PMID- 17066518
OWN - NLM
STAT- MEDLINE
DCOM- 20061215
LR  - 20181113
IS  - 0513-5796 (Print)
IS  - 1976-2437 (Electronic)
IS  - 0513-5796 (Linking)
VI  - 47
IP  - 5
DP  - 2006 Oct 31
TI  - Inflammatory gene expression patterns revealed by DNA microarray analysis in 
      TNF-alpha-treated SGBS human adipocytes.
PG  - 729-36
AB  - We report here the use of human inflammation arrays to study the inflammatory 
      gene expression profile of TNF-alpha- treated human SGBS adipocytes. Human 
      preadipocytes (SGBS) were induced to differentiate in primary culture, and 
      adipocyte differentiation was confirmed, using Oil Red O staining. We treated the 
      differentiated adipocytes with TNF-alpha, and RNA from differentiated adipocytes 
      with or without TNF-alpha treatment was hybridized to MWG human inflammation 
      arrays to compare expression profiles. Eleven genes were up- or down-regulated in 
      TNF-alpha-treated adipocytes. As revealed by array analysis, among 6 up-regulated 
      genes, only eotaxin-1, monocyte chemoattractant protein-1 (MCP-1), and vascular 
      cell adhesion molecule 1 isoform a precursor (VCAM1) were confirmed by real-time 
      polymerase chain reaction (PCR). Similarly, among 5 down-regulated genes, only 
      IL-1 family member 5 (IL1F5), a disintegrin and metalloprotease with 
      thrombospondin motifs-1 preproprotein (ADAMTS1), fibronectin 1 isoform 1 
      preprotein (FN1), and matrix metalloproteinase 15 preprotein (MMP15) were 
      confirmed by real-time PCR. There was a substantial increase (50-fold) in 
      eotaxin-1 in response to TNF-alpha. Taken together, we have identified several 
      inflammatory molecules expressed in SGBS adipocytes and discovered molecular 
      factors explaining the relationship between obesity and atherosclerosis, focusing 
      on inflammatory cytokines expressed in the TNF-alpha-treated SGBS cells. Further 
      investigation into the role of these up- or down-regulated cytokine genes during 
      the pathological processes leading to the development of atherosclerosis is 
      warranted.
FAU - Do, Myoung-Sool
AU  - Do MS
AD  - School of Life and Food Sciences, Handong Global University Pohang, Korea. 
      msdo@handong.edu
FAU - Jeong, Hun-Soon
AU  - Jeong HS
FAU - Choi, Bong-Hyuk
AU  - Choi BH
FAU - Hunter, Leif
AU  - Hunter L
FAU - Langley, Stuart
AU  - Langley S
FAU - Pazmany, Laszlo
AU  - Pazmany L
FAU - Trayhurn, Paul
AU  - Trayhurn P
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Korea (South)
TA  - Yonsei Med J
JT  - Yonsei medical journal
JID - 0414003
RN  - 0 (Inflammation Mediators)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Adipocytes/cytology/drug effects/*metabolism
MH  - Cell Differentiation
MH  - Cells, Cultured
MH  - Gene Expression Profiling
MH  - Gene Expression Regulation/*drug effects
MH  - Humans
MH  - Inflammation Mediators/*metabolism
MH  - Oligonucleotide Array Sequence Analysis
MH  - Polymerase Chain Reaction
MH  - Tumor Necrosis Factor-alpha/*pharmacology
PMC - PMC2687760
EDAT- 2006/10/27 09:00
MHDA- 2006/12/16 09:00
PMCR- 2006/10/31
CRDT- 2006/10/27 09:00
PHST- 2006/10/27 09:00 [pubmed]
PHST- 2006/12/16 09:00 [medline]
PHST- 2006/10/27 09:00 [entrez]
PHST- 2006/10/31 00:00 [pmc-release]
AID - 200610729 [pii]
AID - 10.3349/ymj.2006.47.5.729 [doi]
PST - ppublish
SO  - Yonsei Med J. 2006 Oct 31;47(5):729-36. doi: 10.3349/ymj.2006.47.5.729.