PPARα activation abolishes LDL-stimulated IL-8 production via AP-1 deactivation in human aortic smooth muscle cells

Sungwoo Ryoo; Misun Won; Dong Uk Kim; Lila Kim; Gyoonhee Han; Seung Kiel Park; Naofumi Mukaida; Piljae Maeng; Hyang Sook Yoo; Kwang Lae Hoe

doi:10.1016/j.bbrc.2004.04.031

PPARα activation abolishes LDL-stimulated IL-8 production via AP-1 deactivation in human aortic smooth muscle cells

Sungwoo Ryoo, Misun Won, Dong Uk Kim, Lila Kim, Gyoonhee Han, Seung Kiel Park, Naofumi Mukaida, Piljae Maeng, Hyang Sook Yoo, Kwang Lae Hoe

Research output: Contribution to journal › Article › peer-review

14 Citations (Scopus)

Abstract

Native low density lipoprotein (n-LDL) is a major risk factor for cardiovascular diseases by inducing inflammatory processes and vascular smooth muscle cell proliferation in vessel cells. It has previously been reported that LDL enhances inflammatory reactions by the up-regulation of interleukin (IL)-8 via the activation of p38 kinase and activator protein (AP)-1 in human aortic smooth muscle cells (hAoSMCs). The findings of this study show, for the first time, that the peroxisome proliferator-activated receptor (PPARα) agonist, fenofibrate, completely abolishes the LDL-induced IL-8 up-regulation at the transcriptional level. Pretreatment of hAoSMCs with fenofibrate abolishes the effects of LDL on AP-1 activation without affecting nuclear factor (NF)-κB. In contrast, fenofibrate failed to modulate the activation state of p38 and JNK kinases or the levels of c-fos and phospho-Jun. These data suggest that AP-1 is likely to be located at the crossroads between LDL signaling and the regulation of IL-8 modulation by PPARα.

Original language	English
Pages (from-to)	329-334
Number of pages	6
Journal	Biochemical and Biophysical Research Communications
Volume	318
Issue number	2
DOIs	https://doi.org/10.1016/j.bbrc.2004.04.031
Publication status	Published - 2004 May 28

Bibliographical note

Funding Information:
This work was supported by the Molecular and Cellular BioDiscovery Research Program and 21st Century Frontier R&D Program from the Ministry of Science and Technology of Korea and by Korea Research Institute of Bioscience and Biotechnology. We thank Professor S.-W. Kwon at the Asan Medical Center for his help in the preparation of LDL.

All Science Journal Classification (ASJC) codes

Biophysics
Biochemistry
Molecular Biology
Cell Biology

UN SDGs

This output contributes to the following Sustainable Development Goal(s)

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Ryoo, Sungwoo ; Won, Misun ; Kim, Dong Uk ; Kim, Lila ; Han, Gyoonhee ; Park, Seung Kiel ; Mukaida, Naofumi ; Maeng, Piljae ; Yoo, Hyang Sook ; Hoe, Kwang Lae. / PPARα activation abolishes LDL-stimulated IL-8 production via AP-1 deactivation in human aortic smooth muscle cells. In: Biochemical and Biophysical Research Communications. 2004 ; Vol. 318, No. 2. pp. 329-334.

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title = "PPARα activation abolishes LDL-stimulated IL-8 production via AP-1 deactivation in human aortic smooth muscle cells",

abstract = "Native low density lipoprotein (n-LDL) is a major risk factor for cardiovascular diseases by inducing inflammatory processes and vascular smooth muscle cell proliferation in vessel cells. It has previously been reported that LDL enhances inflammatory reactions by the up-regulation of interleukin (IL)-8 via the activation of p38 kinase and activator protein (AP)-1 in human aortic smooth muscle cells (hAoSMCs). The findings of this study show, for the first time, that the peroxisome proliferator-activated receptor (PPARα) agonist, fenofibrate, completely abolishes the LDL-induced IL-8 up-regulation at the transcriptional level. Pretreatment of hAoSMCs with fenofibrate abolishes the effects of LDL on AP-1 activation without affecting nuclear factor (NF)-κB. In contrast, fenofibrate failed to modulate the activation state of p38 and JNK kinases or the levels of c-fos and phospho-Jun. These data suggest that AP-1 is likely to be located at the crossroads between LDL signaling and the regulation of IL-8 modulation by PPARα.",

author = "Sungwoo Ryoo and Misun Won and Kim, {Dong Uk} and Lila Kim and Gyoonhee Han and Park, {Seung Kiel} and Naofumi Mukaida and Piljae Maeng and Yoo, {Hyang Sook} and Hoe, {Kwang Lae}",

note = "Funding Information: This work was supported by the Molecular and Cellular BioDiscovery Research Program and 21st Century Frontier R&D Program from the Ministry of Science and Technology of Korea and by Korea Research Institute of Bioscience and Biotechnology. We thank Professor S.-W. Kwon at the Asan Medical Center for his help in the preparation of LDL.",

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PPARα activation abolishes LDL-stimulated IL-8 production via AP-1 deactivation in human aortic smooth muscle cells. / Ryoo, Sungwoo; Won, Misun; Kim, Dong Uk; Kim, Lila; Han, Gyoonhee; Park, Seung Kiel; Mukaida, Naofumi; Maeng, Piljae; Yoo, Hyang Sook; Hoe, Kwang Lae.

In: Biochemical and Biophysical Research Communications, Vol. 318, No. 2, 28.05.2004, p. 329-334.

Research output: Contribution to journal › Article › peer-review

TY - JOUR

T1 - PPARα activation abolishes LDL-stimulated IL-8 production via AP-1 deactivation in human aortic smooth muscle cells

AU - Ryoo, Sungwoo

AU - Won, Misun

AU - Kim, Dong Uk

AU - Kim, Lila

AU - Han, Gyoonhee

AU - Park, Seung Kiel

AU - Mukaida, Naofumi

AU - Maeng, Piljae

AU - Yoo, Hyang Sook

AU - Hoe, Kwang Lae

N1 - Funding Information: This work was supported by the Molecular and Cellular BioDiscovery Research Program and 21st Century Frontier R&D Program from the Ministry of Science and Technology of Korea and by Korea Research Institute of Bioscience and Biotechnology. We thank Professor S.-W. Kwon at the Asan Medical Center for his help in the preparation of LDL.

PY - 2004/5/28

Y1 - 2004/5/28

N2 - Native low density lipoprotein (n-LDL) is a major risk factor for cardiovascular diseases by inducing inflammatory processes and vascular smooth muscle cell proliferation in vessel cells. It has previously been reported that LDL enhances inflammatory reactions by the up-regulation of interleukin (IL)-8 via the activation of p38 kinase and activator protein (AP)-1 in human aortic smooth muscle cells (hAoSMCs). The findings of this study show, for the first time, that the peroxisome proliferator-activated receptor (PPARα) agonist, fenofibrate, completely abolishes the LDL-induced IL-8 up-regulation at the transcriptional level. Pretreatment of hAoSMCs with fenofibrate abolishes the effects of LDL on AP-1 activation without affecting nuclear factor (NF)-κB. In contrast, fenofibrate failed to modulate the activation state of p38 and JNK kinases or the levels of c-fos and phospho-Jun. These data suggest that AP-1 is likely to be located at the crossroads between LDL signaling and the regulation of IL-8 modulation by PPARα.

AB - Native low density lipoprotein (n-LDL) is a major risk factor for cardiovascular diseases by inducing inflammatory processes and vascular smooth muscle cell proliferation in vessel cells. It has previously been reported that LDL enhances inflammatory reactions by the up-regulation of interleukin (IL)-8 via the activation of p38 kinase and activator protein (AP)-1 in human aortic smooth muscle cells (hAoSMCs). The findings of this study show, for the first time, that the peroxisome proliferator-activated receptor (PPARα) agonist, fenofibrate, completely abolishes the LDL-induced IL-8 up-regulation at the transcriptional level. Pretreatment of hAoSMCs with fenofibrate abolishes the effects of LDL on AP-1 activation without affecting nuclear factor (NF)-κB. In contrast, fenofibrate failed to modulate the activation state of p38 and JNK kinases or the levels of c-fos and phospho-Jun. These data suggest that AP-1 is likely to be located at the crossroads between LDL signaling and the regulation of IL-8 modulation by PPARα.

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JO - Biochemical and Biophysical Research Communications

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PPARα activation abolishes LDL-stimulated IL-8 production via AP-1 deactivation in human aortic smooth muscle cells

Abstract

Bibliographical note

All Science Journal Classification (ASJC) codes

UN SDGs

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