Molecular Behavior of HMGB1 in the Cochlea Following Noise Exposure and in vitro

Xiao, Lv; Sun, Yan; Liu, Chengqi; Zheng, Zhong; Shen, Ying; Xia, Liang; Yang, Guang; Feng, Yuanming

doi:10.3389/fcell.2021.642946

Cited by 4 publications

(4 citation statements)

References 54 publications

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“…Moreover, upregulation of HMGB1 expression in glial cells of the spiral ganglion regions was linked to cochlear pathogenesis after acoustic trauma. 24 Similar changes in HMGB1 expression were also observed in the SGNs of amikacin-treated rats. 67 Previous studies have shown that HMGB1 can promote neural stem cell proliferation.…”

Section: Discussionsupporting

confidence: 53%

“…22 Two recent studies have shown that abnormal HMGB1 expression in the mouse cochlea is associated with noise-induced hearing loss and contributes to the ototoxicity of cisplatin to the inner ear. [23][24][25] In a recent study, Xiao et al reported on the cytoplasmic accumulation of HMGB1 in cochlear hair cells, which mediated noise-induced cochlear damage. 26 While the crucial role of HMGB1 in the cochlea was confirmed, its exact function of HMGB1 in the mammalian auditory systems remained ambiguous.…”

Section: Introductionmentioning

confidence: 99%

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Developmental expression of high-mobility group box 1 (HMGB1) in the mouse cochlea

Liu,

Ming,

Zhao

et al. 2023

Eur J Histochem

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The expression changes of high-mobility group box 1 (HMGB1) in the mouse cochlea have recently been implicated in noise-induced hearing loss, suggesting that HMGB1 participates in regulating cochlear function. However, the precise role of HMGB1 in the auditory system remains largely unclear. This study aimed to investigate its function in the developing mouse cochlea by examining the expression pattern of HMGB1 in the mouse cochlea from embryonic day (E) 18.5 to postnatal day (P) 28 using double immunofluorescence on frozen sections. Our findings revealed that HMGB1 was extensively expressed in the cell nucleus across various regions of the mouse cochlea, including the organ of Corti. Furthermore, its expression underwent developmental regulation during mouse cochlear development. Specifically, HMGB1 was found to be localized in the tympanic border cells at each developmental stage, coinciding with the gradual anatomical in this region during development. In addition, HMGB1 was expressed in the greater epithelial ridge (GER) and supporting cells of the organ of Corti, as validated by the supporting cell marker Sox2 at P1 and P8. However, at P14, the expression of HMGB1 disappeared from the GER, coinciding with the degeneration of the GER into the inner sulcus cells. Moreover, we observed that HMGB1 co-localized with Ki-67-positive proliferating cells in several cochlear regions during late embryonic and early postnatal stages, including the GER, the tympanic border cells, cochlear lateral wall, and cochlear nerves. Furthermore, by dual-staining Ki-67 with neuronal marker TUJ1 and glial marker Sox10, we determined the expression of Ki-67 in the neonatal glial cells. Our spatial-temporal analysis demonstrated that HMGB1 exhibited distinct expression patterns during mouse cochlear development. The co-localization of HMGB1 with Ki-67-positive proliferating cells suggested that HMGB1 may play a role in cochlear development.

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Section: Discussionsupporting

confidence: 53%

Section: Introductionmentioning

confidence: 99%

Developmental expression of high-mobility group box 1 (HMGB1) in the mouse cochlea

Liu,

Ming,

Zhao

et al. 2023

Eur J Histochem

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“…Using a guinea pig model of noise-induced hearing loss, an increase in HMGB1 expression was observed in the cochlea after noise exposure, while a decrease in HMGB1 expression was noted in the cochlea after pretreatment with dexamethasone [40]. In vitro experiments conducted on a mouse auditory cell line demonstrated that knocking down the HMGB1 gene could protect cells from damage induced by hydrogen peroxide stress [41]. Moreover, inhibiting HMGB1 using neutralizing anti-HMGB1 antibodies before noise exposure successfully reduced oxidative stress and subsequent inflammation [42].…”

Section: Discussionmentioning

confidence: 98%

HMGB1 Carried by Small Extracellular Vesicles Potentially Plays a Role in Promoting Acquired Middle Ear Cholesteatoma

Łuczak,

Dżaman,

Zaręba

et al. 2023

Diagnostics

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Cholesteatoma is a specific medical condition involving the abnormal, non-cancerous growth of skin-like tissue in the middle ear, potentially leading to a collection of debris and even infections. The receptor for advanced glycation (RAGE) and its ligand, high-mobility box 1 (HMGB1), are both known to be overexpressed in cholesteatoma and play a potential role in the pathogenesis of the disease. In this study, we investigated the role of small extracellular vesicles (sEVs) in carrying HMGB1 and inducing disease-promoting effects in cholesteatoma. No significant differences in the concentration of isolated sEVs in the plasma of cholesteatoma patients (n = 17) and controls (n = 22) were found (p > 0.05); however, cholesteatoma-derived sEVs carried significantly higher levels of HMGB1 (p < 0.05). In comparison to sEVs isolated from the plasma of controls, cholesteatoma-derived sEVs significantly enhanced keratinocyte proliferation and IL-6 production (p < 0.05), potentially by engaging multiple activation pathways including MAPKp44/p42, STAT3, and the NF-κB pathway. Thus, HMGB1(+) sEVs emerge as a novel factor potentially promoting cholesteatoma progression.

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“…HMGB1 acts as an indicator of cell damage, which accelerates inflammation in neighbor cells and stimulates professional scavengers. Its direct binding to the toll-like receptor 4 (TLR4) initiates NIHL via the NF-κB and MAPK signaling pathways 59 . Translocation of HMGB1 from the nucleus to the cytosol is the prerequisite for its intracellular function and subsequent cellular release.…”

Section: Underlying Mechanisms and Therapeutic Strategiesmentioning

confidence: 99%

Intrinsic mechanism and pharmacologic treatments of noise-induced hearing loss

Xu¹,

Gu²,

Wang³

et al. 2023

Theranostics

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Noise accounts for one-third of hearing loss worldwide. Regretfully, noise-induced hearing loss (NIHL) is deemed to be irreversible due to the elusive pathogenic mechanisms that have not been fully elucidated. The complex interaction between genetic and environmental factors, which influences numerous downstream molecular and cellular events, contributes to the NIHL. In clinical settings, there are no effective therapeutic drugs other than steroids, which are the only treatment option for patients with NIHL. Therefore, the need for treatment of NIHL that is currently unmet, along with recent progress in our understanding of the underlying regulatory mechanisms, has led to a lot of new literatures focusing on this therapeutic field. The emergence of novel technologies that modify local drug delivery to the inner ear has led to the development of promising therapeutic approaches, which are currently under clinical investigation. In this comprehensive review, we focus on outlining and analyzing the basics and potential therapeutics of NIHL, as well as the application of biomaterials and nanomedicines in inner ear drug delivery. The objective of this review is to provide an incentive for NIHL's fundamental research and future clinical translation.

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Molecular Behavior of HMGB1 in the Cochlea Following Noise Exposure and in vitro

Cited by 4 publications

References 54 publications

Developmental expression of high-mobility group box 1 (HMGB1) in the mouse cochlea

Developmental expression of high-mobility group box 1 (HMGB1) in the mouse cochlea

HMGB1 Carried by Small Extracellular Vesicles Potentially Plays a Role in Promoting Acquired Middle Ear Cholesteatoma

Intrinsic mechanism and pharmacologic treatments of noise-induced hearing loss

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