Comparison of PPARδ and PPARγ in inhibiting the pro-inflammatory effects of C-reactive protein in endothelial cells

Yao Jen Liang, Yuan Chun Liu, Chao Yi Chen, Ling Ping Lai, Kou Gi Shyu, Shiow Jen Juang, Bao Wei Wang, Jyh Gang Leu

研究成果: 雜誌貢獻文章

17 引文 (Scopus)

摘要

Background: Inflammation associated with endothelial cell dysfunction is a key step of atherogenesis. C-reactive protein (CRP), used to serve as a nonspecific clinical inflammation marker, has now emerged as a new marker for cardiovascular diseases. Recently, PPARδ has revealed benefits for dealing with inflammation. The relationship between CRP-induced inflammation and PPARδ agonist remains unclear. Methods: Human umbilical vein endothelial cells (HUVECs) were separated into the following groups: 25 μg CRP alone for 15 hours; CRP-treated with 1 μM PPARδ(L-165041) or 10 μM PPARγ(troglitazone) agonists, and untreated HUVECs. This research focused on the CRP underlying signaling pathways and the effects of PPAR agonists on monocyte attachment to endothelial cells. Results: Levels of interleukin-6 (IL-6) and IL-8 increased by CRP were both significantly attenuated by pretreatment with PPARδ or PPARγ agonists, but the needed dose of PPARδ to reach the same effect was less than PPARγ agonist. After incubation with CRP, immunoblotting showed a significant increase in NF-κB activation and CD32 receptor. These changes were associated with a significant increase of MCP-1 and VCAM-1 expression. PPARδ treatment not only decreased these pro-inflammatory effects in HUVECs but also significantly attenuated monocyte adhesion to endothelial cells in less dosage than PPARγ. Conclusions: The results suggest that PPARδ attenuated CRP-induced pro-inflammatory effects may through CD32 and NF-κB pathway. PPARδ may serve as a more potent therapeutic target than PPARγ in atherosclerosis or inflammatory therapy. Crown
原文英語
頁(從 - 到)361-367
頁數7
期刊International Journal of Cardiology
143
發行號3
DOIs
出版狀態已發佈 - 九月 3 2010

指紋

Peroxisome Proliferator-Activated Receptors
C-Reactive Protein
Endothelial Cells
Human Umbilical Vein Endothelial Cells
Inflammation
troglitazone
4-(3-(2-propyl-3-hydroxy-4-acetyl)phenoxy)propyloxyphenoxy acetic acid
Monocytes
Atherosclerosis
Vascular Cell Adhesion Molecule-1
Crowns
Interleukin-8
Immunoblotting

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

引用此文

Comparison of PPARδ and PPARγ in inhibiting the pro-inflammatory effects of C-reactive protein in endothelial cells. / Liang, Yao Jen; Liu, Yuan Chun; Chen, Chao Yi; Lai, Ling Ping; Shyu, Kou Gi; Juang, Shiow Jen; Wang, Bao Wei; Leu, Jyh Gang.

於: International Journal of Cardiology, 卷 143, 編號 3, 03.09.2010, p. 361-367.

研究成果: 雜誌貢獻文章

Liang, Yao Jen ; Liu, Yuan Chun ; Chen, Chao Yi ; Lai, Ling Ping ; Shyu, Kou Gi ; Juang, Shiow Jen ; Wang, Bao Wei ; Leu, Jyh Gang. / Comparison of PPARδ and PPARγ in inhibiting the pro-inflammatory effects of C-reactive protein in endothelial cells. 於: International Journal of Cardiology. 2010 ; 卷 143, 編號 3. 頁 361-367.
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AU - Liang, Yao Jen

AU - Liu, Yuan Chun

AU - Chen, Chao Yi

AU - Lai, Ling Ping

AU - Shyu, Kou Gi

AU - Juang, Shiow Jen

AU - Wang, Bao Wei

AU - Leu, Jyh Gang

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N2 - Background: Inflammation associated with endothelial cell dysfunction is a key step of atherogenesis. C-reactive protein (CRP), used to serve as a nonspecific clinical inflammation marker, has now emerged as a new marker for cardiovascular diseases. Recently, PPARδ has revealed benefits for dealing with inflammation. The relationship between CRP-induced inflammation and PPARδ agonist remains unclear. Methods: Human umbilical vein endothelial cells (HUVECs) were separated into the following groups: 25 μg CRP alone for 15 hours; CRP-treated with 1 μM PPARδ(L-165041) or 10 μM PPARγ(troglitazone) agonists, and untreated HUVECs. This research focused on the CRP underlying signaling pathways and the effects of PPAR agonists on monocyte attachment to endothelial cells. Results: Levels of interleukin-6 (IL-6) and IL-8 increased by CRP were both significantly attenuated by pretreatment with PPARδ or PPARγ agonists, but the needed dose of PPARδ to reach the same effect was less than PPARγ agonist. After incubation with CRP, immunoblotting showed a significant increase in NF-κB activation and CD32 receptor. These changes were associated with a significant increase of MCP-1 and VCAM-1 expression. PPARδ treatment not only decreased these pro-inflammatory effects in HUVECs but also significantly attenuated monocyte adhesion to endothelial cells in less dosage than PPARγ. Conclusions: The results suggest that PPARδ attenuated CRP-induced pro-inflammatory effects may through CD32 and NF-κB pathway. PPARδ may serve as a more potent therapeutic target than PPARγ in atherosclerosis or inflammatory therapy. Crown

AB - Background: Inflammation associated with endothelial cell dysfunction is a key step of atherogenesis. C-reactive protein (CRP), used to serve as a nonspecific clinical inflammation marker, has now emerged as a new marker for cardiovascular diseases. Recently, PPARδ has revealed benefits for dealing with inflammation. The relationship between CRP-induced inflammation and PPARδ agonist remains unclear. Methods: Human umbilical vein endothelial cells (HUVECs) were separated into the following groups: 25 μg CRP alone for 15 hours; CRP-treated with 1 μM PPARδ(L-165041) or 10 μM PPARγ(troglitazone) agonists, and untreated HUVECs. This research focused on the CRP underlying signaling pathways and the effects of PPAR agonists on monocyte attachment to endothelial cells. Results: Levels of interleukin-6 (IL-6) and IL-8 increased by CRP were both significantly attenuated by pretreatment with PPARδ or PPARγ agonists, but the needed dose of PPARδ to reach the same effect was less than PPARγ agonist. After incubation with CRP, immunoblotting showed a significant increase in NF-κB activation and CD32 receptor. These changes were associated with a significant increase of MCP-1 and VCAM-1 expression. PPARδ treatment not only decreased these pro-inflammatory effects in HUVECs but also significantly attenuated monocyte adhesion to endothelial cells in less dosage than PPARγ. Conclusions: The results suggest that PPARδ attenuated CRP-induced pro-inflammatory effects may through CD32 and NF-κB pathway. PPARδ may serve as a more potent therapeutic target than PPARγ in atherosclerosis or inflammatory therapy. Crown

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