MIF protects against oxygen-glucose deprivation-induced ototoxicity in HEI-OC1 cochlear cells by enhancement of Akt-Nrf2-HO-1 pathway

Zhu, Wei; Jin, Xin; Ma, Yong-Chi; Liu, Zhi-Biao

doi:10.1016/j.bbrc.2018.06.058

Cited by 18 publications

(11 citation statements)

References 21 publications

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“…31,32 Our previous study showed that MIF protected cochlear cells from oxygen-glucose deprivation (OGD)induced injury. 33 Therefore, the present study showed that SSNHL patients with the À173C allele had higher MIF levels and, considering the apparent protective role of MIF in the cochlea, also had improved cochlear steroid responsiveness.…”

Section: Discussionsupporting

confidence: 54%

Correlations of MIF polymorphism and serum levels of MIF with glucocorticoid sensitivity of sudden sensorineural hearing loss

Zhu

Jin

et al. 2019

J Int Med Res

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Objective This study explored the relationship between macrophage migration inhibitory factor (MIF) gene polymorphism (−173G/C) and glucocorticoid sensitivity in sudden sensorineural hearing loss (SSNHL). Methods A total of 120 patients with SSNHL were divided into a glucocorticoid-sensitive group and a glucocorticoid-resistant group. A group of 93 healthy individuals served as the control group. Serum MIF levels of the participants were measured and MIF genotyping was performed. Results The frequency of the MIF −173C allele was significantly higher in glucocorticoid-sensitive patients than in glucocorticoid-resistant patients. Serum MIF levels were significantly higher in SSNHL patients than in healthy controls, and higher in the glucocorticoid-sensitive group than in the glucocorticoid-resistant group of SSNHL patients, which was unexpected. Compared with patients with the GG genotype, patients with the −173C allele (GC and CC genotypes) had significantly higher levels of serum MIF and superoxide dismutase activity and lower levels of tumor necrosis factor-α and malondialdehyde. Conclusion The MIF −173G/C polymorphism is associated with glucocorticoid sensitivity in SSNHL patients. The C allele can result in higher MIF production, reduced oxidative stress, and greater glucocorticoid sensitivity.

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Section: Discussionsupporting

confidence: 54%

Correlations of MIF polymorphism and serum levels of MIF with glucocorticoid sensitivity of sudden sensorineural hearing loss

Zhu

Jin

et al. 2019

J Int Med Res

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“…In addition, Nrf2, a key redoxregulated gene, has a critical role in alleviating oxidative stress, and the level of Nrf2 in the nuclei is decreased in patients with neurological disorders (Niedzielska et al, 2016). Recently, accumulating studies have reported that activated nuclear Nrf2 further regulates several endogenous redox-regulated enzymes, such as heme oxygenase-1 (HO-1) via the PI3K/Akt pathways (Zhu et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

The Protective Effect of DiDang Tang Against AlCl3-Induced Oxidative Stress and Apoptosis in PC12 Cells Through the Activation of SIRT1-Mediated Akt/Nrf2/HO-1 Pathway

et al. 2020

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Aluminum (Al) is considered a pathological factor for various neurological and neurodegenerative diseases, such as Alzheimer's disease (AD) and Parkinson's disease (PD). The neurotoxicity of aluminum can cause oxidative brain damage, trigger apoptosis, and ultimately cause irreversible damage to neurons. DiDang Tang (DDT), a classic formula within traditional Chinese medicine for promoting blood circulation and removing blood stasis and collaterals, is widely used for the treatment of stroke and AD. In this study, models of oxidative stress and apoptosis were established using AlCl 3 , and the effects of DDT were evaluated. We found that DDT treatment for 48 h significantly increased cell viability and reduced the release of lactate dehydrogenase (LDH) in AlCl 3induced PC12 cells. Moreover, DDT attenuated AlCl 3 -induced oxidative stress damage by increasing antioxidant activities and apoptosis through mitochondrial apoptotic pathways. Additionally, DDT treatment significantly activated the Sirtuin 1 (SIRT1) -mediated Akt/ nuclear factor E2 related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathways to limit AlCl 3mediated neurotoxicity. Our data indicated that DDT potently inhibited AlCl 3 -induced oxidative-stress damage and apoptosis in neural cells by activating the SIRT1-mediated Akt/Nrf2/HO-1 pathway, which provides further support for the beneficial effects of DDT on Al-induced neurotoxicity.

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“…Among the identified signaling pathways, PI3K is a powerful candidate for improving the survival of HCs. In recent decades, intensive investigations have been carried out towards PI3K pathway activation for the treatment of aminoglycoside-induced [60][61][62], sudden sensory neural [63,64], noise-induced [65,66], and autosomaldominant hereditary [67] hearing loss. PI3K plays a key role in various cellular processes, including cell survival, growth, and proliferation.…”

Section: Pi3k/akt Signalingmentioning

confidence: 99%

“…By identifying the different expressions of miRNAs in SSNHL patients, it was found that most of the significantly altered miRNAs were abundant in the nervous system, which indicated that putative targeted miRNAs are enriched in the PI3K/Akt, Ras, and MAPK signaling pathways to affect the survival of cochlea HCs [63]. In terms of exhibiting a protective effect on cochlear cells, macrophage migration inhibitory factor (MIF), as a proinflammatory cytokine, can protect cochlear cells from oxygen-glucose deprivation-(OGD-) induced injury by activating the Akt-Nrf2-HO-1 pathway 3 Neural Plasticity [64]. It is known that insulin-like growth factor 1 (IGF1) plays an important role in the treatment of SNHL [78][79][80].…”

Section: Pi3k/akt Signalingmentioning

confidence: 99%

Key Signaling Pathways Regulate the Development and Survival of Auditory Hair Cells

et al. 2021

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The loss of auditory sensory hair cells (HCs) is the most common cause of sensorineural hearing loss (SNHL). As the main sound transmission structure in the cochlea, it is necessary to maintain the normal shape and survival of HCs. In this review, we described and summarized the signaling pathways that regulate the development and survival of auditory HCs in SNHL. The role of the mitogen-activated protein kinase (MAPK), phosphoinositide-3 kinase/protein kinase B (PI3K/Akt), Notch/Wnt/Atoh1, calcium channels, and oxidative stress/reactive oxygen species (ROS) signaling pathways are the most relevant. The molecular interactions of these signaling pathways play an important role in the survival of HCs, which may provide a theoretical basis and possible therapeutic interventions for the treatment of hearing loss.

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MIF protects against oxygen-glucose deprivation-induced ototoxicity in HEI-OC1 cochlear cells by enhancement of Akt-Nrf2-HO-1 pathway

Cited by 18 publications

References 21 publications

Correlations of MIF polymorphism and serum levels of MIF with glucocorticoid sensitivity of sudden sensorineural hearing loss

Correlations of MIF polymorphism and serum levels of MIF with glucocorticoid sensitivity of sudden sensorineural hearing loss

The Protective Effect of DiDang Tang Against AlCl3-Induced Oxidative Stress and Apoptosis in PC12 Cells Through the Activation of SIRT1-Mediated Akt/Nrf2/HO-1 Pathway

Key Signaling Pathways Regulate the Development and Survival of Auditory Hair Cells

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