Trehalose protects against cisplatin-induced cochlear hair cell damage by activating TFEB-mediated autophagy

Li, Zhuangzhuang; Yao, Qinke; Tian, Ye; Jiang, Yan; Xu, Maoxiang; Wang, Hui; Xiong, Yuanping; Jia, Fei; Wen, Li; Yu, Dian; Shi, Haibo

doi:10.1016/j.bcp.2021.114904

Cited by 21 publications

(11 citation statements)

References 68 publications

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“…Our previous study determined that cisplatin damaged HEI-OC1 cells appropriately at a concentration of 20 μm for 24 h ( Li et al, 2022 ). HEI-OC1 cells were treated with different Sal concentrations (0–100 μM) for 24 h to determine its toxicity.…”

Section: Resultsmentioning

confidence: 99%

“…Next, the cochlea was cultured on glass coverslips coated with Cell-Tak in four-well plates (BD Biosciences, Franklin Lakes, NJ, United States) with DMEM/F12 growth medium (11330-032; Gibco) containing B-27 supplement (17504-44; Gibco), N-2 supplement (17502-048; Gibco), and ampicillin (50 g/mL, A5354-10ML; Sangon Biotech Co., Ltd.) at 37°C in an incubator environment of 5% CO 2 and 95% O 2 . After incubation for a day, we pretreated cochlear explants with or without Sal (10 μM) and then co-treated them with 20 μM cisplatin for 24 h. Cisplatin at a concentration of 20 μM was selected based on our previous study ( Li et al, 2022 ). After removing the cisplatin-containing medium, the cochlear explants were recovered in normal medium for 36 h.…”

Section: Methodsmentioning

confidence: 99%

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Salubrinal Protects Against Cisplatin-Induced Cochlear Hair Cell Endoplasmic Reticulum Stress by Regulating Eukaryotic Translation Initiation Factor 2α Signalling

Wen

et al. 2022

Front. Mol. Neurosci.

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ObjectiveCisplatin is a broad-spectrum anti-tumour drug commonly used in clinical practice. However, its ototoxicity greatly limits its clinical application, and no effective method is available to prevent this effect. Endoplasmic reticulum stress (ERS) is reportedly involved in cisplatin ototoxicity, but the exact mechanism remains unclear. Therefore, this study aimed to investigate the role of eukaryotic translation initiation factor 2α (eIF2α) signalling and its dephosphorylation inhibitor salubrinal in cisplatin ototoxicity.MethodsWe evaluated whether salubrinal could protect against cisplatin-induced damage in House Ear Institute-Organ of Corti 1 (HEI-OC1) cells and mouse cochlear explants. By knocking down eIF2α, we elucidated the vital role of eIF2α in cisplatin-induced damage in HEI-OC1 cells. Whole-mount immunofluorescent staining and confocal microscopy of mouse cochlear explants and HEI-OC1 cells were performed to analyse cisplatin-induced damage in cochlear hair cells and the auditory cell line.ResultsData suggested salubrinal attenuated cisplatin-induced hair cell injury by inhibiting apoptosis. In addition, salubrinal significantly reduced ERS levels in hair cells via eIF2α signalling, while eIF2α knockdown inhibited the protective effect of salubrinal.SignificanceSalubrinal and eIF2α signalling play a role in protecting against cisplatin-induced ototoxicity, and pharmacological inhibition of eIF2α-mediated ERS is a potential treatment for cisplatin-induced damage in the cochlea and HEI-OC1 cells.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Salubrinal Protects Against Cisplatin-Induced Cochlear Hair Cell Endoplasmic Reticulum Stress by Regulating Eukaryotic Translation Initiation Factor 2α Signalling

Wen

et al. 2022

Front. Mol. Neurosci.

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“…Moderate autophagy has the positive effect to resist stress damage and inhibit cellular apoptosis 15 . Trehalose protected many pathological conditions‐induced apoptosis by promoting autophagy 16,17 . All this evident indicated that Trehalose might prevent the lipotoxicity‐induced apoptosis of osteoblasts by enhancing autophagy.…”

Section: Introductionmentioning

confidence: 94%

RETRACTED: Trehalose improves palmitic acid‐induced apoptosis of osteoblasts by regulating SIRT3‐medicated autophagy via the AMPK/mTOR/ULK1 pathway

et al. 2022

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Accumulation of lipid substances decreased the activity of osteoblasts. Trehalose is a typical stress metabolite to form a protective membrane on cell surface which has been demonstrated to regulate lipid metabolism. This activity of Trehalose indicates the potential effect of osteoporosis treatment. Our study aimed to determine the therapeutic effect of Trehalose in high fat-induced osteoporosis. We used palmitic acid (PA) to mimic the state of high fat and observed the apoptosis ratio of osteoblasts increased. After adding Trehalose, the apoptosis ratio decreased obviously. Autophagy is a regulatory means involved in the process of apoptosis.We detected the autophagy protein and found that the expression of Beclin-1, Atg5, and LC3 II increased, and p62 decreased after Trehalose treatment. When adding an autophagy inhibitor (3-MA), the expression of Beclin-1, Atg5, and LC3 II decreased, and p62 increased. These results indicated autophagy was an important factor involved in the preventive effect of Trehalose in PA-induced apoptosis. SIRT3 is a mitochondrial gene that can inhibit apoptosis, which has been reported to promote autophagy. We used SIRT3-siRNA to silence the expression of SIRT3 and found the effect of Trehalose was counteracted. The apoptosis ratio increased and the expression of Beclin-1, Atg5, and LC3 II decreased, p62 increased. Additionally, we also fed the mice with a high-fat diet (HFD) and intragastrical Trehalose. The results showed that Trehalose could inhibit the bone mass loss with HFD. Our study revealed the effect and mechanism of Trehalose in the treatment of osteoporosis.

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“…Similarly, pretreatment with novel RIPK1 inhibitors, Cpd-71 and Cpd-2 mitigated CP nephropathy ( Wang et al, 2019 ; Li C. et al, 2022 ). Likewise, Liu et al (2022b) found that the novel heat shock protein (Hsp) 90 inhibitor, C-316-1 facilitates ubiquitination and degradation of RIPK1, thereby inhibiting RIPK1-mediated necroptosis and subsequently attenuating CP-induced AKI. Recently, several investigators further emphasized the significance of this contribution by showing that the protective and detrimental effects of various proteins in the CP-induced AKI model were mediated via modulation of necroptosis signaling.…”

Section: Necroptosis In Cp-induced Acute Kidney Injury (Aki)mentioning

confidence: 99%

Autophagy and necroptosis in cisplatin-induced acute kidney injury: Recent advances regarding their role and therapeutic potential

Alassaf

Attia

2023

Front. Pharmacol.

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Cisplatin (CP) is a broad-spectrum antineoplastic agent, used to treat many different types of malignancies due to its high efficacy and low cost. However, its use is largely limited by acute kidney injury (AKI), which, if left untreated, may progress to cause irreversible chronic renal dysfunction. Despite substantial research, the exact mechanisms of CP-induced AKI are still so far unclear and effective therapies are lacking and desperately needed. In recent years, necroptosis, a novel subtype of regulated necrosis, and autophagy, a form of homeostatic housekeeping mechanism have witnessed a burgeoning interest owing to their potential to regulate and alleviate CP-induced AKI. In this review, we elucidate in detail the molecular mechanisms and potential roles of both autophagy and necroptosis in CP-induced AKI. We also explore the potential of targeting these pathways to overcome CP-induced AKI according to recent advances.

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Trehalose protects against cisplatin-induced cochlear hair cell damage by activating TFEB-mediated autophagy

Cited by 21 publications

References 68 publications

Salubrinal Protects Against Cisplatin-Induced Cochlear Hair Cell Endoplasmic Reticulum Stress by Regulating Eukaryotic Translation Initiation Factor 2α Signalling

Salubrinal Protects Against Cisplatin-Induced Cochlear Hair Cell Endoplasmic Reticulum Stress by Regulating Eukaryotic Translation Initiation Factor 2α Signalling

RETRACTED: Trehalose improves palmitic acid‐induced apoptosis of osteoblasts by regulating SIRT3‐medicated autophagy via the AMPK/mTOR/ULK1 pathway

Autophagy and necroptosis in cisplatin-induced acute kidney injury: Recent advances regarding their role and therapeutic potential

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