PMID- 19161676
OWN - NLM
STAT- MEDLINE
DCOM- 20090319
LR  - 20090123
IS  - 1743-2928 (Electronic)
IS  - 1351-0002 (Linking)
VI  - 14
IP  - 1
DP  - 2009
TI  - Expression of extracellular superoxide dismutase during adipose differentiation 
      in 3T3-L1 cells.
PG  - 34-40
LID - 10.1179/135100009X392467 [doi]
AB  - Obesity is known to be the primary causal component in metabolic syndrome. 
      Adipocytes in obese patients exhibit increased oxidative stress via the 
      activation of reactive oxygen species (ROS)-producing systems and inactivation of 
      antioxidant enzymes. Extracellular superoxide dismutase (EC-SOD) is an 
      anti-inflammatory enzyme that protects cells from the damaging effects of ROS. An 
      earlier report showed that plasma EC-SOD levels in type 2 diabetic patients were 
      significantly and inversely related to body mass index and homeostasis model 
      assessment-insulin resistance index. Moreover, the administration of 
      pioglitazone, an antidiabetic agent, significantly increased the plasma level of 
      EC-SOD. In this report, the expression of EC-SOD was compared to other 
      adipocytokines in mice 3T3-L1 pre-adipocytes. EC-SOD expression levels were 
      increased after the induction of differentiation and then declined, which was 
      similar to adiponectin and transcription factors such as peroxisome 
      proliferator-activated receptor-gamma (PPAR-gamma) and CCAAT/enhancer-binding 
      protein-alpha (C/EBP-alpha). On the other hand, the expression levels of 
      pro-inflammatory adipocytokines, such as tumor necrosis factor-alpha (TNF-alpha) 
      and monocyte chemo-attractant protein-1 (MCP-1), increased markedly in the 
      development stage of cells. It was observed that the expression of EC-SOD in 
      differentiated 3T3-L1 cells co-cultured with LPS-stimulated J774 macrophages was 
      up-regulated, while the addition of TNF-alpha down-regulated EC-SOD and 
      adiponectin expression in adipocytes. It is known that infiltrated and activated 
      macrophages produce extracellular ROS at high levels in adipose tissue. It is 
      possible that the expression of EC-SOD in adipocytes was stimulated to protect 
      them from oxidative stress in the co-culture system.
FAU - Adachi, Tetsuo
AU  - Adachi T
AD  - Laboratory of Clinical Pharmaceutics, Gifu Pharmaceutical University, Gifu, 
      Japan. adachi@gifu-pu.ac.jp
FAU - Toishi, Taisuke
AU  - Toishi T
FAU - Wu, Haoshu
AU  - Wu H
FAU - Kamiya, Tetsuro
AU  - Kamiya T
FAU - Hara, Hirokazu
AU  - Hara H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Redox Rep
JT  - Redox report : communications in free radical research
JID - 9511366
RN  - 0 (Adiponectin)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
SB  - IM
MH  - 3T3-L1 Cells
MH  - Adipocytes/cytology/drug effects/*metabolism
MH  - Adiponectin/genetics
MH  - Animals
MH  - Cell Differentiation/drug effects/*genetics
MH  - Cell Line
MH  - Chemokine CCL2/genetics
MH  - Coculture Techniques
MH  - Gene Expression/drug effects
MH  - *Gene Expression Profiling
MH  - Lipopolysaccharides/pharmacology
MH  - Macrophages/cytology/drug effects/metabolism
MH  - Mice
MH  - RNA, Messenger/genetics/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Superoxide Dismutase/*genetics
MH  - Time Factors
MH  - Tumor Necrosis Factor-alpha/genetics/pharmacology
EDAT- 2009/01/24 09:00
MHDA- 2009/03/20 09:00
CRDT- 2009/01/24 09:00
PHST- 2009/01/24 09:00 [entrez]
PHST- 2009/01/24 09:00 [pubmed]
PHST- 2009/03/20 09:00 [medline]
AID - 10.1179/135100009X392467 [doi]
PST - ppublish
SO  - Redox Rep. 2009;14(1):34-40. doi: 10.1179/135100009X392467.