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Kidney Week

Abstract: FR-PO373

Niban Protein Regulates Apoptosis in HK-2 Cells via Caspase-Dependent Pathway

Session Information

  • CKD: Mechanisms - II
    November 08, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: CKD (Non-Dialysis)

  • 2103 CKD (Non-Dialysis): Mechanisms

Authors

  • Tang, Shiqi, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China
  • Wang, Jianwen, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China
  • Liu, Jishi, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China
  • Zhang, Hao, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China
Background

To investigate whether Niban protein plays a role in renal interstitial fibrosis by regulating apoptosis of renal tubular epithelial cells.

Methods

Unilateral ureteral obstruction (UUO) model was established by using 24 C57B / 6J mice, which were divided into sham operation group, UUO 3 day group, UUO 7 day group and UUO 14 day group. Renal pathological changes were observed by HE staining and Masson staining, Immunohistochemistry was used to detect the expression of Niban, collagen I, collagen III and E-cadherin, Western blot was used to detect the expression of Niban, E-cadherin, collagen I, caspase3, P53, Bip and Chop, TUNEL assays were used to detected apoptosis; Niban siRNA were transfected in HK-2 cells to silence the expression of Niban, Niban plasmid were transfected in HK-2 cells to overexpresse the expression of Niban, Angiotensin II (Ang II) is used to induce apoptosis in HK-2 cells, while tunicamycin (TM) induces endoplasmic reticulum stress response, Western blot was used to detect the expression of Niban, α-SMA, E-cadherin, caspase8, caspase9, caspase12, Bip and Chop.

Results

1. Apoptosis increased in the UUO model, with the development of obstruction, Niban’s expression decreased gradually, the expression of P53, Bip and Chop gradually increased, reached the peak on days 7, and the expression decreased to the normal level on days 14. 2. After AngII stimulates HK-2 cells, Niban expression is decreased and apoptosis is increased. Silencing of Niban up-regulated the levels of caspase 8, caspase 9, α-SMA and apoptosis, while down-regulated the level of E-cadherin. Overexpression of Niban down-regulated the level of caspase 8, caspase 9, α-SMA, and apoptosis, while up-regulated the levels of E-cadherin. 3. After tunicamycin stimulated HK-2 cells, the expression of Niban decreased, compared with the control group,while the endoplasmic reticulum stress marker proteins Bip and Chop increased significantly. Inhibition of Niban expression, the expression of Bip and Chop in HK-2 cells increased, but it was not statistical difference;after stimulation with tunicamycin, the expression of Bip and Chop in HK-2 cells was significantly increased, and there was a statistically significant difference between the two groups compared with Niban siRNA group.

Conclusion

Niban protein is involved in apoptosis regulation in HK-2 cells, and most likely via Caspase-dependent pathway.

Funding

  • Government Support - Non-U.S.