Id1/NR2B Receptor Pathway Regulates Rat Cochlear Sensory Epithelial Cell Survival after Radiation

Chen, Junming; Zhou, Xiaowei; Zou, Tuanming; Wang, Bochen; Yu, Youjun; Lin, Feng Yen; Chen, Kangsong; Lai, Yanbing; Sun, Kai

doi:10.1159/000493084

Cited by 5 publications

(5 citation statements)

References 34 publications

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“…In our cell culture experiments, consistent with many previous inner ear studies [[78], [79], [80], [81], [82]], we also used the HC-like OC-1 cell line, which is an immortalized cochlear sensory epithelial cell line that was derived from the organ of Corti of rats and that expresses multiple HC markers. OC-1 cells were cultured in a 37 °C incubator with 5% CO 2 in MEM supplemented with 20 mM HEPES, 2 mM l -glutamine, 10 mL/L nonessential amino acids, 0.4 μg/mL hydrocortisone, 5 μg/mL insulin, 2.5 μg/mL transferrin, 10 ng/mL EGF, 10% fetal bovine serum (FBS, Gibco, 10099141), 50 μg/mL streptomycin, and 50 units/mL penicillin.…”

Section: Methodsmentioning

confidence: 98%

The nuclear transcription factor FoxG1 affects the sensitivity of mimetic aging hair cells to inflammation by regulating autophagy pathways

et al. 2020

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Inflammation is a self-defense response to protect individuals from infection and tissue damage, but excessive or persistent inflammation can have adverse effects on cell survival. Many individuals become especially susceptible to chronic-inflammation-induced sensorineural hearing loss as they age, but the intrinsic molecular mechanism behind aging individuals' increased risk of hearing loss remains unclear. FoxG1 (forkhead box transcription factor G1) is a key transcription factor that plays important roles in hair cell survival through the regulation of mitochondrial function, but how the function of FoxG1 changes during aging and under inflammatory conditions is unknown. In this study, we first found that FoxG1 expression and autophagy both increased gradually in the low concentration lipopolysaccharide (LPS)-induced inflammation model, while after high concentration of LPS treatment both FoxG1 expression and autophagy levels decreased as the concentration of LPS increased. We then used siRNA to downregulate Foxg1 expression in hair cell-like OC-1 cells and found that cell death and apoptosis were significantly increased after LPS injury. Furthermore, we used d-galactose (D-gal) to create an aging model with hair cell-like OC-1 cells and cochlear explant cultures in vitro and found that the expression of Foxg1 and the level of autophagy were both decreased after D-gal and LPS co-treatment. Lastly, we knocked down the expression of Foxg1 under aged inflammation conditions and found increased numbers of dead and apoptotic cells. Together these results suggest that FoxG1 affects the sensitivity of mimetic aging hair cells to inflammation by regulating autophagy pathways.

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Section: Methodsmentioning

confidence: 98%

The nuclear transcription factor FoxG1 affects the sensitivity of mimetic aging hair cells to inflammation by regulating autophagy pathways

et al. 2020

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“…Cell Culture and Nrf2 KO Cell Line Construction. In our experiments, we used HEI-OC1 cells constructed by the House Ear Institute from the organ of Corti, which is consistent with many previous inner ear studies [14][15][16][17]. This is an immortalized cochlear sensory epithelial cell line that expresses multiple hair cell markers.…”

Section: Methodsmentioning

confidence: 88%

Nrf2 Knockout Affected the Ferroptosis Signaling Pathway against Cisplatin-Induced Hair Cell-Like HEI-OC1 Cell Death

Wang

Gao

et al. 2022

Oxidative Medicine and Cellular Longevity

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Cisplatin is a well-known and widely used anticancer drug with high therapeutic efficacy in solid tumors; however, side effects are common with its use. Because cisplatin can be retained in the cochlea, ototoxicity leading to hearing loss limits its clinical applications. Here, we report that Nrf2 knockout (KO) strongly increased cisplatin resistance in HEI-OC1 cells, which are immortalized cells from the murine organ of Corti. The underlying mechanism of this phenomenon was uncovered, and an important novel therapeutic target for combating cisplatin-induced hearing loss was identified. Preliminary investigations determined that Nrf2 KO markedly decreased TfR1 protein levels and increased GPX4 protein levels. Thus, ferroptosis may protect organisms from cisplatin-induced cell death. Furthermore, Nrf2 KO cells were resistant to the classical ferroptosis inducers RSL3 and erastin, providing solid evidence that Nrf2 KO inhibits ferroptosis and that knocking out Nrf2 may be a new clinical strategy to prevent cisplatin-induced hearing loss.

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“…Our cell culture experiments used the HC‐like OC‐1 cell line, as in many previous studies 28–32 . OC‐1 is an immortalized cochlear sensory epithelial cell line that was derived from the organ of Corti (OC) of rats on postnatal day 5.…”

Section: Methodsmentioning

confidence: 99%

“…SCC‐7 cells were grown in RPMI‐1640 complete medium (Gibco). All cells were incubated in a humidified incubator at 37°C with 5% CO 2 , as in previous studies 30,33 . Cells were subcultured with 0.25% trypsin (Gibco) at 80–90% confluence.…”

Section: Methodsmentioning

confidence: 99%

“…Our cell culture experiments used the HC-like OC-1 cell line, as in many previous studies. [28][29][30][31][32] OC-1 is an immortalized cochlear sensory epithelial cell line that was derived from the organ of Corti (OC) of rats on postnatal day 5. The human NPC cell lines CNE-2 and HNE-1 were kindly provided by Professor Hongling Jin (HUST, Wuhan).…”

Section: Cell Culturementioning

confidence: 99%

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Glutathione carbon dots as an intracellular reactive oxygen species scavenger for reducing cisplatin‐induced ototoxicity

Tu,

Fan,

et al. 2023

VIEW

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It is widely recognized that platinum‐based chemotherapy, particularly cisplatin therapy, can cause ototoxicity. At present, there are no Food and Drug Administration‐approved drugs to prevent or alleviate ototoxicity. Ototoxicity is generally believed to be caused by excessive reactive oxygen species production in the inner ear. Accordingly, a variety of antioxidants have been developed to protect against ototoxicity. To improve the efficiency of drug delivery to the cochlea, here, we synthesized simple and easy‐to‐obtain glutathione carbon dots (GSH CDs) with ultra‐small dimensions. The experimental results revealed that the GSH CDs have strong free‐radical scavenging activity and can restore mitochondrial function, maintain hair cell stability, and protect hair cells from cisplatin‐induced oxidative stress. Thus, GSH CDs may serve as a new therapeutic agent for preventing cisplatin‐induced ototoxicity.

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Id1/NR2B Receptor Pathway Regulates Rat Cochlear Sensory Epithelial Cell Survival after Radiation

Cited by 5 publications

References 34 publications

The nuclear transcription factor FoxG1 affects the sensitivity of mimetic aging hair cells to inflammation by regulating autophagy pathways

The nuclear transcription factor FoxG1 affects the sensitivity of mimetic aging hair cells to inflammation by regulating autophagy pathways

Nrf2 Knockout Affected the Ferroptosis Signaling Pathway against Cisplatin-Induced Hair Cell-Like HEI-OC1 Cell Death

Glutathione carbon dots as an intracellular reactive oxygen species scavenger for reducing cisplatin‐induced ototoxicity

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