PMID- 15562246
OWN - NLM
STAT- MEDLINE
DCOM- 20050412
LR  - 20220318
IS  - 0193-1849 (Print)
IS  - 0193-1849 (Linking)
VI  - 288
IP  - 4
DP  - 2005 Apr
TI  - Expression and secretion of inflammation-related adipokines by human adipocytes 
      differentiated in culture: integrated response to TNF-alpha.
PG  - E731-40
AB  - The expression profile of a series of adipokine genes linked to inflammation has 
      been examined by quantitative PCR during the differentiation of human 
      preadipocytes to adipocytes in primary culture, together with the integrated 
      effects of TNF-alpha on the expression of these adipokines in the differentiated 
      adipocytes. Expression of the genes encoding adiponectin, leptin, and haptoglobin 
      was highly differentiation dependent, the mRNA being undetectable 
      predifferentiation with the level peaking 9-15 days postdifferentiation. Although 
      angiotensinogen (AGT) and monocyte chemoattractant protein-1 (MCP-1) were both 
      expressed before differentiation, the mRNA level increased markedly on 
      differentiation. The expression of nerve growth factor (NGF) and plasminogen 
      activator inhibitor-1 (PAI-1) fell after differentiation, whereas that of 
      TNF-alpha and IL-6 changed little. Measurement of adiponectin, leptin, MCP-1, and 
      NGF in the medium by ELISA showed that the protein secretion pattern paralleled 
      cellular mRNA levels. Treatment of differentiated human adipocytes with TNF-alpha 
      (5 or 100 ng/ml for 24 h) significantly decreased the level of adiponectin, AGT, 
      and haptoglobin mRNA (by 2- to 4-fold), whereas that of leptin and PAI-1 was 
      unchanged. In contrast, TNF-alpha induced substantial increases in IL-6, 
      TNF-alpha, metallothionein, MCP-1, and NGF mRNAs, the largest increase being with 
      MCP-1 (14.5-fold). MCP-1 and NGF secretion increased 8- to 10-fold with 
      TNF-alpha, whereas leptin and adiponectin did not change. These results 
      demonstrate that there are major quantitative changes in adipokine gene 
      expression during differentiation of human adipocytes and that TNF-alpha has a 
      pleiotropic effect on inflammation-related adipokine production, the synthesis of 
      MCP-1 and NGF being highly induced by the cytokine.
FAU - Wang, Bohan
AU  - Wang B
AD  - Neuroendocrine and Obesity Biology Unit, School of Clinical Sciences, University 
      of Liverpool, Liverpool, UK.
FAU - Jenkins, John R
AU  - Jenkins JR
FAU - Trayhurn, Paul
AU  - Trayhurn P
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20041123
PL  - United States
TA  - Am J Physiol Endocrinol Metab
JT  - American journal of physiology. Endocrinology and metabolism
JID - 100901226
RN  - 0 (Adiponectin)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cytokines)
RN  - 0 (Haptoglobins)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 0 (Interleukin-6)
RN  - 0 (Leptin)
RN  - 0 (Plasminogen Activator Inhibitor 1)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 11002-13-4 (Angiotensinogen)
RN  - 9038-94-2 (Metallothionein)
RN  - 9061-61-4 (Nerve Growth Factor)
SB  - IM
MH  - Adipocytes/drug effects/immunology/metabolism/*physiology
MH  - Adiponectin
MH  - Adult
MH  - Angiotensinogen/biosynthesis/metabolism
MH  - Cell Differentiation/immunology
MH  - Chemokine CCL2/biosynthesis/metabolism
MH  - Cytokines/*biosynthesis/metabolism
MH  - Female
MH  - Gene Expression
MH  - Haptoglobins/biosynthesis/metabolism
MH  - Humans
MH  - Intercellular Signaling Peptides and Proteins/biosynthesis/metabolism
MH  - Interleukin-6/biosynthesis/metabolism
MH  - Leptin/biosynthesis/metabolism
MH  - Metallothionein/biosynthesis/metabolism
MH  - Middle Aged
MH  - Nerve Growth Factor/pharmacology
MH  - Plasminogen Activator Inhibitor 1/biosynthesis/metabolism
MH  - RNA, Messenger/biosynthesis/genetics
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 2004/11/25 09:00
MHDA- 2005/04/13 09:00
CRDT- 2004/11/25 09:00
PHST- 2004/11/25 09:00 [pubmed]
PHST- 2005/04/13 09:00 [medline]
PHST- 2004/11/25 09:00 [entrez]
AID - 00475.2004 [pii]
AID - 10.1152/ajpendo.00475.2004 [doi]
PST - ppublish
SO  - Am J Physiol Endocrinol Metab. 2005 Apr;288(4):E731-40. doi: 
      10.1152/ajpendo.00475.2004. Epub 2004 Nov 23.