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Article

Endoplasmic reticulum stress associated apoptosis as a novel mechanism in indoxyl sulfate‑induced cardiomyocyte toxicity

  • Authors:
    • Xiao Tan
    • Xue‑Sen Cao
    • Pan Zhang
    • Fang‑Fang Xiang
    • Jie Teng
    • Jian‑Zhou Zou
    • Xiao‑Qiang Ding
  • View Affiliations / Copyright

    Affiliations: Shanghai Key Laboratory of Kidney and Blood Purification, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China, Department of Nephrology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China
  • Pages: 5117-5122
    |
    Published online on: September 20, 2018
       https://doi.org/10.3892/mmr.2018.9496
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Abstract

Indoxyl sulfate (IS), a typical uremic toxin, is of great importance in the development of chronic kidney disease. In addition to its nephrotoxicity, previous studies have provided increasing evidence for its cardiovascular toxicity. The mechanism underlying IS‑induced cardiovascular toxicity has been elusive to date. The present study aimed to evaluate whether IS treatment could induce apoptosis of H9C2 cells, and used the endoplasmic reticulum (ER) stress‑modulator 4‑phenylbutyric acid (4‑PBA) to evaluate whether IS‑induced apoptosis is indeed associated with ERS. To evaluate whether IS induces apoptosis in H9C2 cardiomyocytes, cells were exposed to increasing concentrations of IS (500, 1,000, and 2,000 µM) for 24 h, and apoptosis was detected by flow cytometry. To determine whether IS‑induced apoptosis is associated with ERS, cells were divided into 4 groups: control group, PBA group, IS group and PBA+IS group. IS dose‑dependently induced apoptosis, and increased the expression of ER chaperones in H9C2 cells. Additionally, 4‑PBA treatment decreased IS‑induced apoptosis, and reduced ERS‑associated protein expression induced by IS. Therefore, the mechanism may be associated with the CCAAT‑enhancer‑binding protein homologous protein and c‑Jun N‑terminal kinase signaling pathways.
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Copy and paste a formatted citation
Spandidos Publications style
Tan X, Cao XS, Zhang P, Xiang FF, Teng J, Zou JZ and Ding XQ: Endoplasmic reticulum stress associated apoptosis as a novel mechanism in indoxyl sulfate‑induced cardiomyocyte toxicity. Mol Med Rep 18: 5117-5122, 2018.
APA
Tan, X., Cao, X., Zhang, P., Xiang, F., Teng, J., Zou, J., & Ding, X. (2018). Endoplasmic reticulum stress associated apoptosis as a novel mechanism in indoxyl sulfate‑induced cardiomyocyte toxicity. Molecular Medicine Reports, 18, 5117-5122. https://doi.org/10.3892/mmr.2018.9496
MLA
Tan, X., Cao, X., Zhang, P., Xiang, F., Teng, J., Zou, J., Ding, X."Endoplasmic reticulum stress associated apoptosis as a novel mechanism in indoxyl sulfate‑induced cardiomyocyte toxicity". Molecular Medicine Reports 18.6 (2018): 5117-5122.
Chicago
Tan, X., Cao, X., Zhang, P., Xiang, F., Teng, J., Zou, J., Ding, X."Endoplasmic reticulum stress associated apoptosis as a novel mechanism in indoxyl sulfate‑induced cardiomyocyte toxicity". Molecular Medicine Reports 18, no. 6 (2018): 5117-5122. https://doi.org/10.3892/mmr.2018.9496
Copy and paste a formatted citation
x
Spandidos Publications style
Tan X, Cao XS, Zhang P, Xiang FF, Teng J, Zou JZ and Ding XQ: Endoplasmic reticulum stress associated apoptosis as a novel mechanism in indoxyl sulfate‑induced cardiomyocyte toxicity. Mol Med Rep 18: 5117-5122, 2018.
APA
Tan, X., Cao, X., Zhang, P., Xiang, F., Teng, J., Zou, J., & Ding, X. (2018). Endoplasmic reticulum stress associated apoptosis as a novel mechanism in indoxyl sulfate‑induced cardiomyocyte toxicity. Molecular Medicine Reports, 18, 5117-5122. https://doi.org/10.3892/mmr.2018.9496
MLA
Tan, X., Cao, X., Zhang, P., Xiang, F., Teng, J., Zou, J., Ding, X."Endoplasmic reticulum stress associated apoptosis as a novel mechanism in indoxyl sulfate‑induced cardiomyocyte toxicity". Molecular Medicine Reports 18.6 (2018): 5117-5122.
Chicago
Tan, X., Cao, X., Zhang, P., Xiang, F., Teng, J., Zou, J., Ding, X."Endoplasmic reticulum stress associated apoptosis as a novel mechanism in indoxyl sulfate‑induced cardiomyocyte toxicity". Molecular Medicine Reports 18, no. 6 (2018): 5117-5122. https://doi.org/10.3892/mmr.2018.9496
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