Dysregulation of microRNA-125b is involved in the pathogenesis of post-operative infection via modulating the STAT3/procalcitonin (PCT) signaling pathway

Abstract

Introduction Procalcitonin (PCT) has been reported to function as a predictive biomarker of post-operative infection. In this study, we aimed to explore the mechanisms underlying the regulation of PCT expression. Material and methods 72 children diagnosed with post-operative infection and 58 children without post-operative infection were recruited in this study. Computational analysis, luciferase assay, real-time PCR, Western-blot analysis, and assays of post-operative C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and PCT were performed to investigate the mechanisms underlying the regulation of PCT expression. Results MiR-125b was found to repress STAT3 expression with putative binding sites in 3’UTR of STAT3. The levels of PCT and miR-125b in non-infection group remained stable from day 0 to day 5, while the level of PCT was increased in the infection group along with a decreased level of miR-125b from day 1 to day 5. The post-operative levels of CRP and ESR in both non-infection and infection groups were evidently increased in a time-dependent manner, but the levels of miR-106b and miR-20a in both non-infection and infection groups remained stable. The area under the curve (AUC) values of PCT, CRP, ESR, miR-125b, miR-106b and miR-20a demonstrated that only miR-125b and PCT were involved in infection. Transfection with miR-125b reduced STAT3 expression, while the activation of STAT3 by lipopolysaccharide (LPS) treatment up-regulated PCT production. Finally, miR-125b down-regulated the expression of PCT by targeting STAT3. Conclusions Taken together, we suggested that miR-125b was involved in the prognosis and diagnosis of posteroperative infection by modulating the signaling pathway of miR-125b/STAT3/PCT. Powered by TCPDF (www.tcpdf.org) Pr ep int Dysregulation of microRNA-125b is involved in the pathogenesis of post-operative infection via modulating the STAT3/procalcitonin (PCT) signaling pathway Li Wang1, Mingzhu Yang2, Xuan Jin3* 1. Laboratory, Affiliated Hospital of Shaanxi University of Chinese Medicine, Xianyang, Shaanxi, 712000, China 2. Pediatrics Department, Xianyang Central Hospital, Xianyang, Shaanxi, 712000, China 3. Pediatrics Department, Affiliated Hospital of Shaanxi University of Chinese Medicine, Xianyang, Shaanxi, 712000, China *Corresponding author: Xuan Jin Institution: Pediatrics Department, Affiliated Hospital of Shaanxi University of Chinese Medicine, Xianyang, Shaanxi, 712000, China Address: No.2, Yangxi Road, Xianyang, Shaanxi, 712000, China Email: [email protected]