CXCL10型
急性肾小管坏死
再灌注损伤
细胞生长
肾缺血
坏死
缺血
急性肾损伤
肾
医学
内分泌学
内科学
生物
病理
免疫学
趋化因子
炎症
生物化学
作者
Kengo Furuichi,Takashi Wada,Shinji Kitajikma,Tadasi Toyama,Tomoko Okumura,Akinori Hara,Hiroshi Kawachi,Fujio Shimizu,Takeshi Sugaya,Naofumi Mukaida,Shosaku Narumi,Kouji Matsushima,Shuichi Kaneko
出处
期刊:Nephron Experimental Nephrology
[S. Karger AG]
日期:2008-06-03
卷期号:109 (1): e29-e38
被引量:14
摘要
Although renal tubular cell proliferation after acute tubular necrosis is an important and essential response in the recovery of renal dysfunction in acute renal failure, the precise factors and mechanisms of tubular cell regeneration remain unclear. Here, we describe our studies using a neutralizing antibody (Ab) against interferon-inducible protein of 10 kDa (IP-10; CXCL10) that indicate a role for CXCL10 in tubular cell proliferation after renal ischemia-reperfusion injury. Tissue necrosis and interstitial infiltrating numbers were comparable between anti-CXCL10 Ab-treated and control mice treated with IgG at the 24 and 48 h time points after reperfusion. In contrast, the numbers of Ki67-positive proliferating tubular cells were significantly increased in anti-CXCL10 Ab-treated mice 48 h after reperfusion. In accordance with the in vivo findings,in vitro studies using murine tubular epithelial cells indicated an antiproliferative effect of CXCL10 upon the intensity of cell proliferation and the number of Ki67-positive cells. These data suggest that CXCL10 plays a role in the regulation of tubular cell proliferation following renal ischemia-reperfusion injury.
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