• Yuefei Xiao, Nainin Yang, Qingxian Zhang, Yiping Wang, Songtao Yang, and Zhanxiao Liu.
• Department of Nephrology, Aerospace Center Hospital, Aerospace Clinical Medical College, Peking University, No.15 Yuquan Road, Haidian District, Beijing, 100049, People's Republic of China, yuefeixiaobj@163.com.
• Inflammation. 2014 Oct 1; 37 (5): 1895-901.

AbstractAcute kidney injury-induced organ fibrosis is recognized as a major risk factor for the development of chronic kidney disease, which remains one of the leading causes of death in the developed world. However, knowledge on molecules that may suppress the fibrogenic response after injury is lacking. The long pentraxin 3 (PTX3), a novel acute renal injury marker, has been reported to be involved in chronic renal injury, but the mechanism is still unknown. In this experiment, the mice subjected to acute kidney injury showed a slow recovery of kidney function compared with PTX3-treated animals. Collagen expression was absent in sham-operated kidneys; however, their expression was significantly increased after reperfusion. And, these changes were reduced in PTX3-treated mouse kidney. Fibrosis was associated with increased expression of IL-6 and extensive activation of Stat3. Administration of IL-6 increased collagen I expression and Stat3 activation in vitro in renal epithelial cells subjected to hypoxia-reoxygenation, which was suppressed by PTX3. Furthermore, we found that the decreased serum creatinine level and the reduced expression of collagen and smooth muscle actin induced by PTX3 were abolished by additional administration of IL-6. The associated p-Stat3 expression which was reduced by PTX3 administration was also inverted by additional IL-6 treatment. Our data suggest that PTX3 inhibits acute renal injury-induced interstitial fibrosis through suppression of IL-6/Stat3 pathway.

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