دورية أكاديمية
Endoplasmic reticulum stress associated apoptosis as a novel mechanism in indoxyl sulfate‑induced cardiomyocyte toxicity.
| العنوان: | Endoplasmic reticulum stress associated apoptosis as a novel mechanism in indoxyl sulfate‑induced cardiomyocyte toxicity. |
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| المؤلفون: | Tan X; Shanghai Key Laboratory of Kidney and Blood Purification, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China., Cao XS; Department of Nephrology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China., Zhang P; Shanghai Key Laboratory of Kidney and Blood Purification, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China., Xiang FF; Department of Nephrology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China., Teng J; Department of Nephrology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China., Zou JZ; Department of Nephrology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China., Ding XQ; Shanghai Key Laboratory of Kidney and Blood Purification, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China. |
| المصدر: | Molecular medicine reports [Mol Med Rep] 2018 Dec; Vol. 18 (6), pp. 5117-5122. Date of Electronic Publication: 2018 Sep 20. |
| نوع المنشور: | Journal Article |
| اللغة: | English |
| بيانات الدورية: | Publisher: D. A. Spandidos Country of Publication: Greece NLM ID: 101475259 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1791-3004 (Electronic) Linking ISSN: 17912997 NLM ISO Abbreviation: Mol Med Rep Subsets: MEDLINE |
| أسماء مطبوعة: | Original Publication: Athens, Greece : D. A. Spandidos |
| مواضيع طبية MeSH: | Apoptosis* , Endoplasmic Reticulum Stress*, Indican/*pharmacology , Myocytes, Cardiac/*drug effects , Myocytes, Cardiac/*metabolism, Animals ; Biomarkers ; Cell Line ; Flow Cytometry ; MAP Kinase Kinase 4/metabolism ; Signal Transduction |
| مستخلص: | 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. |
| فهرسة مساهمة: | Keywords: uremic toxin; indoxyl sulfate; cardiomyocyte; apoptosis; endoplasmic reticulum stress |
| المشرفين على المادة: | 0 (Biomarkers) EC 2.7.12.2 (MAP Kinase Kinase 4) N187WK1Y1J (Indican) |
| تواريخ الأحداث: | Date Created: 20181002 Date Completed: 20190128 Latest Revision: 20220113 |
| رمز التحديث: | 20221213 |
| DOI: | 10.3892/mmr.2018.9496 |
| PMID: | 30272270 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder | تدمد: | 1791-3004 |
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| DOI: | 10.3892/mmr.2018.9496 |