Gene expression of TWEAK/Fn14 and IP-10/CXCR3 in glomerulus and tubulointerstitium of patients with lupus nephritis
Gene expression of TWEAK/Fn14 and IP-10/CXCR3 in glomerulus and tubulointerstitium of patients with lupus nephritis
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DOI：
10.1111/j.1440-1797.2011.01449.x
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发表时间：
2011-05-01
期刊：
影响因子：
2.5
通讯作者：
Szeto, Cheuk-Chun
中科院分区：
文献类型：
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作者：
Lu, Jianxin;Kwan, Bonnie Ching-Ha;Szeto, Cheuk-Chun
目的：探讨肿瘤坏死因子样细胞凋亡弱诱导剂(TWEAK)/Fn14和干扰素诱导蛋白(IP-10)/CXCR3轴在狼疮性肾炎发病中的作用。方法：测定42例狼疮性肾炎患者（LN组）和10例健康对照者肾小球和小管间质中TWEAK、Fn14、IP-10和CXCR3 mRNA的表达。结果：与对照组相比，LN组患者肾小球中TWEAK和Fn14的表达较高，而肾小球中CXCR3的表达较低。同样，LN组的TWEAK和Fn14的小管间质表达高于对照组，而CXCR3的小管间质表达低于对照组。V型肾炎的肾小球TWEAK表达明显高于IV型肾炎。肾小球中CXCR3表达与蛋白尿显著相关（r = -0.532, P = 0.019），而小管间质中CXCR3表达与血清肌酐显著相关（r = -0.447, P = 0.029）。结论：狼疮性肾炎患者肾内TWEAK、Fn14表达升高，CXCR3表达降低。肾内CXCR3的表达与蛋白尿和肾功能相关。我们的研究结果提示，TWEAK/Fn14和IP-10/CXCR3轴可能参与狼疮性肾炎的发病机制。
Aim: The role of the tumour necrosis factor-like weak inducer of apoptosis (TWEAK)/Fn14 and interferon-inducible protein (IP-10)/CXCR3 axis in the pathogenesis of lupus nephritis were studied.Methods: The mRNA expression of TWEAK, Fn14, IP-10 and CXCR3 were quantified in the glomerulus and tubulointerstitium of 42 patients with lupus nephritis (LN group) and 10 healthy controls.Results: As compared to controls, LN patients had higher glomerular expression of TWEAK and Fn14, but glomerular CXCR3 expression was lower in the LN group. Similarly, the LN group had higher tubulointerstitial expression of TWEAK and Fn14, but lower tubulointerstitial expression of CXCR3, than controls. Glomerular TWEAK expression of class V nephritis was significantly higher than class IV nephritis. Glomerular expression of CXCR3 significantly correlated with proteinuria (r = -0.532; P = 0.019), whereas tubulointerstitial CXCR3 significantly correlated with serum creatinine (r = -0.447; P = 0.029).Conclusion: In patients with lupus nephritis, there is an increase in intra-renal expression of TWEAK and Fn14, and a decrease in CXCR3 expression. Intra-renal expression of CXCR3 correlates with proteinuria and renal function. Our findings suggest that the TWEAK/Fn14 and IP-10/CXCR3 axis may contribute to the pathogenesis of lupus nephritis.