Differential Levels of Endoplasmic Reticulum Stress in Peripheral Blood Mononuclear Cells from Patients with Sudden Sensorineural Hearing Loss

Zhi-biao, Liu; Fei, Bing; Du, Xiaoping; Dai, Yifei; She, Wandong

doi:10.12659/msm.927328

Cited by 2 publications

(2 citation statements)

References 32 publications

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“…Levels of p-PERK, p-eIF2a, ATF4, and CHOP were significantly elevated in PBMCs extracted from patients with SSNHL compared with those from healthy controls. After treatment with a corticosteroid, levels of ATF4 and CHOP were significantly reduced in PBMCs from improved patients, although neither ATF4 nor CHOP changed significantly in PBMCs from unimproved patients [ 36 ]. Thus, UPR mediated through PERK may play a significant role in the pathogenesis of SSNHL, and the response to ER stress may be one of the factors affecting prognosis after corticosteroid treatment.…”

Section: Resultsmentioning

confidence: 99%

“…These findings may support the hypothesis that thrombus formation in the cochlea causes hearing loss. Levels of PERK pathway-related proteins, including p-PERK, p-eIF2a, ATF4, and CHOP, were significantly elevated in PBMCs extracted from patients with SSNHL compared with those from healthy controls [ 36 ]. Thus, UPR mediated through PERK pathway may play a significant role in the pathogenesis of SSNHL.…”

Section: Discussionmentioning

confidence: 99%

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Update on Findings about Sudden Sensorineural Hearing Loss and Insight into Its Pathogenesis

Yamada

Kita

Shinmura

et al. 2022

JCM

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Sudden sensorineural hearing loss (SSNHL) is routinely encountered and is one of the most common emergent diseases in otolaryngology clinics. However, the etiology of SSNHL remains unclear. Due to the inaccessibility of the living human inner ear for biopsy, studies investigating the etiology of SSNHL have been performed by analyzing data obtained from examinations using peripheral blood or imaging. We updated the findings obtained from serological, magnetic resonance imaging, genetic, and viral examinations to reveal the etiology of SSNHL. Regarding viral examination, we focused on sensorineural hearing loss associated with coronavirus disease (COVID-19) because the number of correlated reports has been increasing after the outbreak. The updated findings revealed the following three possible mechanisms underlying the development of SSNHL: thrombosis and resulting vascular obstruction in the cochlea, asymptomatic viral infection and resulting damage to the cochlea, and cochlear inflammation and resulting damage to the cochlea. Thrombosis and viral infection are predominant, and cochlear inflammation can be secondarily induced through viral infection or even thrombosis. The findings about sensorineural hearing loss associated with COVID-19 supported the possibility that asymptomatic viral infection is one of the etiologies of SSNHL, and the virus can infect inner ear tissues and directly damage them.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Update on Findings about Sudden Sensorineural Hearing Loss and Insight into Its Pathogenesis

Yamada

Kita

Shinmura

et al. 2022

JCM

View full text Add to dashboard Cite

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Inhibition of Extracellular Signal-Regulated Kinase Downregulates Endoplasmic Reticulum Stress-Induced Apoptosis and Decreases Brain Injury in a Cardiac Arrest Rat Model

Yuan

et al. 2022

Physiol Res

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Cerebral ischemia-reperfusion injury (CIRI) is the predominant cause of neurological disability after cardiac arrest/cardiopulmonary resuscitation (CA/CPR). The endoplasmic reticulum stress (ERs)-induced apoptosis plays an important role in neuronal survival/death in CIRI. Our previous studies reported that the extracellular signal-regulated kinase (ERK) inhibitor, PD98059, alleviates CIRI after CA/CPR. Whether ERs-induced apoptosis is involved in the neuroprotection of PD98059 remains unknown. This study aims to investigate the effects of ERK inhibition by PD98059 on ERs-induced apoptosis after CIRI in the CA/CPR rat model. The baseline characteristics of male adult Sprague-Dawley (SD) rats in all groups were evaluated before CA/CPR. The SD rats that survived from CA/CPR were randomly divided into 3 groups (n=12/group): normal saline group (1 ml/kg), dimethylsulfoxide (DMSO, the solvent of PD98059, 1 ml/kg) group, PD98059 group (0.3 mg/kg). Another 12 SD rats were randomly selected as the Sham group. Twenty-four hours after resuscitation, neural injury was assessed by survival rate, neurological deficit scores (NDS) and Nissl staining; apoptosis of brain cells was detected using terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining; mRNA expression and protein levels of ERs-related protein BIP, PERK, ATF4 and CHOP were checked with RT-PCR and Western Blot. The results showed that there were no significant differences in baseline characteristics before CA/CPR among all groups. PD98059 significantly improved survival rate and NDS, increased the Nissl bodies in neurons, reduced apoptosis, downregulated the mRNA transcription and expression levels of BIP, PERK, ATF4 and CHOP at 24 h after CA/CPR. Our results demonstrate that inhibition of ERK by PD98059 alleviates ERs-induced apoptosis via BIP-PERK-ATF4-CHOP signaling pathway and mitigates CIRI in the CA/CPR rat model.

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Differential Levels of Endoplasmic Reticulum Stress in Peripheral Blood Mononuclear Cells from Patients with Sudden Sensorineural Hearing Loss

Cited by 2 publications

References 32 publications

Update on Findings about Sudden Sensorineural Hearing Loss and Insight into Its Pathogenesis

Update on Findings about Sudden Sensorineural Hearing Loss and Insight into Its Pathogenesis

Inhibition of Extracellular Signal-Regulated Kinase Downregulates Endoplasmic Reticulum Stress-Induced Apoptosis and Decreases Brain Injury in a Cardiac Arrest Rat Model

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