Ang II induces capillary formation from endothelial cells via the AT1R-dependent inositol requiring enzyme 1 pathway
•Mechanisms of angiogenesis induced by Ang II are incompletely understood.•We found that IRE1 signaling mediate the angiogenic response induced by Ang II•AT1R-mediated the IRE1/JNK/p38 MAPK pathway involved in those process.•We reported a new mechanism for Ang II induced angiogenesis. Previous studi...
Gespeichert in:
| Veröffentlicht in: | Biochemical and biophysical research communications 2013-05, Vol.434 (3), p.552-558 |
|---|---|
| Hauptverfasser: | , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 558 |
|---|---|
| container_issue | 3 |
| container_start_page | 552 |
| container_title | Biochemical and biophysical research communications |
| container_volume | 434 |
| creator | Wang, Xiang Bai, Yong-Ping Hong, Dan Gao, Hai-Chao Li, Ling-Fang Li, Chuan-Chang Zhu, Ling-Ping Sun, Quan Zhang, Guo-Gang |
| description | •Mechanisms of angiogenesis induced by Ang II are incompletely understood.•We found that IRE1 signaling mediate the angiogenic response induced by Ang II•AT1R-mediated the IRE1/JNK/p38 MAPK pathway involved in those process.•We reported a new mechanism for Ang II induced angiogenesis.
Previous studies have demonstrated an important interaction between angiotension II type 1 receptor (AT1R) and angiotension II (Ang II) -induced capillary formation from endothelial cells and vascular endothelial growth factor (VEGF). However, the underlying mechanism remains elusive. Recent studies revealed that the unfolded protein response regulates an angiogenic response by the kidney epithelium during ischemic stress. Therefore, in the present study, we investigated the effects of Ang II on AT1R-mediated capillary formation from endothelial cells and the possible involvement of the IRE1/JNK/p38 MAPK pathway. Our results show that Ang II (1nmol/L) induced the expression of VEGF and enhanced capillary formation from endothelial cells in the Matrigel assay. This effect was significantly depressed by the AT1R blocker losartan and different inhibitors (irestatin, IRE1 specific inhibitor; SP600125, JNK specific inhibitor; SB203580, p38 MAPK specific inhibitor) but not by the AT2R blocker PD123319. Next, we investigated the effect of Ang II on the IRE1/JNK/p38 MAPK pathway and the 78kDA glucose regulated protein 78 (GRP78) activity in HUVECs and the role of the AT1 Receptor. The results show that Ang II activated both the IRE1/JNK/p38 MAPK pathway and GRP78 binding activity. These effects were markedly inhibited by the AT1R blocker losartan. The IRE1 specific inhibitor irestatin, the JNK specific inhibitor SP600125, and the p38 MAPK specific inhibitor SB203580 significantly inhibited Ang II-induced capillary formation from endothelial cells and VEGF expression but had no effect on GRP78. Collectively, these findings suggest for the first time that Ang II promotes capillary formation by inducing the expression of VEGF via Ang II type 1 receptor-mediated stimulation of the IRE1/JNK/p38 MAPK pathway. |
| doi_str_mv | 10.1016/j.bbrc.2013.03.113 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1350891793</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0006291X13005925</els_id><sourcerecordid>1350891793</sourcerecordid><originalsourceid>FETCH-LOGICAL-c426t-c8c230264ea65ff35fd7f93edd54a16b81a400dee7fa2f75102d010613e110e23</originalsourceid><addsrcrecordid>eNp9kEFrFDEUgIModlv9Ax4kRy8zvpfMzO6Al6VUXSgIUsFbyCYvNsvMZJpkWtZfb5atHj0FHt_7yPsYe4dQI2D38VDv99HUAlDWIGtE-YKtEHqoBELzkq0AoKtEjz8v2GVKBwDEputfswsh241sAFYsb6dffLfjfrKLocSNnv0w6HjkLsRRZx8m7mIYOU025HsavB64oWFI_NFrXiZ8e4ffK0tzIWjKxRSSz2HgkR4WH33x0_T7OBJHPut8_6SPb9grp4dEb5_fK_bj883d9dfq9tuX3fX2tjKN6HJlNkZIEF1Dumudk62za9dLsrZtNHb7DepygyVaOy3cukUQFhA6lIQIJOQV-3D2zjE8LJSyGn06fV5PFJakULaw6XHdy4KKM2piSCmSU3P0Y-mgENSptjqoU211qq1AqlK7LL1_9i_7key_lb95C_DpDFC58tFTVMl4mgxZH8lkZYP_n_8PeYqRUg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1350891793</pqid></control><display><type>article</type><title>Ang II induces capillary formation from endothelial cells via the AT1R-dependent inositol requiring enzyme 1 pathway</title><source>MEDLINE</source><source>ScienceDirect Journals (5 years ago - present)</source><creator>Wang, Xiang ; Bai, Yong-Ping ; Hong, Dan ; Gao, Hai-Chao ; Li, Ling-Fang ; Li, Chuan-Chang ; Zhu, Ling-Ping ; Sun, Quan ; Zhang, Guo-Gang</creator><creatorcontrib>Wang, Xiang ; Bai, Yong-Ping ; Hong, Dan ; Gao, Hai-Chao ; Li, Ling-Fang ; Li, Chuan-Chang ; Zhu, Ling-Ping ; Sun, Quan ; Zhang, Guo-Gang</creatorcontrib><description>•Mechanisms of angiogenesis induced by Ang II are incompletely understood.•We found that IRE1 signaling mediate the angiogenic response induced by Ang II•AT1R-mediated the IRE1/JNK/p38 MAPK pathway involved in those process.•We reported a new mechanism for Ang II induced angiogenesis.
Previous studies have demonstrated an important interaction between angiotension II type 1 receptor (AT1R) and angiotension II (Ang II) -induced capillary formation from endothelial cells and vascular endothelial growth factor (VEGF). However, the underlying mechanism remains elusive. Recent studies revealed that the unfolded protein response regulates an angiogenic response by the kidney epithelium during ischemic stress. Therefore, in the present study, we investigated the effects of Ang II on AT1R-mediated capillary formation from endothelial cells and the possible involvement of the IRE1/JNK/p38 MAPK pathway. Our results show that Ang II (1nmol/L) induced the expression of VEGF and enhanced capillary formation from endothelial cells in the Matrigel assay. This effect was significantly depressed by the AT1R blocker losartan and different inhibitors (irestatin, IRE1 specific inhibitor; SP600125, JNK specific inhibitor; SB203580, p38 MAPK specific inhibitor) but not by the AT2R blocker PD123319. Next, we investigated the effect of Ang II on the IRE1/JNK/p38 MAPK pathway and the 78kDA glucose regulated protein 78 (GRP78) activity in HUVECs and the role of the AT1 Receptor. The results show that Ang II activated both the IRE1/JNK/p38 MAPK pathway and GRP78 binding activity. These effects were markedly inhibited by the AT1R blocker losartan. The IRE1 specific inhibitor irestatin, the JNK specific inhibitor SP600125, and the p38 MAPK specific inhibitor SB203580 significantly inhibited Ang II-induced capillary formation from endothelial cells and VEGF expression but had no effect on GRP78. Collectively, these findings suggest for the first time that Ang II promotes capillary formation by inducing the expression of VEGF via Ang II type 1 receptor-mediated stimulation of the IRE1/JNK/p38 MAPK pathway.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2013.03.113</identifier><identifier>PMID: 23583400</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Angiogenesis ; Angiotensin II - pharmacology ; Angiotension II ; AT1 receptor ; Base Sequence ; Capillaries - drug effects ; Cells, Cultured ; DNA Primers ; Endoplasmic Reticulum - metabolism ; Endoribonucleases - metabolism ; Endothelium, Vascular - cytology ; Endothelium, Vascular - drug effects ; GRP78 ; Humans ; IRE1 ; MAP Kinase Signaling System ; MAPKs ; Protein-Serine-Threonine Kinases - metabolism ; Receptor, Angiotensin, Type 1 - metabolism ; Reverse Transcriptase Polymerase Chain Reaction</subject><ispartof>Biochemical and biophysical research communications, 2013-05, Vol.434 (3), p.552-558</ispartof><rights>2013</rights><rights>Crown Copyright © 2013. Published by Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c426t-c8c230264ea65ff35fd7f93edd54a16b81a400dee7fa2f75102d010613e110e23</citedby><cites>FETCH-LOGICAL-c426t-c8c230264ea65ff35fd7f93edd54a16b81a400dee7fa2f75102d010613e110e23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.bbrc.2013.03.113$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3549,27923,27924,45994</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23583400$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Xiang</creatorcontrib><creatorcontrib>Bai, Yong-Ping</creatorcontrib><creatorcontrib>Hong, Dan</creatorcontrib><creatorcontrib>Gao, Hai-Chao</creatorcontrib><creatorcontrib>Li, Ling-Fang</creatorcontrib><creatorcontrib>Li, Chuan-Chang</creatorcontrib><creatorcontrib>Zhu, Ling-Ping</creatorcontrib><creatorcontrib>Sun, Quan</creatorcontrib><creatorcontrib>Zhang, Guo-Gang</creatorcontrib><title>Ang II induces capillary formation from endothelial cells via the AT1R-dependent inositol requiring enzyme 1 pathway</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>•Mechanisms of angiogenesis induced by Ang II are incompletely understood.•We found that IRE1 signaling mediate the angiogenic response induced by Ang II•AT1R-mediated the IRE1/JNK/p38 MAPK pathway involved in those process.•We reported a new mechanism for Ang II induced angiogenesis.
Previous studies have demonstrated an important interaction between angiotension II type 1 receptor (AT1R) and angiotension II (Ang II) -induced capillary formation from endothelial cells and vascular endothelial growth factor (VEGF). However, the underlying mechanism remains elusive. Recent studies revealed that the unfolded protein response regulates an angiogenic response by the kidney epithelium during ischemic stress. Therefore, in the present study, we investigated the effects of Ang II on AT1R-mediated capillary formation from endothelial cells and the possible involvement of the IRE1/JNK/p38 MAPK pathway. Our results show that Ang II (1nmol/L) induced the expression of VEGF and enhanced capillary formation from endothelial cells in the Matrigel assay. This effect was significantly depressed by the AT1R blocker losartan and different inhibitors (irestatin, IRE1 specific inhibitor; SP600125, JNK specific inhibitor; SB203580, p38 MAPK specific inhibitor) but not by the AT2R blocker PD123319. Next, we investigated the effect of Ang II on the IRE1/JNK/p38 MAPK pathway and the 78kDA glucose regulated protein 78 (GRP78) activity in HUVECs and the role of the AT1 Receptor. The results show that Ang II activated both the IRE1/JNK/p38 MAPK pathway and GRP78 binding activity. These effects were markedly inhibited by the AT1R blocker losartan. The IRE1 specific inhibitor irestatin, the JNK specific inhibitor SP600125, and the p38 MAPK specific inhibitor SB203580 significantly inhibited Ang II-induced capillary formation from endothelial cells and VEGF expression but had no effect on GRP78. Collectively, these findings suggest for the first time that Ang II promotes capillary formation by inducing the expression of VEGF via Ang II type 1 receptor-mediated stimulation of the IRE1/JNK/p38 MAPK pathway.</description><subject>Angiogenesis</subject><subject>Angiotensin II - pharmacology</subject><subject>Angiotension II</subject><subject>AT1 receptor</subject><subject>Base Sequence</subject><subject>Capillaries - drug effects</subject><subject>Cells, Cultured</subject><subject>DNA Primers</subject><subject>Endoplasmic Reticulum - metabolism</subject><subject>Endoribonucleases - metabolism</subject><subject>Endothelium, Vascular - cytology</subject><subject>Endothelium, Vascular - drug effects</subject><subject>GRP78</subject><subject>Humans</subject><subject>IRE1</subject><subject>MAP Kinase Signaling System</subject><subject>MAPKs</subject><subject>Protein-Serine-Threonine Kinases - metabolism</subject><subject>Receptor, Angiotensin, Type 1 - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kEFrFDEUgIModlv9Ax4kRy8zvpfMzO6Al6VUXSgIUsFbyCYvNsvMZJpkWtZfb5atHj0FHt_7yPsYe4dQI2D38VDv99HUAlDWIGtE-YKtEHqoBELzkq0AoKtEjz8v2GVKBwDEputfswsh241sAFYsb6dffLfjfrKLocSNnv0w6HjkLsRRZx8m7mIYOU025HsavB64oWFI_NFrXiZ8e4ffK0tzIWjKxRSSz2HgkR4WH33x0_T7OBJHPut8_6SPb9grp4dEb5_fK_bj883d9dfq9tuX3fX2tjKN6HJlNkZIEF1Dumudk62za9dLsrZtNHb7DepygyVaOy3cukUQFhA6lIQIJOQV-3D2zjE8LJSyGn06fV5PFJakULaw6XHdy4KKM2piSCmSU3P0Y-mgENSptjqoU211qq1AqlK7LL1_9i_7key_lb95C_DpDFC58tFTVMl4mgxZH8lkZYP_n_8PeYqRUg</recordid><startdate>20130510</startdate><enddate>20130510</enddate><creator>Wang, Xiang</creator><creator>Bai, Yong-Ping</creator><creator>Hong, Dan</creator><creator>Gao, Hai-Chao</creator><creator>Li, Ling-Fang</creator><creator>Li, Chuan-Chang</creator><creator>Zhu, Ling-Ping</creator><creator>Sun, Quan</creator><creator>Zhang, Guo-Gang</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>7X8</scope></search><sort><creationdate>20130510</creationdate><title>Ang II induces capillary formation from endothelial cells via the AT1R-dependent inositol requiring enzyme 1 pathway</title><author>Wang, Xiang ; Bai, Yong-Ping ; Hong, Dan ; Gao, Hai-Chao ; Li, Ling-Fang ; Li, Chuan-Chang ; Zhu, Ling-Ping ; Sun, Quan ; Zhang, Guo-Gang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c426t-c8c230264ea65ff35fd7f93edd54a16b81a400dee7fa2f75102d010613e110e23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Angiogenesis</topic><topic>Angiotensin II - pharmacology</topic><topic>Angiotension II</topic><topic>AT1 receptor</topic><topic>Base Sequence</topic><topic>Capillaries - drug effects</topic><topic>Cells, Cultured</topic><topic>DNA Primers</topic><topic>Endoplasmic Reticulum - metabolism</topic><topic>Endoribonucleases - metabolism</topic><topic>Endothelium, Vascular - cytology</topic><topic>Endothelium, Vascular - drug effects</topic><topic>GRP78</topic><topic>Humans</topic><topic>IRE1</topic><topic>MAP Kinase Signaling System</topic><topic>MAPKs</topic><topic>Protein-Serine-Threonine Kinases - metabolism</topic><topic>Receptor, Angiotensin, Type 1 - metabolism</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Xiang</creatorcontrib><creatorcontrib>Bai, Yong-Ping</creatorcontrib><creatorcontrib>Hong, Dan</creatorcontrib><creatorcontrib>Gao, Hai-Chao</creatorcontrib><creatorcontrib>Li, Ling-Fang</creatorcontrib><creatorcontrib>Li, Chuan-Chang</creatorcontrib><creatorcontrib>Zhu, Ling-Ping</creatorcontrib><creatorcontrib>Sun, Quan</creatorcontrib><creatorcontrib>Zhang, Guo-Gang</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><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Xiang</au><au>Bai, Yong-Ping</au><au>Hong, Dan</au><au>Gao, Hai-Chao</au><au>Li, Ling-Fang</au><au>Li, Chuan-Chang</au><au>Zhu, Ling-Ping</au><au>Sun, Quan</au><au>Zhang, Guo-Gang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ang II induces capillary formation from endothelial cells via the AT1R-dependent inositol requiring enzyme 1 pathway</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2013-05-10</date><risdate>2013</risdate><volume>434</volume><issue>3</issue><spage>552</spage><epage>558</epage><pages>552-558</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>•Mechanisms of angiogenesis induced by Ang II are incompletely understood.•We found that IRE1 signaling mediate the angiogenic response induced by Ang II•AT1R-mediated the IRE1/JNK/p38 MAPK pathway involved in those process.•We reported a new mechanism for Ang II induced angiogenesis.
Previous studies have demonstrated an important interaction between angiotension II type 1 receptor (AT1R) and angiotension II (Ang II) -induced capillary formation from endothelial cells and vascular endothelial growth factor (VEGF). However, the underlying mechanism remains elusive. Recent studies revealed that the unfolded protein response regulates an angiogenic response by the kidney epithelium during ischemic stress. Therefore, in the present study, we investigated the effects of Ang II on AT1R-mediated capillary formation from endothelial cells and the possible involvement of the IRE1/JNK/p38 MAPK pathway. Our results show that Ang II (1nmol/L) induced the expression of VEGF and enhanced capillary formation from endothelial cells in the Matrigel assay. This effect was significantly depressed by the AT1R blocker losartan and different inhibitors (irestatin, IRE1 specific inhibitor; SP600125, JNK specific inhibitor; SB203580, p38 MAPK specific inhibitor) but not by the AT2R blocker PD123319. Next, we investigated the effect of Ang II on the IRE1/JNK/p38 MAPK pathway and the 78kDA glucose regulated protein 78 (GRP78) activity in HUVECs and the role of the AT1 Receptor. The results show that Ang II activated both the IRE1/JNK/p38 MAPK pathway and GRP78 binding activity. These effects were markedly inhibited by the AT1R blocker losartan. The IRE1 specific inhibitor irestatin, the JNK specific inhibitor SP600125, and the p38 MAPK specific inhibitor SB203580 significantly inhibited Ang II-induced capillary formation from endothelial cells and VEGF expression but had no effect on GRP78. Collectively, these findings suggest for the first time that Ang II promotes capillary formation by inducing the expression of VEGF via Ang II type 1 receptor-mediated stimulation of the IRE1/JNK/p38 MAPK pathway.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>23583400</pmid><doi>10.1016/j.bbrc.2013.03.113</doi><tpages>7</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0006-291X |
| ispartof | Biochemical and biophysical research communications, 2013-05, Vol.434 (3), p.552-558 |
| issn | 0006-291X 1090-2104 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1350891793 |
| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Angiogenesis Angiotensin II - pharmacology Angiotension II AT1 receptor Base Sequence Capillaries - drug effects Cells, Cultured DNA Primers Endoplasmic Reticulum - metabolism Endoribonucleases - metabolism Endothelium, Vascular - cytology Endothelium, Vascular - drug effects GRP78 Humans IRE1 MAP Kinase Signaling System MAPKs Protein-Serine-Threonine Kinases - metabolism Receptor, Angiotensin, Type 1 - metabolism Reverse Transcriptase Polymerase Chain Reaction |
| title | Ang II induces capillary formation from endothelial cells via the AT1R-dependent inositol requiring enzyme 1 pathway |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-08T16%3A03%3A14IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Ang%20II%20induces%20capillary%20formation%20from%20endothelial%20cells%20via%20the%20AT1R-dependent%20inositol%20requiring%20enzyme%201%20pathway&rft.jtitle=Biochemical%20and%20biophysical%20research%20communications&rft.au=Wang,%20Xiang&rft.date=2013-05-10&rft.volume=434&rft.issue=3&rft.spage=552&rft.epage=558&rft.pages=552-558&rft.issn=0006-291X&rft.eissn=1090-2104&rft_id=info:doi/10.1016/j.bbrc.2013.03.113&rft_dat=%3Cproquest_cross%3E1350891793%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1350891793&rft_id=info:pmid/23583400&rft_els_id=S0006291X13005925&rfr_iscdi=true |