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Gene expression of CC chemokines in experimental crescentic glomerulonephritis (CGN)
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SUMMARY
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-1α (MIP-1α), MIP-1β, 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-1α and MIP-1β 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.
Oxford University Press (OUP)
Title: Gene expression of CC chemokines in experimental crescentic glomerulonephritis (CGN)
Description:
SUMMARY
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-1α (MIP-1α), MIP-1β, 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-1α and MIP-1β 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.
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