Enhanced Orai1-mediated store-operated Ca2+ channel/calpain signaling contributes to high glucose-induced podocyte injury
Yu Tao, Sarika Chaudhari, Parisa Yazdizadeh Shotorbani, Yanfeng Ding, Zhenglan Chen, Ramesh B. Kasetti, Gulab Zode, Rong Ma
Abstract
pump on the endoplasmic/sarcoplasmic reticulum membrane, significantly increased the activity of calpain, which was inhibited by BTP2. Finally, the calpain-1/calpain-2 inhibitor calpeptin significantly blunted the nephrin protein reduction induced by HG treatment. Taken together, our results suggest that enhanced signaling via an Orai1/SOCE/Calpain axis contributes to HG-induced podocyte injury.
Topics & Concepts
PodocyteNephrinCalpainORAI1ThapsigarginSTIM1Cell biologyEndoplasmic reticulumChemistrySynaptopodinInternal medicineEndocrinologyBiologyKidneyBiochemistryMedicineProteinuriaEnzymeIon Channels and Receptors