首页|Dexmedetomidine ameliorates high glucose-induced epithelial-mesenchymal transformation in HK-2 cells through the Cdk5/Drp1/ROS pathway
Dexmedetomidine ameliorates high glucose-induced epithelial-mesenchymal transformation in HK-2 cells through the Cdk5/Drp1/ROS pathway
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Epithelial-mesenchymal transformation(EMT)plays an important role in the progression of diabetic nephropathy.Dexmedetomidine(DEX)has shown renoprotective effects against ischemic reperfusion injury;however,whether and how DEX prevents high glucose-induced EMT in renal tubular epithelial cells is incompletely known.Here,we conduct in vitro experiments using HK-2 cells,a human tubular epithelial cell line.Our results demonstrate that high glucose increases the expressions of EMT-related proteins,including Vimentin,Slug,Snail and Twist,while de-creasing the expression of E-cadherin and increasing Cdk5 expression in HK-2 cells.Both Cdk5 knockdown and inhibition by roscovitine increase the expressions of E-cadherin while decreasing the expressions of other EMT-related markers.DEX inhibits Cdk5 expression without affecting cell viability and changes the expressions of EMT-related markers,similar to effects of Cdk5 inhibition.Furthermore,Cdk5 is found to interact with Drp1 at the protein level and mediate the phosphorylation of Drp1.In addition,Drp1 inhibition with mdivi-1 could also restrain the high glucose-induced EMT process in HK-2 cells.Immunofluorescence results show that roscovitine,Mdivi-1 and DEX inhibit high glucose-induced intracellular ROS accumulation,while the oxidant H2O2 eliminates the protective effect of DEX on the EMT process.These results indicate that DEX mitigates high glucose-induced EMT progression in HK-2 cells via inhibition of the Cdk5/Drp1/ROS pathway.
dexmedetomidinehigh glucoseepithelial-mesenchymal transformationcyclin-dependent kinase 5dynamin-related protein 1
Fei Wang、Weilong Xu、Xiaoge Liu、Jun Zhang
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Department of Anesthesiology,Fudan University Shanghai Cancer Center,Shanghai 200032,China
Department of Oncology,Shanghai Medical College,Fudan University,Shanghai 200032,China
Department of Anesthesiology,the Affiliated Hospital of Qingdao University,Qingdao 266000,China
Medical Guidance Supporting Project from Shanghai Municipal Science and Technology Committee
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