PMID- 17184171
OWN - NLM
STAT- MEDLINE
DCOM- 20070510
LR  - 20171116
IS  - 1523-0864 (Print)
IS  - 1523-0864 (Linking)
VI  - 9
IP  - 3
DP  - 2007 Mar
TI  - Effects of PGC-1alpha on TNF-alpha-induced MCP-1 and VCAM-1 expression and 
      NF-kappaB activation in human aortic smooth muscle and endothelial cells.
PG  - 301-7
AB  - Increased oxidative stress in vascular cells is implicated in the pathogenesis of 
      atherosclerosis. Reactive oxygen species (ROS) induce vascular inflammation via 
      the proinflammatory cytokine/NF-kappaB pathway. Several lines of evidence suggest 
      that peroxisome proliferator-activated receptor-gamma coactivator 1-alpha 
      (PGC-1alpha) is an important regulator of intracellular ROS levels. However, no 
      studies have examined the effects of PGC-1alpha on this process. We investigated 
      the effects of PGC-1alpha on inflammatory molecule expression and activity of the 
      redox-sensitive transcription factor, NF-kappaB, in vascular cells. PGC-1alpha 
      expressed in human aortic smooth (HASMCs) and endothelial cells (HAECs) is 
      upregulated by AMP-activated protein kinase activators, including metformin, 
      rosiglitazone and alpha-lipoic acid. Tumor necrosis factor-alpha (TNF-alpha), a 
      major proinflammatory factor in the development of vascular inflammation, 
      stimulates intracellular ROS production through an increase in both mitochondrial 
      ROS and NAD(P)H oxidase activity. Adenovirus-mediated overexpression of the 
      PGC-1alpha gene in HASMCs and HAECs leads to a significant reduction in 
      intracellular and mitochondrial ROS production as well as NAD(P)H oxidase 
      activity. Consequently, NF-kappaB activity and MCP-1 and VCAM-1 induced by 
      TNF-alpha are suppressed. Our data support the possibility that agents 
      stimulating PGC-1alpha expression in the vasculature aid in preventing the 
      development of atherosclerosis.
FAU - Kim, Hye-Jin
AU  - Kim HJ
AD  - Department of Microbiology, Kyungpook National University, Daegu, South Korea.
FAU - Park, Keun-Gyu
AU  - Park KG
FAU - Yoo, Eun-Kyung
AU  - Yoo EK
FAU - Kim, Young-Ho
AU  - Kim YH
FAU - Kim, Yoon-Nyun
AU  - Kim YN
FAU - Kim, Hye-Soon
AU  - Kim HS
FAU - Kim, Hyoung Tae
AU  - Kim HT
FAU - Park, Joong-Yeol
AU  - Park JY
FAU - Lee, Ki-Up
AU  - Lee KU
FAU - Jang, Won Gu
AU  - Jang WG
FAU - Kim, Jung-Guk
AU  - Kim JG
FAU - Kim, Bo-Wan
AU  - Kim BW
FAU - Lee, In-Kyu
AU  - Lee IK
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Antioxid Redox Signal
JT  - Antioxidants & redox signaling
JID - 100888899
RN  - 0 (Chemokine CCL2)
RN  - 0 (DNA Primers)
RN  - 0 (Heat-Shock Proteins)
RN  - 0 (NF-kappa B)
RN  - 0 (PPARGC1A protein, human)
RN  - 0 (Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Transcription Factors)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - EC 1.6.3.- (NADPH Oxidases)
SB  - IM
MH  - Aorta, Thoracic/cytology/drug effects/enzymology/*metabolism
MH  - Base Sequence
MH  - Cells, Cultured
MH  - Chemokine CCL2/*metabolism
MH  - DNA Primers
MH  - Endothelium, Vascular/cytology/drug effects/enzymology/*metabolism
MH  - Heat-Shock Proteins/*physiology
MH  - Humans
MH  - Muscle, Smooth, Vascular/cytology/drug effects/enzymology/*metabolism
MH  - NADPH Oxidases/metabolism
MH  - NF-kappa B/*metabolism
MH  - Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
MH  - Reactive Oxygen Species/metabolism
MH  - Recombinant Proteins/pharmacology
MH  - Transcription Factors/*physiology
MH  - Tumor Necrosis Factor-alpha/*pharmacology
MH  - Vascular Cell Adhesion Molecule-1/*metabolism
EDAT- 2006/12/23 09:00
MHDA- 2007/05/11 09:00
CRDT- 2006/12/23 09:00
PHST- 2006/12/23 09:00 [pubmed]
PHST- 2007/05/11 09:00 [medline]
PHST- 2006/12/23 09:00 [entrez]
AID - 10.1089/ars.2006.1456 [doi]
PST - ppublish
SO  - Antioxid Redox Signal. 2007 Mar;9(3):301-7. doi: 10.1089/ars.2006.1456.