Telmisartan inhibits expression of a receptor for advanced glycation end products (RAGE) in angiotensin-II-exposed endothelial cells and decreases serum levels of soluble RAGE in patients with essential hypertension
There is a growing body of evidence that the advanced glycation end product (AGE)–their receptor (RAGE) system plays a central role in the pathogenesis of diabetic vascular complication. The renin–angiotensin system (RAS) contributes to the development and progression of diabetic angiopathy as well....
Gespeichert in:
| Veröffentlicht in: | Microvascular research 2005-11, Vol.70 (3), p.137-141 |
|---|---|
| Hauptverfasser: | , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 141 |
|---|---|
| container_issue | 3 |
| container_start_page | 137 |
| container_title | Microvascular research |
| container_volume | 70 |
| creator | Nakamura, Kazuo Yamagishi, Sho-ichi Nakamura, Yayoi Takenaka, Katsuhiko Matsui, Takanori Jinnouchi, Yuko Imaizumi, Tsutomu |
| description | There is a growing body of evidence that the advanced glycation end product (AGE)–their receptor (RAGE) system plays a central role in the pathogenesis of diabetic vascular complication. The renin–angiotensin system (RAS) contributes to the development and progression of diabetic angiopathy as well. However, the cross-talk between the AGE–RAGE system and the RAS is not fully understood. In this study, we examined the role of angiotensin II (Ang II) type 1 receptor system for RAGE expression in cultured endothelial cells (ECs) and in patients with essential hypertension. Ang II up-regulated RAGE mRNA levels of microvascular ECs and subsequently increased the soluble form of RAGE (sRAGE) expression in the medium of ECs, both of which were completely blocked by telmisartan, a commercially available Ang II type 1 receptor antagonist. Furthermore, telmisartan was found to decrease serum levels of sRAGE in patients with essential hypertension. These results demonstrate that sRAGE is released from the cell surface of Ang-II-exposed ECs. Our present study indicates that a cross-talk exists between the AGE–RAGE system and the RAS and suggests that serum levels of sRAGE may reflect endothelial RAGE expression. |
| doi_str_mv | 10.1016/j.mvr.2005.10.002 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_68768142</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0026286205000877</els_id><sourcerecordid>68768142</sourcerecordid><originalsourceid>FETCH-LOGICAL-c351t-8870cd4339b93132ce18d37c17885332e6cef808c7382652e6fea4fd6452f96a3</originalsourceid><addsrcrecordid>eNp9UU1vEzEQtRCIhsIP4IJ8QnDY4I_srlecqqotkSohoXJeOfZs48ixF9ubkl_av8MsicSNg2XN-M17nvcIec_ZkjPefNkt94e0FIzVWC8ZEy_IgrOurjrJu5dkgZ2mEqoRF-RNzjvGOK878Zpc8Ea0vJPdgjw_gN-7rFPRgbqwdRtXMoXfY4KcXQw0DlTTBAbGEhMd8Gh70MGApY_-aHSZQRAsHVO0k8HhTz-u7m4-IxnV4dHFAiG7UK3XFbLGjHOIjmUL3mlPDXifEWipBZNAZ8g0Q5r21MMB8An1c_TTxgOdeWfaEUUhoNKTK1uK_8Ri5toeR0h_5WJ4S14N2md4d74vyc_bm4frb9X997v19dV9ZWTNS6VUy4xdSdlt0DMpDHBlZWt4q1QtpYDGwKCYMq1UoqmxHkCvBtusajF0jZaX5OOJF9f_NUEuPbo5L6UDxCn3jWobxVcCgfwENCnmnGDox-T2Oh17zvo5zX7XY5r9nObcwuxw5sOZfNrswf6bOMeHgK8nADoFBwepzwatwXAcRlZ6G91_6P8A36-1DA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>68768142</pqid></control><display><type>article</type><title>Telmisartan inhibits expression of a receptor for advanced glycation end products (RAGE) in angiotensin-II-exposed endothelial cells and decreases serum levels of soluble RAGE in patients with essential hypertension</title><source>MEDLINE</source><source>ScienceDirect Journals (5 years ago - present)</source><creator>Nakamura, Kazuo ; Yamagishi, Sho-ichi ; Nakamura, Yayoi ; Takenaka, Katsuhiko ; Matsui, Takanori ; Jinnouchi, Yuko ; Imaizumi, Tsutomu</creator><creatorcontrib>Nakamura, Kazuo ; Yamagishi, Sho-ichi ; Nakamura, Yayoi ; Takenaka, Katsuhiko ; Matsui, Takanori ; Jinnouchi, Yuko ; Imaizumi, Tsutomu</creatorcontrib><description>There is a growing body of evidence that the advanced glycation end product (AGE)–their receptor (RAGE) system plays a central role in the pathogenesis of diabetic vascular complication. The renin–angiotensin system (RAS) contributes to the development and progression of diabetic angiopathy as well. However, the cross-talk between the AGE–RAGE system and the RAS is not fully understood. In this study, we examined the role of angiotensin II (Ang II) type 1 receptor system for RAGE expression in cultured endothelial cells (ECs) and in patients with essential hypertension. Ang II up-regulated RAGE mRNA levels of microvascular ECs and subsequently increased the soluble form of RAGE (sRAGE) expression in the medium of ECs, both of which were completely blocked by telmisartan, a commercially available Ang II type 1 receptor antagonist. Furthermore, telmisartan was found to decrease serum levels of sRAGE in patients with essential hypertension. These results demonstrate that sRAGE is released from the cell surface of Ang-II-exposed ECs. Our present study indicates that a cross-talk exists between the AGE–RAGE system and the RAS and suggests that serum levels of sRAGE may reflect endothelial RAGE expression.</description><identifier>ISSN: 0026-2862</identifier><identifier>EISSN: 1095-9319</identifier><identifier>DOI: 10.1016/j.mvr.2005.10.002</identifier><identifier>PMID: 16271939</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Administration, Oral ; Age Factors ; Aged ; AGEs ; Ang II type 1 receptor antagonist ; Angiotensin II - metabolism ; Angiotensin II Type 1 Receptor Blockers - pharmacology ; Antioxidants - metabolism ; Benzimidazoles - pharmacology ; Benzoates - pharmacology ; Blotting, Western ; Coronary Artery Disease - blood ; Coronary Artery Disease - metabolism ; Diabetic vascular complication ; Disease Progression ; DNA Primers - chemistry ; Endothelial Cells - cytology ; Endothelium, Vascular - metabolism ; Female ; Humans ; Hypertension ; Male ; Microcirculation ; Middle Aged ; Oxidative Stress ; RAGE ; RAS ; Receptor for Advanced Glycation End Products ; Receptors, Immunologic - blood ; Receptors, Immunologic - metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - metabolism ; Time Factors ; Up-Regulation</subject><ispartof>Microvascular research, 2005-11, Vol.70 (3), p.137-141</ispartof><rights>2005 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c351t-8870cd4339b93132ce18d37c17885332e6cef808c7382652e6fea4fd6452f96a3</citedby><cites>FETCH-LOGICAL-c351t-8870cd4339b93132ce18d37c17885332e6cef808c7382652e6fea4fd6452f96a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.mvr.2005.10.002$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,781,785,3551,27929,27930,46000</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16271939$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nakamura, Kazuo</creatorcontrib><creatorcontrib>Yamagishi, Sho-ichi</creatorcontrib><creatorcontrib>Nakamura, Yayoi</creatorcontrib><creatorcontrib>Takenaka, Katsuhiko</creatorcontrib><creatorcontrib>Matsui, Takanori</creatorcontrib><creatorcontrib>Jinnouchi, Yuko</creatorcontrib><creatorcontrib>Imaizumi, Tsutomu</creatorcontrib><title>Telmisartan inhibits expression of a receptor for advanced glycation end products (RAGE) in angiotensin-II-exposed endothelial cells and decreases serum levels of soluble RAGE in patients with essential hypertension</title><title>Microvascular research</title><addtitle>Microvasc Res</addtitle><description>There is a growing body of evidence that the advanced glycation end product (AGE)–their receptor (RAGE) system plays a central role in the pathogenesis of diabetic vascular complication. The renin–angiotensin system (RAS) contributes to the development and progression of diabetic angiopathy as well. However, the cross-talk between the AGE–RAGE system and the RAS is not fully understood. In this study, we examined the role of angiotensin II (Ang II) type 1 receptor system for RAGE expression in cultured endothelial cells (ECs) and in patients with essential hypertension. Ang II up-regulated RAGE mRNA levels of microvascular ECs and subsequently increased the soluble form of RAGE (sRAGE) expression in the medium of ECs, both of which were completely blocked by telmisartan, a commercially available Ang II type 1 receptor antagonist. Furthermore, telmisartan was found to decrease serum levels of sRAGE in patients with essential hypertension. These results demonstrate that sRAGE is released from the cell surface of Ang-II-exposed ECs. Our present study indicates that a cross-talk exists between the AGE–RAGE system and the RAS and suggests that serum levels of sRAGE may reflect endothelial RAGE expression.</description><subject>Administration, Oral</subject><subject>Age Factors</subject><subject>Aged</subject><subject>AGEs</subject><subject>Ang II type 1 receptor antagonist</subject><subject>Angiotensin II - metabolism</subject><subject>Angiotensin II Type 1 Receptor Blockers - pharmacology</subject><subject>Antioxidants - metabolism</subject><subject>Benzimidazoles - pharmacology</subject><subject>Benzoates - pharmacology</subject><subject>Blotting, Western</subject><subject>Coronary Artery Disease - blood</subject><subject>Coronary Artery Disease - metabolism</subject><subject>Diabetic vascular complication</subject><subject>Disease Progression</subject><subject>DNA Primers - chemistry</subject><subject>Endothelial Cells - cytology</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Female</subject><subject>Humans</subject><subject>Hypertension</subject><subject>Male</subject><subject>Microcirculation</subject><subject>Middle Aged</subject><subject>Oxidative Stress</subject><subject>RAGE</subject><subject>RAS</subject><subject>Receptor for Advanced Glycation End Products</subject><subject>Receptors, Immunologic - blood</subject><subject>Receptors, Immunologic - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - metabolism</subject><subject>Time Factors</subject><subject>Up-Regulation</subject><issn>0026-2862</issn><issn>1095-9319</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9UU1vEzEQtRCIhsIP4IJ8QnDY4I_srlecqqotkSohoXJeOfZs48ixF9ubkl_av8MsicSNg2XN-M17nvcIec_ZkjPefNkt94e0FIzVWC8ZEy_IgrOurjrJu5dkgZ2mEqoRF-RNzjvGOK878Zpc8Ea0vJPdgjw_gN-7rFPRgbqwdRtXMoXfY4KcXQw0DlTTBAbGEhMd8Gh70MGApY_-aHSZQRAsHVO0k8HhTz-u7m4-IxnV4dHFAiG7UK3XFbLGjHOIjmUL3mlPDXifEWipBZNAZ8g0Q5r21MMB8An1c_TTxgOdeWfaEUUhoNKTK1uK_8Ri5toeR0h_5WJ4S14N2md4d74vyc_bm4frb9X997v19dV9ZWTNS6VUy4xdSdlt0DMpDHBlZWt4q1QtpYDGwKCYMq1UoqmxHkCvBtusajF0jZaX5OOJF9f_NUEuPbo5L6UDxCn3jWobxVcCgfwENCnmnGDox-T2Oh17zvo5zX7XY5r9nObcwuxw5sOZfNrswf6bOMeHgK8nADoFBwepzwatwXAcRlZ6G91_6P8A36-1DA</recordid><startdate>20051101</startdate><enddate>20051101</enddate><creator>Nakamura, Kazuo</creator><creator>Yamagishi, Sho-ichi</creator><creator>Nakamura, Yayoi</creator><creator>Takenaka, Katsuhiko</creator><creator>Matsui, Takanori</creator><creator>Jinnouchi, Yuko</creator><creator>Imaizumi, Tsutomu</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>20051101</creationdate><title>Telmisartan inhibits expression of a receptor for advanced glycation end products (RAGE) in angiotensin-II-exposed endothelial cells and decreases serum levels of soluble RAGE in patients with essential hypertension</title><author>Nakamura, Kazuo ; Yamagishi, Sho-ichi ; Nakamura, Yayoi ; Takenaka, Katsuhiko ; Matsui, Takanori ; Jinnouchi, Yuko ; Imaizumi, Tsutomu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c351t-8870cd4339b93132ce18d37c17885332e6cef808c7382652e6fea4fd6452f96a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Administration, Oral</topic><topic>Age Factors</topic><topic>Aged</topic><topic>AGEs</topic><topic>Ang II type 1 receptor antagonist</topic><topic>Angiotensin II - metabolism</topic><topic>Angiotensin II Type 1 Receptor Blockers - pharmacology</topic><topic>Antioxidants - metabolism</topic><topic>Benzimidazoles - pharmacology</topic><topic>Benzoates - pharmacology</topic><topic>Blotting, Western</topic><topic>Coronary Artery Disease - blood</topic><topic>Coronary Artery Disease - metabolism</topic><topic>Diabetic vascular complication</topic><topic>Disease Progression</topic><topic>DNA Primers - chemistry</topic><topic>Endothelial Cells - cytology</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Female</topic><topic>Humans</topic><topic>Hypertension</topic><topic>Male</topic><topic>Microcirculation</topic><topic>Middle Aged</topic><topic>Oxidative Stress</topic><topic>RAGE</topic><topic>RAS</topic><topic>Receptor for Advanced Glycation End Products</topic><topic>Receptors, Immunologic - blood</topic><topic>Receptors, Immunologic - metabolism</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - metabolism</topic><topic>Time Factors</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nakamura, Kazuo</creatorcontrib><creatorcontrib>Yamagishi, Sho-ichi</creatorcontrib><creatorcontrib>Nakamura, Yayoi</creatorcontrib><creatorcontrib>Takenaka, Katsuhiko</creatorcontrib><creatorcontrib>Matsui, Takanori</creatorcontrib><creatorcontrib>Jinnouchi, Yuko</creatorcontrib><creatorcontrib>Imaizumi, Tsutomu</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>Microvascular research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nakamura, Kazuo</au><au>Yamagishi, Sho-ichi</au><au>Nakamura, Yayoi</au><au>Takenaka, Katsuhiko</au><au>Matsui, Takanori</au><au>Jinnouchi, Yuko</au><au>Imaizumi, Tsutomu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Telmisartan inhibits expression of a receptor for advanced glycation end products (RAGE) in angiotensin-II-exposed endothelial cells and decreases serum levels of soluble RAGE in patients with essential hypertension</atitle><jtitle>Microvascular research</jtitle><addtitle>Microvasc Res</addtitle><date>2005-11-01</date><risdate>2005</risdate><volume>70</volume><issue>3</issue><spage>137</spage><epage>141</epage><pages>137-141</pages><issn>0026-2862</issn><eissn>1095-9319</eissn><abstract>There is a growing body of evidence that the advanced glycation end product (AGE)–their receptor (RAGE) system plays a central role in the pathogenesis of diabetic vascular complication. The renin–angiotensin system (RAS) contributes to the development and progression of diabetic angiopathy as well. However, the cross-talk between the AGE–RAGE system and the RAS is not fully understood. In this study, we examined the role of angiotensin II (Ang II) type 1 receptor system for RAGE expression in cultured endothelial cells (ECs) and in patients with essential hypertension. Ang II up-regulated RAGE mRNA levels of microvascular ECs and subsequently increased the soluble form of RAGE (sRAGE) expression in the medium of ECs, both of which were completely blocked by telmisartan, a commercially available Ang II type 1 receptor antagonist. Furthermore, telmisartan was found to decrease serum levels of sRAGE in patients with essential hypertension. These results demonstrate that sRAGE is released from the cell surface of Ang-II-exposed ECs. Our present study indicates that a cross-talk exists between the AGE–RAGE system and the RAS and suggests that serum levels of sRAGE may reflect endothelial RAGE expression.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>16271939</pmid><doi>10.1016/j.mvr.2005.10.002</doi><tpages>5</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0026-2862 |
| ispartof | Microvascular research, 2005-11, Vol.70 (3), p.137-141 |
| issn | 0026-2862 1095-9319 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_68768142 |
| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Administration, Oral Age Factors Aged AGEs Ang II type 1 receptor antagonist Angiotensin II - metabolism Angiotensin II Type 1 Receptor Blockers - pharmacology Antioxidants - metabolism Benzimidazoles - pharmacology Benzoates - pharmacology Blotting, Western Coronary Artery Disease - blood Coronary Artery Disease - metabolism Diabetic vascular complication Disease Progression DNA Primers - chemistry Endothelial Cells - cytology Endothelium, Vascular - metabolism Female Humans Hypertension Male Microcirculation Middle Aged Oxidative Stress RAGE RAS Receptor for Advanced Glycation End Products Receptors, Immunologic - blood Receptors, Immunologic - metabolism Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - metabolism Time Factors Up-Regulation |
| title | Telmisartan inhibits expression of a receptor for advanced glycation end products (RAGE) in angiotensin-II-exposed endothelial cells and decreases serum levels of soluble RAGE in patients with essential hypertension |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-15T18%3A52%3A56IST&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=Telmisartan%20inhibits%20expression%20of%20a%20receptor%20for%20advanced%20glycation%20end%20products%20(RAGE)%20in%20angiotensin-II-exposed%20endothelial%20cells%20and%20decreases%20serum%20levels%20of%20soluble%20RAGE%20in%20patients%20with%20essential%20hypertension&rft.jtitle=Microvascular%20research&rft.au=Nakamura,%20Kazuo&rft.date=2005-11-01&rft.volume=70&rft.issue=3&rft.spage=137&rft.epage=141&rft.pages=137-141&rft.issn=0026-2862&rft.eissn=1095-9319&rft_id=info:doi/10.1016/j.mvr.2005.10.002&rft_dat=%3Cproquest_cross%3E68768142%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=68768142&rft_id=info:pmid/16271939&rft_els_id=S0026286205000877&rfr_iscdi=true |