,Effect of lentiviral vector-mediated KSR1 gene silencing on the proliferation of renal tubular epit

• 作 者: Yang Bai Guanghong Han Kaimin Guo Lili Yu Xiadong Du ying Xu
• 机 构: Department of Ultrasound, The First Hospital of Jilin University, Changchun 130021, China“,”Departme
• 出 处: 生物化学与生物物理学报（英文版）
• 发表日期: 2018年8期
• 关键词: KSR1 renal tubular epithelial cells inflammatory factor expression Ras/MAPK path

Renal ischemia/reperfusion (I/R) is a common cause of acute renal failure in many clinical settings.Our study aimed to elucidate the role of lentiviral vector-mediated KSR1 gene silencing in inflammatory factor expression and proliferation of renal tubular epithelial cells (RTECs) in a rat model of I/R injury.Male Sprague-Dawley (SD) rats were used for I/R model establishment and subject to different treatments,followed by the measurement of neurological severity score (NSS),tumor necrosis factor-α (TNF-α),interleukin (IL)-6,IL-1β,47-kDa heat-shock protein (HSP47),KSR1,and factors related to the Ras/MAPK pathway,as well as cell apoptosis.As compared with the blank group,the neurologic impairment induced by I/R in the siKSR1,U0126,and siKSR1 + U0126 groups was alleviated.Compared with the control group,the other five groups showed increased levels of TNF-α,IL-6,IL-1β,HSP47,N-ras,Raf-1,c-fos,TNF-α,IL-6,p38 MAPK,and cell apoptosis,accompanied by a declined mRNA and protein level of Bcl-2.As compared with the blank and NC groups,the siKSR1,U0126,and siKSR1 + U0126 groups showed decreased levels of TNF-α,IL-6,IL-1β,HSP47,N-ras,Raf-1,c-fos,TNF-α,IL-6,p38 MAPK,cleaved caspase-3,cleaved caspase-9,p53,and cell apoptosis,accompanied by an increased mRNA and protein level of Bcl-2.Our findings demonstrated that KSR1 gene silencing might inhibit the expression of inflammatory factors in RTECs and promote their proliferation by inactivating the Ras/MAPK pathway in the rat model of I/R injury.