The dipeptidyl peptidase-IV inhibitor inhibits the expression of vascular adhesion molecules and inflammatory cytokines in HUVECs via Akt- and AMPK-dependent mechanisms
DC Field | Value | Language |
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dc.contributor.author | Hwang, Hwan-Jin | - |
dc.contributor.author | Chung, Hye Soo | - |
dc.contributor.author | Jung, Tae Woo | - |
dc.contributor.author | Ryu, Ja Young | - |
dc.contributor.author | Hong, Ho Cheol | - |
dc.contributor.author | Seo, Ji A. | - |
dc.contributor.author | Kim, Sin Gon | - |
dc.contributor.author | Kim, Nan Hee | - |
dc.contributor.author | Choi, Kyung Mook | - |
dc.contributor.author | Choi, Dong Seop | - |
dc.contributor.author | Baik, Sei Hyun | - |
dc.contributor.author | Yoo, Hye Jin | - |
dc.date.accessioned | 2021-09-04T17:13:19Z | - |
dc.date.available | 2021-09-04T17:13:19Z | - |
dc.date.created | 2021-06-18 | - |
dc.date.issued | 2015-04-15 | - |
dc.identifier.issn | 0303-7207 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/93835 | - |
dc.description.abstract | Recently, dipeptidyl peptidase-IV (DPP-IV) inhibitor, a major anti-hyperglycemic agent, has received substantial attention as a possible therapeutic target for inflammatory diseases such as atherosclerosis. However, the direct molecular mechanisms through which DPP-IV inhibitor mediates anti-inflammatory effects in vascular endothelial cells have not been clarified. The effects of the DPP-IV inhibitor, gemigliptin, were analyzed in human umbilical vein endothelial cells (HUVECs) and THP-1 cells. Using Western blotting, we demonstrated that gemigliptin efficiently increased the level of AMP-activated protein kinase (AMPK) and Akt phosphorylation in a dose-dependent manner. The levels of lipopolysaccharide (LPS)-mediated phosphorylated nuclear factor-kappa B (NF-kappa B) and c-Jun N-terminal kinase (INK) were significantly decreased after gemigliptin treatment. Furthermore, gemigliptin reduced LPS-induced expression of adhesion molecules and inflammatory cytokines such as vascular cell adhesion molecule-1 (VCAM-1), E-selectin, tumor necrosis factor-alpha (TNF-alpha), monocyte chemoattractant protein-1 (MCP-1), interleukin-1 beta (IL-1 beta), and IL-6 in HUVECs. In macrophage-like THP-1 cells, gemigliptin effectively inhibited LPS- and low-density lipoprotein (LDL)-induced foam cell formation. However, these anti-inflammatory and antiatherosclerotic effects of gemigliptin in HUVECs and ITIP-1 cells were significantly reduced after treatment with an AMPK or an Akt inhibitor. Our results suggest that gemigliptin efficiently inhibited LPS-induced pro-inflammatory effects in vascular endothelial cells by attenuating NF-kappa B and JNK signaling via Akt/AMPK-dependent mechanisms. Therefore, the DPP-IV inhibitor, gemigliptin, may directly protect the vascular endothelium against inflammatory diseases such as atherosclerosis. (C) 2015 Elsevier Ireland Ltd. All rights reserved. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | ELSEVIER IRELAND LTD | - |
dc.subject | ACTIVATED PROTEIN-KINASE | - |
dc.subject | VEIN ENDOTHELIAL-CELLS | - |
dc.subject | ATHEROSCLEROTIC LESION | - |
dc.subject | INSULIN-RESISTANCE | - |
dc.subject | SITAGLIPTIN | - |
dc.subject | SYSTEM | - |
dc.subject | PHOSPHORYLATION | - |
dc.subject | RECRUITMENT | - |
dc.subject | DYSFUNCTION | - |
dc.subject | APOPTOSIS | - |
dc.title | The dipeptidyl peptidase-IV inhibitor inhibits the expression of vascular adhesion molecules and inflammatory cytokines in HUVECs via Akt- and AMPK-dependent mechanisms | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Seo, Ji A. | - |
dc.contributor.affiliatedAuthor | Kim, Sin Gon | - |
dc.contributor.affiliatedAuthor | Kim, Nan Hee | - |
dc.contributor.affiliatedAuthor | Choi, Kyung Mook | - |
dc.contributor.affiliatedAuthor | Choi, Dong Seop | - |
dc.contributor.affiliatedAuthor | Baik, Sei Hyun | - |
dc.contributor.affiliatedAuthor | Yoo, Hye Jin | - |
dc.identifier.doi | 10.1016/j.mce.2015.01.025 | - |
dc.identifier.scopusid | 2-s2.0-84923034778 | - |
dc.identifier.wosid | 000352330300003 | - |
dc.identifier.bibliographicCitation | MOLECULAR AND CELLULAR ENDOCRINOLOGY, v.405, no.C, pp.25 - 34 | - |
dc.relation.isPartOf | MOLECULAR AND CELLULAR ENDOCRINOLOGY | - |
dc.citation.title | MOLECULAR AND CELLULAR ENDOCRINOLOGY | - |
dc.citation.volume | 405 | - |
dc.citation.number | C | - |
dc.citation.startPage | 25 | - |
dc.citation.endPage | 34 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalResearchArea | Endocrinology & Metabolism | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Endocrinology & Metabolism | - |
dc.subject.keywordPlus | ACTIVATED PROTEIN-KINASE | - |
dc.subject.keywordPlus | VEIN ENDOTHELIAL-CELLS | - |
dc.subject.keywordPlus | ATHEROSCLEROTIC LESION | - |
dc.subject.keywordPlus | INSULIN-RESISTANCE | - |
dc.subject.keywordPlus | SITAGLIPTIN | - |
dc.subject.keywordPlus | SYSTEM | - |
dc.subject.keywordPlus | PHOSPHORYLATION | - |
dc.subject.keywordPlus | RECRUITMENT | - |
dc.subject.keywordPlus | DYSFUNCTION | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordAuthor | Dipeptidyl peptidase-IV inhibitors | - |
dc.subject.keywordAuthor | AMP-activated protein kinase | - |
dc.subject.keywordAuthor | Inflammation | - |
dc.subject.keywordAuthor | Endothelial cells | - |
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