#2353 The role of Foxp2 in kidney ischemia-reperfusion injury

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Abstract Background and Aims Our recent study found that the transcription factor of Forkhead box P2(Foxp2) was upregulated in renal tubules from human and mouse models of chronic kidney diseases (CKD) and is involved in the progression of cell cycle arrest and renal fibrosis [1]. However, the role of Foxp2 on kidney injury and the associated mechanisms remain largely unknown. Method Foxp2 expression was detected by immunohistochemical staining on renal biopsies from patients with acute tubular injury. Tubule-specific Foxp2 knockout mice (Foxp2fl/fl,Cre) and the corresponding control (Foxp2fl/fl) were subjected to unilateral ischemia-reperfusion injury (UIRI) for 30 mins, followed by contralateral nephrectomy at one day before sacrifice. Mice were sacrificed at 7-day post-surgery for examination of renal injury and apoptosis. Results Foxp2 expression was increased in nucleus of injured renal tubules. Tubular injury marker kidney injury molecule 1 (Kim1) was significantly decreased in Foxp2 knockout mice compared to that in control mice at 7-day post-surgery. Increased expression levels of Bcl2 associated x (Bax) and p53 were attenuated with the absence of tubular Foxp2 at both mRNA and protein levels. Conclusion Foxp2 plays a pathogenetic role in kidney ischemia-reperfusion injury. Suppression of tubular Foxp2 alleviates apoptotic effects in kidney injury.

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