PMID- 17563062
OWN - NLM
STAT- MEDLINE
DCOM- 20070921
LR  - 20220310
IS  - 1939-327X (Electronic)
IS  - 0012-1797 (Linking)
VI  - 56
IP  - 9
DP  - 2007 Sep
TI  - Adipocyte-derived serum amyloid A3 and hyaluronan play a role in monocyte 
      recruitment and adhesion.
PG  - 2260-73
AB  - Obesity is characterized by adipocyte hypertrophy and macrophage accumulation in 
      adipose tissue. Monocyte chemoattractant protein-1 (MCP-1) plays a role in 
      macrophage recruitment into adipose tissue. However, other adipocyte-derived 
      factors, e.g., hyaluronan and serum amyloid A (SAA), can facilitate monocyte 
      adhesion and chemotaxis, respectively. The objective was to test the potential 
      involvement of these factors in macrophage recruitment. Differentiated 3T3-L1 
      adipocytes made hypertrophic by growth in high glucose conditions were used to 
      study SAA and hyaluronan regulation in vitro. Two mouse models of obesity were 
      used to study their expression in vivo. Nuclear factor-kappaB was upregulated and 
      peroxisome proliferator-activated receptor (PPAR)gamma was downregulated in 
      hypertrophic 3T3-L1 cells, with increased expression of SAA3 and increased 
      hyaluronan production. Rosiglitazone, a PPARgamma agonist, reversed these 
      changes. Hypertrophic adipocytes demonstrated overexpression of SAA3 and 
      hyaluronan synthase 2 in vitro and in vivo in diet-induced and genetic obesity. 
      SAA and hyaluronan existed as part of a complex matrix that increased the 
      adhesion and retention of monocytes. This complex, purified by binding to a 
      biotinylated hyaluronan binding protein affinity column, also showed monocyte 
      chemotactic activity, which was dependent on the presence of SAA3 and hyaluronan 
      but independent of MCP-1. We hypothesize that adipocyte hypertrophy leads to 
      increased production of SAA and hyaluronan, which act in concert to recruit and 
      retain monocytes, thereby leading to local inflammation in adipose tissue.
FAU - Han, Chang Yeop
AU  - Han CY
AD  - Department of Medicine, University of Washington, Seattle, Washington 98195-6426, 
      USA.
FAU - Subramanian, Savitha
AU  - Subramanian S
FAU - Chan, Christina K
AU  - Chan CK
FAU - Omer, Mohamed
AU  - Omer M
FAU - Chiba, Tsuyoshi
AU  - Chiba T
FAU - Wight, Thomas N
AU  - Wight TN
FAU - Chait, Alan
AU  - Chait A
LA  - eng
GR  - DK-02456/DK/NIDDK NIH HHS/United States
GR  - DK-17047/DK/NIDDK NIH HHS/United States
GR  - DK-35816/DK/NIDDK NIH HHS/United States
GR  - HL-079117/HL/NHLBI NIH HHS/United States
GR  - HL-18645/HL/NHLBI NIH HHS/United States
GR  - HL-30086/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20070611
PL  - United States
TA  - Diabetes
JT  - Diabetes
JID - 0372763
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (NF-kappa B)
RN  - 0 (PPAR gamma)
RN  - 0 (Saa3 protein, mouse)
RN  - 0 (Serum Amyloid A Protein)
RN  - 0 (Thiazolidinediones)
RN  - 05V02F2KDG (Rosiglitazone)
RN  - 9004-61-9 (Hyaluronic Acid)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - 3T3 Cells
MH  - Adipocytes/cytology/drug effects/*physiology
MH  - Adipose Tissue/physiopathology
MH  - Animals
MH  - Cell Differentiation/drug effects
MH  - Cell Division/drug effects
MH  - Chemokine CCL2/*genetics
MH  - Glucose/*pharmacology
MH  - Hyaluronic Acid/*metabolism
MH  - Inflammation
MH  - Mice
MH  - NF-kappa B/metabolism
MH  - PPAR gamma/metabolism/physiology
MH  - Rosiglitazone
MH  - Serum Amyloid A Protein/*genetics
MH  - Thiazolidinediones/pharmacology
EDAT- 2007/06/15 09:00
MHDA- 2007/09/22 09:00
CRDT- 2007/06/15 09:00
PHST- 2007/06/15 09:00 [pubmed]
PHST- 2007/09/22 09:00 [medline]
PHST- 2007/06/15 09:00 [entrez]
AID - db07-0218 [pii]
AID - 10.2337/db07-0218 [doi]
PST - ppublish
SO  - Diabetes. 2007 Sep;56(9):2260-73. doi: 10.2337/db07-0218. Epub 2007 Jun 11.