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Article

Role of Calbindin-D28k in Diabetes-Associated Advanced Glycation End-Products-Induced Renal Proximal Tubule Cell Injury

by
Kuo-How Huang
1,†,
Siao-Syun Guan
2,
Wei-Han Lin
3,
Cheng-Tien Wu
4,
Meei-Ling Sheu
5,†,
Chih-Kang Chiang
3,6 and
Shing-Hwa Liu
3,7,8,*
1
Department of Urology, College of Medicine and Hospital, National Taiwan University, Taipei 100, Taiwan
2
Institute of Nuclear Energy Research, Atomic Energy Council, Taoyuan 325, Taiwan
3
Institute of Toxicology, College of Medicine, National Taiwan University, Taipei 100, Taiwan
4
Division of General Surgery, Department of Surgery, Shuang Ho Hospital, Taipei Medical University, New Taipei City 235, Taiwan
5
Institute of Biomedical Sciences, National Chung Hsing University, Taichung 402, Taiwan
6
Departments of Integrated Diagnostics & Therapeutics and Internal Medicine, College of Medicine and Hospital, National Taiwan University, Taipei 100, Taiwan
7
Department of Medical Research, China Medical University Hospital, China Medical University, Taichung 404, Taiwan
8
Department of Pediatrics, National Taiwan University Hospital, Taipei 100, Taiwan
*
Author to whom correspondence should be addressed.
†
These authors contributed equally to this work.
Cells 2019, 8(7), 660; https://doi.org/10.3390/cells8070660
Submission received: 16 May 2019 / Revised: 27 June 2019 / Accepted: 29 June 2019 / Published: 30 June 2019
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Abstract

Diabetes-associated advanced glycation end-products (AGEs) can increase extracellular matrix (ECM) expression and induce renal fibrosis. Calbindin-D28k, which plays a role in calcium reabsorption in renal distal convoluted tubules, is increased in a diabetic kidney. The role of calbindin-D28k in diabetic nephropathy still remains unclear. Here, calbindin-D28k protein expression was unexpectedly induced in the renal tubules of db/db diabetic mice. AGEs induced the calbindin-D28k expression in human renal proximal tubule cells (HK2), but not in mesangial cells. AGEs induced the expression of fibrotic molecules, ECM proteins, epithelial-mesenchymal transition (EMT) markers, and endoplasmic reticulum (ER) stress-related molecules in HK2 cells, which could be inhibited by a receptor for AGE (RAGE) neutralizing antibody. Calbindin-D28k knockdown by siRNA transfection reduced the cell viability and obviously enhanced the protein expressions of fibrotic factors, EMT markers, and ER stress-related molecules in AGEs-treated HK2 cells. Chemical chaperone 4-Phenylbutyric acid counteracted the AGEs-induced ER stress and ECM and EMT markers expressions. Calbindin-D28k siRNA in vivo delivery could enhance renal fibrosis in db/db diabetic mice. These findings suggest that inducible calbindin-D28k protects against AGEs/RAGE axis-induced ER stress-activated ECM induction and cell injury in renal proximal tubule cells.
Keywords: advanced glycation end products; renal proximal tubule; calbindin-D28k; renal fibrosis; diabetic nephropathy advanced glycation end products; renal proximal tubule; calbindin-D28k; renal fibrosis; diabetic nephropathy

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MDPI and ACS Style

Huang, K.-H.; Guan, S.-S.; Lin, W.-H.; Wu, C.-T.; Sheu, M.-L.; Chiang, C.-K.; Liu, S.-H. Role of Calbindin-D28k in Diabetes-Associated Advanced Glycation End-Products-Induced Renal Proximal Tubule Cell Injury. Cells 2019, 8, 660. https://doi.org/10.3390/cells8070660

AMA Style

Huang K-H, Guan S-S, Lin W-H, Wu C-T, Sheu M-L, Chiang C-K, Liu S-H. Role of Calbindin-D28k in Diabetes-Associated Advanced Glycation End-Products-Induced Renal Proximal Tubule Cell Injury. Cells. 2019; 8(7):660. https://doi.org/10.3390/cells8070660

Chicago/Turabian Style

Huang, Kuo-How, Siao-Syun Guan, Wei-Han Lin, Cheng-Tien Wu, Meei-Ling Sheu, Chih-Kang Chiang, and Shing-Hwa Liu. 2019. "Role of Calbindin-D28k in Diabetes-Associated Advanced Glycation End-Products-Induced Renal Proximal Tubule Cell Injury" Cells 8, no. 7: 660. https://doi.org/10.3390/cells8070660

APA Style

Huang, K.-H., Guan, S.-S., Lin, W.-H., Wu, C.-T., Sheu, M.-L., Chiang, C.-K., & Liu, S.-H. (2019). Role of Calbindin-D28k in Diabetes-Associated Advanced Glycation End-Products-Induced Renal Proximal Tubule Cell Injury. Cells, 8(7), 660. https://doi.org/10.3390/cells8070660

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