PMID- 9218837
OWN - NLM
STAT- MEDLINE
DCOM- 19970807
LR  - 20190512
IS  - 0009-9104 (Print)
IS  - 1365-2249 (Electronic)
IS  - 0009-9104 (Linking)
VI  - 109
IP  - 1
DP  - 1997 Jul
TI  - Gene expression of CC chemokines in experimental crescentic glomerulonephritis 
      (CGN).
PG  - 143-8
AB  - CGN is a rapidly progressive glomerular disease. Monocytes/macrophages are 
      frequently observed in glomeruli in cases of CGN and they are considered to play 
      a crucial role in the pathogenesis of this disease. We described previously the 
      glomerular expression of monocyte chemoattractant protein-1 (MCP-1), which is a 
      potent chemoattractant for monocytes and a member of CC chemokine family, in an 
      experimental model of CGN. In the present study we investigated the expression of 
      mRNAs for other CC chemokines, namely, MCP-3, macrophage inflammatory 
      protein-1alpha (MIP-1alpha), MIP-1beta, RANTES and TCA3, all of which are 
      chemotactic for monocytes, in the CGN model. First, we established a reverse 
      transcriptase-polymerase chain reaction (RT-PCR) method by which mRNA for each of 
      the CC chemokines could be amplified separately, and then we measured the levels 
      of the expression of mRNAs for the chemokines in diseased glomeruli at several 
      time points after induction of CGN. The mRNAs for all CC chemokines examined were 
      expressed in glomeruli of rats with CGN. Moreover, induction of the gene 
      expression of MIP-1alpha and MIP-1beta seemed to occur earlier than that of the 
      others. CC chemokines may contribute to the recruitment and activation of 
      monocytes in CGN, and each individual CC chemokine may play an overlapping but 
      distinct role in the pathogenesis of this disease.
FAU - Natori, Y
AU  - Natori Y
AD  - Division of Pathophysiology, Research Institute, International Medical Centre of 
      Japan, Tokyo.
FAU - Sekiguchi, M
AU  - Sekiguchi M
FAU - Ou, Z
AU  - Ou Z
FAU - Natori, Y
AU  - Natori Y
LA  - eng
PT  - Journal Article
PL  - England
TA  - Clin Exp Immunol
JT  - Clinical and experimental immunology
JID - 0057202
RN  - 0 (CCL1 protein, human)
RN  - 0 (CCL7 protein, human)
RN  - 0 (Ccl7 protein, rat)
RN  - 0 (Chemokine CCL1)
RN  - 0 (Chemokine CCL3)
RN  - 0 (Chemokine CCL4)
RN  - 0 (Chemokine CCL5)
RN  - 0 (Chemokine CCL7)
RN  - 0 (Chemokines)
RN  - 0 (Chemokines, CC)
RN  - 0 (Cytokines)
RN  - 0 (Macrophage Inflammatory Proteins)
RN  - 0 (Monocyte Chemoattractant Proteins)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Animals
MH  - Basement Membrane/immunology
MH  - Chemokine CCL1
MH  - Chemokine CCL3
MH  - Chemokine CCL4
MH  - Chemokine CCL5/genetics/metabolism
MH  - Chemokine CCL7
MH  - Chemokines/*genetics/*metabolism
MH  - Chemokines, CC
MH  - Chemotaxis
MH  - Cytokines/genetics/metabolism
MH  - Gene Expression
MH  - Glomerulonephritis/*genetics/*immunology
MH  - Kidney Glomerulus/immunology/metabolism/pathology
MH  - Macrophage Inflammatory Proteins/genetics/metabolism
MH  - Monocyte Chemoattractant Proteins/genetics/metabolism
MH  - Monocytes/immunology
MH  - Polymerase Chain Reaction
MH  - RNA, Messenger/metabolism
MH  - Rats
PMC - PMC1904711
EDAT- 1997/07/01 00:00
MHDA- 1997/07/01 00:01
PMCR- 1998/07/01
CRDT- 1997/07/01 00:00
PHST- 1997/07/01 00:00 [pubmed]
PHST- 1997/07/01 00:01 [medline]
PHST- 1997/07/01 00:00 [entrez]
PHST- 1998/07/01 00:00 [pmc-release]
AID - 10.1046/j.1365-2249.1997.4271321.x [doi]
PST - ppublish
SO  - Clin Exp Immunol. 1997 Jul;109(1):143-8. doi: 10.1046/j.1365-2249.1997.4271321.x.