Jian-Min</creatorcontrib><title>Antagonistic effects of endostatin-vascular endothelial growth inhibitor chimeric recombinant adenovirus on homocysteine-induced vascular endothelial cells injury in vitro and in vivo</title><title>Medicine (Baltimore)</title><addtitle>Medicine (Baltimore)</addtitle><description>The study is inclined to investigate the antagonistic effects of endostatin-vascular endothelial growth inhibitor chimeric recombinant adenovirus (Ad-hENDO-VEGI) on homocysteine (Hcy)-induced vascular endothelial cells (VECs) injury in vitro and in vivo.
Human VECs cell line ECV304 was selected and infected with Ad-hENDO-VEGI. The LDH leakage, SOD activity, and MDA levels were measured by the automatic biochemical analyzer. Cell survival rate was counted by Trypanblau dying. The TNF-α and MCP-1 protein expressions were detected by ELISA assay. The protein expressions of fusion protein of Ad-hENDO-VEGI, nuclear factor kappa B p65 (NF-kappa B p65), and NF-kappa B inhibitor alpha (I-kappa B-α) were detected by Western blotting. A rat model of hyper-homocysteinemia was constructed. Thirty-six Wistar rats were randomly divided into 3 groups: the control group, the model group, and the Ad-hENDO-VEGI group. Serum Hcy levels in rats were measured with enzymatic cycling method. Endothelial vasodilation function was evaluated with the treatment of sodium nitroprusside and acetylcholine.
After Ad-hENDO-VEGI infection, high expressions (41 kD) of fusion proteins in ECV304 cells were observed. The injury severity of Hcy on ECV304 cells had a dose-dependent manner, and the injury reached a steady stage at 1.0 mmol/L. Thus, 1.0 mmol/L Hcy was selected for further experiments. With an increase of Ad-hENDO-VEGI in ECV304 cells after Hcy treatment, LDH leakage, MDA, TNF-α, MCP-1, and nuclear NF-kappa B p65 protein expression were gradually decreased, and cell survival rate, SOD activity, and I-kappa B-α protein expression were gradually increased. Compared with the control group, the model group had a higher Hcy level and attenuated vasodilator response. The Ad-hENDO-VEGI group exhibited a lower Hcy level and enhanced vasodilator response than the model group.
These results indicated that Ad-hENDO-VEGI could down-regulate NF-kappa B p65 expression and suppress inflammatory response, thereby alleviating Hcy-induced VECs injury.</description><subject>Adenoviridae</subject><subject>Animals</subject><subject>Cells, Cultured</subject><subject>Chimera</subject><subject>Clinical Trial/Experimental Study</subject><subject>Endostatins</subject><subject>Endothelial Cells - drug effects</subject><subject>Endothelial Cells - virology</subject><subject>Homocysteine - pharmacology</subject><subject>Homocysteine - physiology</subject><subject>Humans</subject><subject>Male</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Vascular Endothelial Growth Factors - antagonists & inhibitors</subject><issn>0025-7974</issn><issn>1536-5964</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptks9u1DAQxiMEokvhCZCQj1xSbCe2kwtS1fJPasUFzpZjjzcujl1sJ6t9Ml6PbLdUBeHLyJ5vfjPWN1X1muAzgnvx7vryDD86jPTiSbUhrOE163n7tNpgTFktetGeVC9yvsGYNIK2z6sTKjrWdRxvql_noahtDC4XpxFYC7pkFC2CYGIuqrhQLyrr2at091ZG8E55tE1xV0bkwugGV2JCenQTpBWSQMdpcEGFgpSBEBeX5pUZ0BinqPe5gAtQu2BmDQb9l67B-7zCb-a0XwNaXEkRqWCOlyW-rJ5Z5TO8uo-n1fePH75dfK6vvn76cnF-VeuWYVZb3FFi2cCBC2uahlgFQBVnfdNS2mBKaW8MKE0HNojecE7VQHHLLcNAO9GcVu-P3Nt5mMBoCCUpL2-Tm1Tay6ic_DsT3Ci3cZGM9YTgbgW8vQek-HOGXOTk8uF7KkCcsyRdSzrcMo5XaXOU6hRzTmAf2hAsD5bL60v5r-Vr1ZvHEz7U_PF4FbRHwS76Ain_8PMOkhxB-TLe8ZjoaU0x4evEBNf4sDfNb6KDvZc</recordid><startdate>20161101</startdate><enddate>20161101</enddate><creator>Cui, Zhen-Tian</creator><creator>Liu, Jian-Ping</creator><creator>Yao, Jian-Min</creator><general>The Authors. Published by Wolters Kluwer Health, Inc. All rights reserved</general><general>Wolters Kluwer Health</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20161101</creationdate><title>Antagonistic effects of endostatin-vascular endothelial growth inhibitor chimeric recombinant adenovirus on homocysteine-induced vascular endothelial cells injury in vitro and in vivo</title><author>Cui, Zhen-Tian ; Liu, Jian-Ping ; Yao, Jian-Min</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4505-f0821f5b6e67fd331faee2a6593422302229ddeac2b5b79d662ab2046f50e2873</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adenoviridae</topic><topic>Animals</topic><topic>Cells, Cultured</topic><topic>Chimera</topic><topic>Clinical Trial/Experimental Study</topic><topic>Endostatins</topic><topic>Endothelial Cells - drug effects</topic><topic>Endothelial Cells - virology</topic><topic>Homocysteine - pharmacology</topic><topic>Homocysteine - physiology</topic><topic>Humans</topic><topic>Male</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Vascular Endothelial Growth Factors - antagonists & inhibitors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cui, Zhen-Tian</creatorcontrib><creatorcontrib>Liu, Jian-Ping</creatorcontrib><creatorcontrib>Yao, Jian-Min</creatorcontrib><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>Medicine (Baltimore)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cui, Zhen-Tian</au><au>Liu, Jian-Ping</au><au>Yao, Jian-Min</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Antagonistic effects of endostatin-vascular endothelial growth inhibitor chimeric recombinant adenovirus on homocysteine-induced vascular endothelial cells injury in vitro and in vivo</atitle><jtitle>Medicine (Baltimore)</jtitle><addtitle>Medicine (Baltimore)</addtitle><date>2016-11-01</date><risdate>2016</risdate><volume>95</volume><issue>44</issue><spage>e5197</spage><epage>e5197</epage><pages>e5197-e5197</pages><issn>0025-7974</issn><eissn>1536-5964</eissn><abstract>The study is inclined to investigate the antagonistic effects of endostatin-vascular endothelial growth inhibitor chimeric recombinant adenovirus (Ad-hENDO-VEGI) on homocysteine (Hcy)-induced vascular endothelial cells (VECs) injury in vitro and in vivo.
Human VECs cell line ECV304 was selected and infected with Ad-hENDO-VEGI. The LDH leakage, SOD activity, and MDA levels were measured by the automatic biochemical analyzer. Cell survival rate was counted by Trypanblau dying. The TNF-α and MCP-1 protein expressions were detected by ELISA assay. The protein expressions of fusion protein of Ad-hENDO-VEGI, nuclear factor kappa B p65 (NF-kappa B p65), and NF-kappa B inhibitor alpha (I-kappa B-α) were detected by Western blotting. A rat model of hyper-homocysteinemia was constructed. Thirty-six Wistar rats were randomly divided into 3 groups: the control group, the model group, and the Ad-hENDO-VEGI group. Serum Hcy levels in rats were measured with enzymatic cycling method. Endothelial vasodilation function was evaluated with the treatment of sodium nitroprusside and acetylcholine.
After Ad-hENDO-VEGI infection, high expressions (41 kD) of fusion proteins in ECV304 cells were observed. The injury severity of Hcy on ECV304 cells had a dose-dependent manner, and the injury reached a steady stage at 1.0 mmol/L. Thus, 1.0 mmol/L Hcy was selected for further experiments. With an increase of Ad-hENDO-VEGI in ECV304 cells after Hcy treatment, LDH leakage, MDA, TNF-α, MCP-1, and nuclear NF-kappa B p65 protein expression were gradually decreased, and cell survival rate, SOD activity, and I-kappa B-α protein expression were gradually increased. Compared with the control group, the model group had a higher Hcy level and attenuated vasodilator response. The Ad-hENDO-VEGI group exhibited a lower Hcy level and enhanced vasodilator response than the model group.
These results indicated that Ad-hENDO-VEGI could down-regulate NF-kappa B p65 expression and suppress inflammatory response, thereby alleviating Hcy-induced VECs injury.</abstract><cop>United States</cop><pub>The Authors. Published by Wolters Kluwer Health, Inc. All rights reserved</pub><pmid>27858860</pmid><doi>10.1097/MD.0000000000005197</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0025-7974 |
| ispartof | Medicine (Baltimore), 2016-11, Vol.95 (44), p.e5197-e5197 |
| issn | 0025-7974 1536-5964 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5591108 |
| source | Wolters Kluwer Open Health; MEDLINE; DOAJ Directory of Open Access Journals; IngentaConnect Free/Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Alma/SFX Local Collection |
| subjects | Adenoviridae Animals Cells, Cultured Chimera Clinical Trial/Experimental Study Endostatins Endothelial Cells - drug effects Endothelial Cells - virology Homocysteine - pharmacology Homocysteine - physiology Humans Male Rats Rats, Wistar Vascular Endothelial Growth Factors - antagonists & inhibitors |
| title | Antagonistic effects of endostatin-vascular endothelial growth inhibitor chimeric recombinant adenovirus on homocysteine-induced vascular endothelial cells injury in vitro and in vivo |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-27T16%3A19%3A37IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Antagonistic%20effects%20of%20endostatin-vascular%20endothelial%20growth%20inhibitor%20chimeric%20recombinant%20adenovirus%20on%20homocysteine-induced%20vascular%20endothelial%20cells%20injury%20in%20vitro%20and%20in%20vivo&rft.jtitle=Medicine%20(Baltimore)&rft.au=Cui,%20Zhen-Tian&rft.date=2016-11-01&rft.volume=95&rft.issue=44&rft.spage=e5197&rft.epage=e5197&rft.pages=e5197-e5197&rft.issn=0025-7974&rft.eissn=1536-5964&rft_id=info:doi/10.1097/MD.0000000000005197&rft_dat=%3Cproquest_pubme%3E1841804560%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1841804560&rft_id=info:pmid/27858860&rfr_iscdi=true |