PMID- 14520519
OWN - NLM
STAT- MEDLINE
DCOM- 20031126
LR  - 20220316
IS  - 1023-3830 (Print)
IS  - 1023-3830 (Linking)
VI  - 52
IP  - 10
DP  - 2003 Oct
TI  - Monocyte chemoattractant protein (MCP)-1 production via functionally 
      reconstituted Fcalpha receptor (CD89) on glomerular mesangial cells.
PG  - 428-32
AB  - BACKGROUND: Fc alpha receptor (FcalphaR; CD89) is the receptor for Fc portion of 
      IgA in various cells, and displays various immunological responses on binding. It 
      is important to analyze the mesangial functions via FcalphaR in the pathogenesis 
      of IgA nephropathy. However, it is still controversial whether FcalphaR is 
      expressed on mesangial cells. To assess biological functions of FcalphaR on the 
      mesangial cells, we established mesangial transfectants that expressed FcalphaR 
      with or without FcRgamma chain that is a common signaling molecule of FcRs. The 
      production of monocyte chemoattractant protein-1 (MCP-1) by mesangial cells is 
      known to contribute to cellular infiltration into glomeruli and subsequent 
      glomerular injuries. METHODS: Murine mesangial cell lines (SV40 MES 13) were 
      transfected with cDNA of the human FcalphaR. Furthermore, we co-transfected some 
      of the FcalphaR transfectants with cDNA of human FcRgamma chain. The tyrosine 
      phosphorylation of the intra-mesangial proteins after FcalphaR cross-linking was 
      examined by immunoprecipitation. MCP-1 production from each transfectant 
      stimulated with heat aggregated IgA was determined by sandwich ELISA. RESULTS: 
      Two kinds of mesangial transfectants stably expressed human FcalphaR with or 
      without FcRgamma chain (FcalphaR(+), FcalphaR(+)/gamma(+)). Phosphorylation of 
      FcRgamma chain and syk kinase was detected in FcalphaR(+) and 
      FcalphaR(+)/gamma(+) cells, but not in untransfected cells. Aggregated IgA 
      induced significantly higher MCP-1 production in FcalphaR(+)/gamma(+) than those 
      in FcalphaR(+) or untransfected control. CONCLUSIONS: Present study demonstrated 
      that FcalphaR and FcRgamma chain could be reconstituted in mesangial cells and 
      mediated MCP-1 production by aggregated IgA in a dose-dependent manner. Current 
      data would argue that FcalphaR can be activated in mesangial cells through their 
      own machinery, although underlying mechanisms for FcalphaR induction in mesangial 
      cells remain unclear.
FAU - Tsuge, T
AU  - Tsuge T
AD  - Department of Internal Medicine, Juntendo University School of Medicine, 2-1-1 
      Hongo, 113-8421 Tokyo, Japan, Bunkyo-ku.
FAU - Suzuki, Y
AU  - Suzuki Y
FAU - Shimokawa, T
AU  - Shimokawa T
FAU - Horikoshi, S
AU  - Horikoshi S
FAU - Okumura, K
AU  - Okumura K
FAU - Ra, C
AU  - Ra C
FAU - Tomino, Y
AU  - Tomino Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Switzerland
TA  - Inflamm Res
JT  - Inflammation research : official journal of the European Histamine Research 
      Society ... [et al.]
JID - 9508160
RN  - 0 (Antigens, CD)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Enzyme Precursors)
RN  - 0 (Fc(alpha) receptor)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (Receptors, Fc)
RN  - 42HK56048U (Tyrosine)
RN  - 63231-63-0 (RNA)
RN  - EC 2.7.10.1 (Protein-Tyrosine Kinases)
RN  - EC 2.7.10.2 (SYK protein, human)
RN  - EC 2.7.10.2 (Syk Kinase)
RN  - EC 2.7.10.2 (Syk protein, mouse)
SB  - IM
MH  - Animals
MH  - Antigens, CD/*metabolism
MH  - Cells, Cultured
MH  - Chemical Phenomena
MH  - Chemistry, Physical
MH  - Chemokine CCL2/*biosynthesis/genetics
MH  - Enzyme Precursors/biosynthesis/genetics
MH  - Glomerular Mesangium/cytology/*metabolism
MH  - Intracellular Signaling Peptides and Proteins
MH  - Mice
MH  - Phosphorylation
MH  - Protein-Tyrosine Kinases/biosynthesis/genetics
MH  - RNA/biosynthesis/genetics
MH  - Receptors, Fc/*metabolism
MH  - Syk Kinase
MH  - Transfection
MH  - Tyrosine/metabolism
EDAT- 2003/10/02 05:00
MHDA- 2003/12/03 05:00
CRDT- 2003/10/02 05:00
PHST- 2003/10/02 05:00 [pubmed]
PHST- 2003/12/03 05:00 [medline]
PHST- 2003/10/02 05:00 [entrez]
AID - 10.1007/s00011-003-1200-x [doi]
PST - ppublish
SO  - Inflamm Res. 2003 Oct;52(10):428-32. doi: 10.1007/s00011-003-1200-x.