Gene expression of CC chemokines in experimental crescentic glomerulonephritis (CGN)
Gene expression of CC chemokines in experimental crescentic glomerulonephritis (CGN)
复制标题
DOI：
10.1046/j.1365-2249.1997.4271321.x
复制
发表时间：
1997-07-01
影响因子：
4.6
通讯作者：
Natori, Y
中科院分区：
文献类型：
--
作者：
Natori, Y;Sekiguchi, M;Natori, Y
CGN是一种快速进展的肾小球疾病。在CGN的情况下，在肾小球中经常观察到单核细胞/巨噬细胞，并且它们被认为在这种疾病的发病机制中起关键作用。我们先前描述了单核细胞趋化蛋白-1（MCP-1）在CGN实验模型中的肾小球表达，MCP-1是一种有效的单核细胞趋化因子，也是CC趋化因子家族的成员。在本研究中，我们研究了其他CC趋化因子，即MCP-3，巨噬细胞炎性蛋白-1 α（MIP-1 α），MIP-1 β，RANTES和TCA 3的mRNA表达，所有这些都是趋化单核细胞，在CGN模型。首先，我们建立了一种逆转录-聚合酶链反应（RT-PCR）方法，通过该方法可以分别扩增每种CC趋化因子的mRNA，然后我们测量了诱导CGN后几个时间点病变肾小球中趋化因子mRNA的表达水平。检测的所有CC趋化因子的mRNA在CGN大鼠肾小球中表达。此外，MIP-1 α和MIP-1 β的基因表达的诱导似乎比其他的更早发生。CC趋化因子可能有助于CGN中单核细胞的募集和活化，并且每个单独的CC趋化因子可能在这种疾病的发病机制中发挥重叠但不同的作用。
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-1 alpha (MIP-1 alpha), MIP-1 beta, 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-1 alpha and MIP-1 beta 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.