Role of mast cells in the development of renal fibrosis: use of mast cell-deficient rats.
Role of mast cells in the development of renal fibrosis: use of mast cell-deficient rats.
复制标题
肥大细胞在肾纤维化发展中的作用：使用肥大细胞缺陷大鼠。
DOI：
10.1111/j.1523-1755.2004.00629.x
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发表时间：
2004
影响因子：
19.6
通讯作者：
Natori,Yasuhiro
中科院分区：
文献类型：
--
作者：
Miyazawa,Shinobu;Hotta,Osamu;Doi,Naoko;Natori,Yumiko;Nishikawa,Kiyotaka;Natori,Yasuhiro
Role of mast cells in the development of renal fibrosis: Use of mast cell–deficient rats.BackgroundRecent clinical studies have shown that the number of interstitial mast cells increases in various types of renal disease and correlates well with the magnitude of interstitial fibrosis. The present study was conducted to assess the role of mast cells in renal fibrosis by examining an experimental glomerular disease.MethodsA rat model of chronic glomerular disease, puromycin aminonucleoside-nephrosis, was induced in mast cell–deficient (Ws/Ws) and normal (+/+) rats.ResultsThe area of interstitial fibrosis was widely distributed at 6 weeks in both groups of rats; however, unexpectedly, the area of interstitial fibrosis was greater inWs/Wsrats than in +/+ littermates. Biochemical analysis of the hydroxyproline content confirmed the more severe fibrosis in theWs/Wsrats. The number of mast cells increased in bothWs/Wsand +/+ rats, concomitant with the development of interstitial fibrosis, but was confirmed to be lower inWs/Wsthan in +/+ rats. There were no differences in the numbers of interstitial macrophages and T lymphocytes between the two groups. Reverse transcription-polymerase chain reaction analysis of cytokine expression revealed that the level of mRNA for transforming growth factor-β (TGF-β), a potent profibrotic cytokine, was higher inWs/Wsrats. In addition, heparin, one of the major components of mast cells, inhibited the expression of TGF-β mRNA in rat fibroblasts in culture.ConclusionThese results suggest that mast cells do not play a major role in the pathogenesis of interstitial fibrosis in puromycin aminonucleoside nephrosis. Rather, they might be protective or ameliorative in this model through the inhibition of TGF-β production by heparin, and possibly in other models and also in humans.
