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Kidney Week

Abstract: TH-PO945

Stanniocalcin-1 Inhibits ER Stress-Induced Apoptosis and Renal Fibrosis via Restoration of ER-Mitochondrial Calcium Communication

Session Information

Category: CKD (Non-Dialysis)

  • 1903 CKD (Non-Dialysis): Mechanisms


  • Yang, Eun mi, Chonnam National University Medical School, Gwangju, Korea (the Republic of)
  • Kim, Soo Wan, Chonnam National University Medical School, Gwangju, Korea (the Republic of)
  • Bae, Eun Hui, Chonnam National University Hospital, Gwangju, Korea (the Republic of)
  • Ma, Seong Kwon, Chonnam National University Medical School, Gwangju, Korea (the Republic of)
  • Park, Jung Sun, chonnam national university, Gwang Ju, Korea (the Republic of)

Endoplasmic reticulum (ER) stress is a common feature of several physiological and pathological conditions. ER stress-associated apoptosis plays a role in organ remodeling after insult, and overwhelming ER stress lead to renal cell apoptosis and subsequent fibrosis. Stanniocalcin-1 (STC-1) is a multifunctional glycoprotein which is targeted to the mitochondria to exert putative anti-apoptotic effects. The present study aimed to investigate the effects of STC-1 in ER stress-induced apoptosis and renal fibrosis in human renal proximal tubular (HK-2) cells.


HK2 cells pretreated with STC-1 (200 ng/ml) for 1 hours followed by treatment with TGF-β (10 ng/ml) for 24 hours. The protein expression of ER stress, apoptosis, and fibrosis markers was determined by semiquantitative immunoblotting. The level of reactive oxygen species (ROS) was determined by fluorescent microscopy immunofluorescence. Using microscopy and immunocytochemistry, immunolabelling of Ca2+, calcium sensing receptor and inositol 1,4,5-trisphosphate receptor (IP3R) was detected.


TGF-β treatment induced ER stress via upregulation of PERK-eIF2-ATF signaling, and suppressed cytosolic calcium concentration via downregulation of IP3R. Pretreatment of STC-1 attenuated the TGF-β induced up-regulation of PERK-eIF2-ATF4 signaling and restored the cytosolic Ca concentration, thus reducing apoptosis. TGF-β treatment induced mitochondrial ROS generation and cytosolic cytochrome c release. STC-1 pretreatment significantly blocked mitochondrial ROS generation and cytosolic cytochrome C release. TGF-β treatment also induced upregulation of E-cadherin, collagen IV and fibronectin and downregulation of N-cadherin, which was counteracted by STC-1 pretreatment.


Restoration of ER-mitochondrial calcium signal by STC-1 attenuated ER stress induced apoptosis and fibrosis in HK2 cells. The present study suggested that the STC-1 may serve as a potential treatment for renal fibrotic disease.


  • Government Support - Non-U.S.