The glucagon-like peptide 1 receptor agonist enhances intrinsic peroxisome proliferator-activated receptor γ activity in endothelial cells
•PPARγ activation was involved in the GLP-1-mediated anti-inflammatory action.•Exendin-4 enhanced endogenous PPARγ transcriptional activity in HUVECs.•H89, a PKA inhibitor, abolished GLP-1-induced PPARγ enhancement.•The anti-inflammatory effects of GLP-1 may be explained by PPARγ activation. Recent...
Gespeichert in:
| Veröffentlicht in: | Biochemical and biophysical research communications 2014-08, Vol.451 (2), p.339-344 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 344 |
|---|---|
| container_issue | 2 |
| container_start_page | 339 |
| container_title | Biochemical and biophysical research communications |
| container_volume | 451 |
| creator | Onuma, Hirohisa Inukai, Kouichi Kitahara, Atsuko Moriya, Rie Nishida, Susumu Tanaka, Toshiaki Katsuta, Hidenori Takahashi, Kazuto Sumitani, Yoshikazu Hosaka, Toshio Ishida, Hitoshi |
| description | •PPARγ activation was involved in the GLP-1-mediated anti-inflammatory action.•Exendin-4 enhanced endogenous PPARγ transcriptional activity in HUVECs.•H89, a PKA inhibitor, abolished GLP-1-induced PPARγ enhancement.•The anti-inflammatory effects of GLP-1 may be explained by PPARγ activation.
Recent studies have suggested glucagon-like peptide-1 (GLP-1) signaling to exert anti-inflammatory effects on endothelial cells, although the precise underlying mechanism remains to be elucidated. In the present study, we investigated whether PPARγ activation is involved in the GLP-1-mediated anti-inflammatory action on endothelial cells. When we treated HUVEC cells with 0.2ng/ml exendin-4, a GLP-1 receptor agonist, endogenous PPARγ transcriptional activity was significantly elevated, by approximately 20%, as compared with control cells. The maximum PPARγ activity enhancing effect of exendin-4 was observed 12h after the initiation of incubation with exendin-4. As H89, a PKA inhibitor, abolished GLP-1-induced PPARγ enhancement, the signaling downstream from GLP-1 cross-talk must have been involved in PPARγ activation. In conclusion, our results suggest that GLP-1 has the potential to induce PPARγ activity, partially explaining the anti-inflammatory effects of GLP-1 on endothelial cells. Cross-talk between GLP-1 signaling and PPARγ activation would have major impacts on treatments for patients at high risk for cardiovascular disease. |
| doi_str_mv | 10.1016/j.bbrc.2014.07.136 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_osti_</sourceid><recordid>TN_cdi_osti_scitechconnect_22416722</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0006291X14013990</els_id><sourcerecordid>1557083516</sourcerecordid><originalsourceid>FETCH-LOGICAL-c454t-d2f8fce735f7bae1d4386da4cc22038afae2167e9a40e98a1980f6e993fc095c3</originalsourceid><addsrcrecordid>eNp9kU1uFDEQhS1ERIbABVggS2zYdKfsdv9JbFAEASkSmyCxszzlcsZDT3uwPRE5A8fhHpwpbibAjpUt-3tPr-ox9kJALUB059t6vY5YSxCqhr4WTfeIrQSMUEkB6jFbAUBXyVF8OWVPU9oCCKG68Qk7lW3BBmhX7Mf1hvjNdEBzE-Zq8l-J72mfvSUueCQs9xD58ulT5jRvzIyUuJ9z9HPyWOgYvvsUdkUYw-QdRVMklcHsb00m-8_l10_--9Xnu2JQzGzIG5q8mTjSNKVn7MSZKdHzh_OMfX7_7vriQ3X16fLjxdurClWrcmWlGxxS37SuXxsSVjVDZ41ClBKawThDUnQ9jUYBjYMRZVLX0Tg2DmFssTljr46-IWWvE_pMuMEwz4RZS6mKWMpCvT5SZaxvB0pZ73xacpqZwiFp0bY9DE0ruoLKI4oxpBTJ6X30OxPvtAC9VKW3eqlKL1Vp6HWpqohePvgf1juyfyV_uinAmyNAZRe3nuISlcr6rY9LUhv8__zvAUFfqQg</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1557083516</pqid></control><display><type>article</type><title>The glucagon-like peptide 1 receptor agonist enhances intrinsic peroxisome proliferator-activated receptor γ activity in endothelial cells</title><source>MEDLINE</source><source>Access via ScienceDirect (Elsevier)</source><creator>Onuma, Hirohisa ; Inukai, Kouichi ; Kitahara, Atsuko ; Moriya, Rie ; Nishida, Susumu ; Tanaka, Toshiaki ; Katsuta, Hidenori ; Takahashi, Kazuto ; Sumitani, Yoshikazu ; Hosaka, Toshio ; Ishida, Hitoshi</creator><creatorcontrib>Onuma, Hirohisa ; Inukai, Kouichi ; Kitahara, Atsuko ; Moriya, Rie ; Nishida, Susumu ; Tanaka, Toshiaki ; Katsuta, Hidenori ; Takahashi, Kazuto ; Sumitani, Yoshikazu ; Hosaka, Toshio ; Ishida, Hitoshi</creatorcontrib><description>•PPARγ activation was involved in the GLP-1-mediated anti-inflammatory action.•Exendin-4 enhanced endogenous PPARγ transcriptional activity in HUVECs.•H89, a PKA inhibitor, abolished GLP-1-induced PPARγ enhancement.•The anti-inflammatory effects of GLP-1 may be explained by PPARγ activation.
Recent studies have suggested glucagon-like peptide-1 (GLP-1) signaling to exert anti-inflammatory effects on endothelial cells, although the precise underlying mechanism remains to be elucidated. In the present study, we investigated whether PPARγ activation is involved in the GLP-1-mediated anti-inflammatory action on endothelial cells. When we treated HUVEC cells with 0.2ng/ml exendin-4, a GLP-1 receptor agonist, endogenous PPARγ transcriptional activity was significantly elevated, by approximately 20%, as compared with control cells. The maximum PPARγ activity enhancing effect of exendin-4 was observed 12h after the initiation of incubation with exendin-4. As H89, a PKA inhibitor, abolished GLP-1-induced PPARγ enhancement, the signaling downstream from GLP-1 cross-talk must have been involved in PPARγ activation. In conclusion, our results suggest that GLP-1 has the potential to induce PPARγ activity, partially explaining the anti-inflammatory effects of GLP-1 on endothelial cells. Cross-talk between GLP-1 signaling and PPARγ activation would have major impacts on treatments for patients at high risk for cardiovascular disease.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2014.07.136</identifier><identifier>PMID: 25109805</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>60 APPLIED LIFE SCIENCES ; ADHESION ; Anilides - pharmacology ; CARDIOVASCULAR DISEASES ; Colforsin - pharmacology ; COMPARATIVE EVALUATIONS ; Cyclic AMP-Dependent Protein Kinases - antagonists & inhibitors ; Cyclic AMP-Dependent Protein Kinases - metabolism ; Endothelial Cells - drug effects ; Endothelial Cells - metabolism ; Gene Expression - drug effects ; GLP-1 ; GLUCAGON ; Glucagon-Like Peptide-1 Receptor ; HOMEOSTASIS ; HUMAN POPULATIONS ; Human Umbilical Vein Endothelial Cells ; Humans ; HUVEC ; INCUBATION ; INFLAMMATION ; INSULIN ; Intercellular Adhesion Molecule-1 - genetics ; Intercellular Adhesion Molecule-1 - metabolism ; Isoquinolines - pharmacology ; MOLECULES ; NADP ; NADPH Oxidase 1 ; NADPH Oxidases - genetics ; NADPH Oxidases - metabolism ; NF-kappa B - metabolism ; OXIDASES ; PATIENTS ; Peptides - pharmacology ; PHOSPHATES ; Phosphorylation ; PLASMINOGEN ; PPAR gamma - antagonists & inhibitors ; PPAR gamma - metabolism ; PPARγ ; Protein Kinase Inhibitors - pharmacology ; Receptor Cross-Talk ; RECEPTORS ; Receptors, Glucagon - agonists ; Signal Transduction - drug effects ; SUBSTRATES ; Sulfonamides - pharmacology ; Thiazolidinediones - pharmacology ; Vascular Cell Adhesion Molecule-1 - genetics ; Vascular Cell Adhesion Molecule-1 - metabolism ; VEINS ; Venoms - pharmacology</subject><ispartof>Biochemical and biophysical research communications, 2014-08, Vol.451 (2), p.339-344</ispartof><rights>2014</rights><rights>Copyright © 2014. Published by Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c454t-d2f8fce735f7bae1d4386da4cc22038afae2167e9a40e98a1980f6e993fc095c3</citedby><cites>FETCH-LOGICAL-c454t-d2f8fce735f7bae1d4386da4cc22038afae2167e9a40e98a1980f6e993fc095c3</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.2014.07.136$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,780,784,885,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25109805$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://www.osti.gov/biblio/22416722$$D View this record in Osti.gov$$Hfree_for_read</backlink></links><search><creatorcontrib>Onuma, Hirohisa</creatorcontrib><creatorcontrib>Inukai, Kouichi</creatorcontrib><creatorcontrib>Kitahara, Atsuko</creatorcontrib><creatorcontrib>Moriya, Rie</creatorcontrib><creatorcontrib>Nishida, Susumu</creatorcontrib><creatorcontrib>Tanaka, Toshiaki</creatorcontrib><creatorcontrib>Katsuta, Hidenori</creatorcontrib><creatorcontrib>Takahashi, Kazuto</creatorcontrib><creatorcontrib>Sumitani, Yoshikazu</creatorcontrib><creatorcontrib>Hosaka, Toshio</creatorcontrib><creatorcontrib>Ishida, Hitoshi</creatorcontrib><title>The glucagon-like peptide 1 receptor agonist enhances intrinsic peroxisome proliferator-activated receptor γ activity in endothelial cells</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>•PPARγ activation was involved in the GLP-1-mediated anti-inflammatory action.•Exendin-4 enhanced endogenous PPARγ transcriptional activity in HUVECs.•H89, a PKA inhibitor, abolished GLP-1-induced PPARγ enhancement.•The anti-inflammatory effects of GLP-1 may be explained by PPARγ activation.
Recent studies have suggested glucagon-like peptide-1 (GLP-1) signaling to exert anti-inflammatory effects on endothelial cells, although the precise underlying mechanism remains to be elucidated. In the present study, we investigated whether PPARγ activation is involved in the GLP-1-mediated anti-inflammatory action on endothelial cells. When we treated HUVEC cells with 0.2ng/ml exendin-4, a GLP-1 receptor agonist, endogenous PPARγ transcriptional activity was significantly elevated, by approximately 20%, as compared with control cells. The maximum PPARγ activity enhancing effect of exendin-4 was observed 12h after the initiation of incubation with exendin-4. As H89, a PKA inhibitor, abolished GLP-1-induced PPARγ enhancement, the signaling downstream from GLP-1 cross-talk must have been involved in PPARγ activation. In conclusion, our results suggest that GLP-1 has the potential to induce PPARγ activity, partially explaining the anti-inflammatory effects of GLP-1 on endothelial cells. Cross-talk between GLP-1 signaling and PPARγ activation would have major impacts on treatments for patients at high risk for cardiovascular disease.</description><subject>60 APPLIED LIFE SCIENCES</subject><subject>ADHESION</subject><subject>Anilides - pharmacology</subject><subject>CARDIOVASCULAR DISEASES</subject><subject>Colforsin - pharmacology</subject><subject>COMPARATIVE EVALUATIONS</subject><subject>Cyclic AMP-Dependent Protein Kinases - antagonists & inhibitors</subject><subject>Cyclic AMP-Dependent Protein Kinases - metabolism</subject><subject>Endothelial Cells - drug effects</subject><subject>Endothelial Cells - metabolism</subject><subject>Gene Expression - drug effects</subject><subject>GLP-1</subject><subject>GLUCAGON</subject><subject>Glucagon-Like Peptide-1 Receptor</subject><subject>HOMEOSTASIS</subject><subject>HUMAN POPULATIONS</subject><subject>Human Umbilical Vein Endothelial Cells</subject><subject>Humans</subject><subject>HUVEC</subject><subject>INCUBATION</subject><subject>INFLAMMATION</subject><subject>INSULIN</subject><subject>Intercellular Adhesion Molecule-1 - genetics</subject><subject>Intercellular Adhesion Molecule-1 - metabolism</subject><subject>Isoquinolines - pharmacology</subject><subject>MOLECULES</subject><subject>NADP</subject><subject>NADPH Oxidase 1</subject><subject>NADPH Oxidases - genetics</subject><subject>NADPH Oxidases - metabolism</subject><subject>NF-kappa B - metabolism</subject><subject>OXIDASES</subject><subject>PATIENTS</subject><subject>Peptides - pharmacology</subject><subject>PHOSPHATES</subject><subject>Phosphorylation</subject><subject>PLASMINOGEN</subject><subject>PPAR gamma - antagonists & inhibitors</subject><subject>PPAR gamma - metabolism</subject><subject>PPARγ</subject><subject>Protein Kinase Inhibitors - pharmacology</subject><subject>Receptor Cross-Talk</subject><subject>RECEPTORS</subject><subject>Receptors, Glucagon - agonists</subject><subject>Signal Transduction - drug effects</subject><subject>SUBSTRATES</subject><subject>Sulfonamides - pharmacology</subject><subject>Thiazolidinediones - pharmacology</subject><subject>Vascular Cell Adhesion Molecule-1 - genetics</subject><subject>Vascular Cell Adhesion Molecule-1 - metabolism</subject><subject>VEINS</subject><subject>Venoms - pharmacology</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU1uFDEQhS1ERIbABVggS2zYdKfsdv9JbFAEASkSmyCxszzlcsZDT3uwPRE5A8fhHpwpbibAjpUt-3tPr-ox9kJALUB059t6vY5YSxCqhr4WTfeIrQSMUEkB6jFbAUBXyVF8OWVPU9oCCKG68Qk7lW3BBmhX7Mf1hvjNdEBzE-Zq8l-J72mfvSUueCQs9xD58ulT5jRvzIyUuJ9z9HPyWOgYvvsUdkUYw-QdRVMklcHsb00m-8_l10_--9Xnu2JQzGzIG5q8mTjSNKVn7MSZKdHzh_OMfX7_7vriQ3X16fLjxdurClWrcmWlGxxS37SuXxsSVjVDZ41ClBKawThDUnQ9jUYBjYMRZVLX0Tg2DmFssTljr46-IWWvE_pMuMEwz4RZS6mKWMpCvT5SZaxvB0pZ73xacpqZwiFp0bY9DE0ruoLKI4oxpBTJ6X30OxPvtAC9VKW3eqlKL1Vp6HWpqohePvgf1juyfyV_uinAmyNAZRe3nuISlcr6rY9LUhv8__zvAUFfqQg</recordid><startdate>20140822</startdate><enddate>20140822</enddate><creator>Onuma, Hirohisa</creator><creator>Inukai, Kouichi</creator><creator>Kitahara, Atsuko</creator><creator>Moriya, Rie</creator><creator>Nishida, Susumu</creator><creator>Tanaka, Toshiaki</creator><creator>Katsuta, Hidenori</creator><creator>Takahashi, Kazuto</creator><creator>Sumitani, Yoshikazu</creator><creator>Hosaka, Toshio</creator><creator>Ishida, Hitoshi</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><scope>OTOTI</scope></search><sort><creationdate>20140822</creationdate><title>The glucagon-like peptide 1 receptor agonist enhances intrinsic peroxisome proliferator-activated receptor γ activity in endothelial cells</title><author>Onuma, Hirohisa ; Inukai, Kouichi ; Kitahara, Atsuko ; Moriya, Rie ; Nishida, Susumu ; Tanaka, Toshiaki ; Katsuta, Hidenori ; Takahashi, Kazuto ; Sumitani, Yoshikazu ; Hosaka, Toshio ; Ishida, Hitoshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c454t-d2f8fce735f7bae1d4386da4cc22038afae2167e9a40e98a1980f6e993fc095c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>60 APPLIED LIFE SCIENCES</topic><topic>ADHESION</topic><topic>Anilides - pharmacology</topic><topic>CARDIOVASCULAR DISEASES</topic><topic>Colforsin - pharmacology</topic><topic>COMPARATIVE EVALUATIONS</topic><topic>Cyclic AMP-Dependent Protein Kinases - antagonists & inhibitors</topic><topic>Cyclic AMP-Dependent Protein Kinases - metabolism</topic><topic>Endothelial Cells - drug effects</topic><topic>Endothelial Cells - metabolism</topic><topic>Gene Expression - drug effects</topic><topic>GLP-1</topic><topic>GLUCAGON</topic><topic>Glucagon-Like Peptide-1 Receptor</topic><topic>HOMEOSTASIS</topic><topic>HUMAN POPULATIONS</topic><topic>Human Umbilical Vein Endothelial Cells</topic><topic>Humans</topic><topic>HUVEC</topic><topic>INCUBATION</topic><topic>INFLAMMATION</topic><topic>INSULIN</topic><topic>Intercellular Adhesion Molecule-1 - genetics</topic><topic>Intercellular Adhesion Molecule-1 - metabolism</topic><topic>Isoquinolines - pharmacology</topic><topic>MOLECULES</topic><topic>NADP</topic><topic>NADPH Oxidase 1</topic><topic>NADPH Oxidases - genetics</topic><topic>NADPH Oxidases - metabolism</topic><topic>NF-kappa B - metabolism</topic><topic>OXIDASES</topic><topic>PATIENTS</topic><topic>Peptides - pharmacology</topic><topic>PHOSPHATES</topic><topic>Phosphorylation</topic><topic>PLASMINOGEN</topic><topic>PPAR gamma - antagonists & inhibitors</topic><topic>PPAR gamma - metabolism</topic><topic>PPARγ</topic><topic>Protein Kinase Inhibitors - pharmacology</topic><topic>Receptor Cross-Talk</topic><topic>RECEPTORS</topic><topic>Receptors, Glucagon - agonists</topic><topic>Signal Transduction - drug effects</topic><topic>SUBSTRATES</topic><topic>Sulfonamides - pharmacology</topic><topic>Thiazolidinediones - pharmacology</topic><topic>Vascular Cell Adhesion Molecule-1 - genetics</topic><topic>Vascular Cell Adhesion Molecule-1 - metabolism</topic><topic>VEINS</topic><topic>Venoms - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Onuma, Hirohisa</creatorcontrib><creatorcontrib>Inukai, Kouichi</creatorcontrib><creatorcontrib>Kitahara, Atsuko</creatorcontrib><creatorcontrib>Moriya, Rie</creatorcontrib><creatorcontrib>Nishida, Susumu</creatorcontrib><creatorcontrib>Tanaka, Toshiaki</creatorcontrib><creatorcontrib>Katsuta, Hidenori</creatorcontrib><creatorcontrib>Takahashi, Kazuto</creatorcontrib><creatorcontrib>Sumitani, Yoshikazu</creatorcontrib><creatorcontrib>Hosaka, Toshio</creatorcontrib><creatorcontrib>Ishida, Hitoshi</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>OSTI.GOV</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Onuma, Hirohisa</au><au>Inukai, Kouichi</au><au>Kitahara, Atsuko</au><au>Moriya, Rie</au><au>Nishida, Susumu</au><au>Tanaka, Toshiaki</au><au>Katsuta, Hidenori</au><au>Takahashi, Kazuto</au><au>Sumitani, Yoshikazu</au><au>Hosaka, Toshio</au><au>Ishida, Hitoshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The glucagon-like peptide 1 receptor agonist enhances intrinsic peroxisome proliferator-activated receptor γ activity in endothelial cells</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2014-08-22</date><risdate>2014</risdate><volume>451</volume><issue>2</issue><spage>339</spage><epage>344</epage><pages>339-344</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>•PPARγ activation was involved in the GLP-1-mediated anti-inflammatory action.•Exendin-4 enhanced endogenous PPARγ transcriptional activity in HUVECs.•H89, a PKA inhibitor, abolished GLP-1-induced PPARγ enhancement.•The anti-inflammatory effects of GLP-1 may be explained by PPARγ activation.
Recent studies have suggested glucagon-like peptide-1 (GLP-1) signaling to exert anti-inflammatory effects on endothelial cells, although the precise underlying mechanism remains to be elucidated. In the present study, we investigated whether PPARγ activation is involved in the GLP-1-mediated anti-inflammatory action on endothelial cells. When we treated HUVEC cells with 0.2ng/ml exendin-4, a GLP-1 receptor agonist, endogenous PPARγ transcriptional activity was significantly elevated, by approximately 20%, as compared with control cells. The maximum PPARγ activity enhancing effect of exendin-4 was observed 12h after the initiation of incubation with exendin-4. As H89, a PKA inhibitor, abolished GLP-1-induced PPARγ enhancement, the signaling downstream from GLP-1 cross-talk must have been involved in PPARγ activation. In conclusion, our results suggest that GLP-1 has the potential to induce PPARγ activity, partially explaining the anti-inflammatory effects of GLP-1 on endothelial cells. Cross-talk between GLP-1 signaling and PPARγ activation would have major impacts on treatments for patients at high risk for cardiovascular disease.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>25109805</pmid><doi>10.1016/j.bbrc.2014.07.136</doi><tpages>6</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0006-291X |
| ispartof | Biochemical and biophysical research communications, 2014-08, Vol.451 (2), p.339-344 |
| issn | 0006-291X 1090-2104 |
| language | eng |
| recordid | cdi_osti_scitechconnect_22416722 |
| source | MEDLINE; Access via ScienceDirect (Elsevier) |
| subjects | 60 APPLIED LIFE SCIENCES ADHESION Anilides - pharmacology CARDIOVASCULAR DISEASES Colforsin - pharmacology COMPARATIVE EVALUATIONS Cyclic AMP-Dependent Protein Kinases - antagonists & inhibitors Cyclic AMP-Dependent Protein Kinases - metabolism Endothelial Cells - drug effects Endothelial Cells - metabolism Gene Expression - drug effects GLP-1 GLUCAGON Glucagon-Like Peptide-1 Receptor HOMEOSTASIS HUMAN POPULATIONS Human Umbilical Vein Endothelial Cells Humans HUVEC INCUBATION INFLAMMATION INSULIN Intercellular Adhesion Molecule-1 - genetics Intercellular Adhesion Molecule-1 - metabolism Isoquinolines - pharmacology MOLECULES NADP NADPH Oxidase 1 NADPH Oxidases - genetics NADPH Oxidases - metabolism NF-kappa B - metabolism OXIDASES PATIENTS Peptides - pharmacology PHOSPHATES Phosphorylation PLASMINOGEN PPAR gamma - antagonists & inhibitors PPAR gamma - metabolism PPARγ Protein Kinase Inhibitors - pharmacology Receptor Cross-Talk RECEPTORS Receptors, Glucagon - agonists Signal Transduction - drug effects SUBSTRATES Sulfonamides - pharmacology Thiazolidinediones - pharmacology Vascular Cell Adhesion Molecule-1 - genetics Vascular Cell Adhesion Molecule-1 - metabolism VEINS Venoms - pharmacology |
| title | The glucagon-like peptide 1 receptor agonist enhances intrinsic peroxisome proliferator-activated receptor γ activity in endothelial cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-21T10%3A24%3A48IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_osti_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=The%20glucagon-like%20peptide%201%20receptor%20agonist%20enhances%20intrinsic%20peroxisome%20proliferator-activated%20receptor%20%CE%B3%20activity%20in%20endothelial%20cells&rft.jtitle=Biochemical%20and%20biophysical%20research%20communications&rft.au=Onuma,%20Hirohisa&rft.date=2014-08-22&rft.volume=451&rft.issue=2&rft.spage=339&rft.epage=344&rft.pages=339-344&rft.issn=0006-291X&rft.eissn=1090-2104&rft_id=info:doi/10.1016/j.bbrc.2014.07.136&rft_dat=%3Cproquest_osti_%3E1557083516%3C/proquest_osti_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1557083516&rft_id=info:pmid/25109805&rft_els_id=S0006291X14013990&rfr_iscdi=true |