2D Ti3C2TxMXene couples electrical stimulation to promote proliferation and neural differentiation of neural stem cells

Guo, Rongrong; Xing, Miao; Zhao, Wanyu; Zhou, Shan; Hu, Yangnan; Liao, Menghui; Wang, Shengping; Yang, Xiaowei; Chai, Renjie; Tang, Mingliang

doi:10.1016/j.actbio.2020.12.035

Cited by 95 publications

(90 citation statements)

References 65 publications

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“…Hearing loss is one of the major disabilities worldwide, which is often induced by loss of sensory hair cells [25][26][27][28][29] and spiral ganglion neurons [30][31][32][33][34] in the inner ear cochlea. Hearing loss could be caused by genetic factors, aging, chronic cochlear infections, infectious diseases, ototoxic drugs, and noise exposure [35][36][37][38][39][40][41][42], and genetic factors account for around 70% of the hearing loss.…”

Section: Discussionmentioning

confidence: 99%

Next-Generation Sequencing Identifies Pathogenic Variants in HGF, POU3F4, TECTA, and MYO7A in Consanguineous Pakistani Deaf Families

et al. 2021

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Background. Approximately 70% of congenital deafness is attributable to genetic causes. Incidence of congenital deafness is known to be higher in families with consanguineous marriage. In this study, we investigated the genetic causes in three consanguineous Pakistani families segregating with prelingual, severe-to-profound deafness. Results. Through targeted next-generation sequencing of 414 genes known to be associated with deafness, homozygous variants c.536del (p. Leu180Serfs ∗ 20) in TECTA, c.3719 G>A (p. Arg1240Gln) in MYO7A, and c.482+1986_1988del in HGF were identified as the pathogenic causes of enrolled families. Interestingly, in one large consanguineous family, an additional c.706G>A (p. Glu236Lys) variant in the X-linked POU3F4 gene was also identified in multiple affected family members causing deafness. Genotype-phenotype cosegregation was confirmed in all participating family members by Sanger sequencing. Conclusions. Our results showed that the genetic causes of deafness are highly heterogeneous. Even within a single family, the affected members with apparently indistinguishable clinical phenotypes may have different pathogenic variants.

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Section: Discussionmentioning

confidence: 99%

Next-Generation Sequencing Identifies Pathogenic Variants in HGF, POU3F4, TECTA, and MYO7A in Consanguineous Pakistani Deaf Families

et al. 2021

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“…Hair cells (HCs) and spiral ganglion neurons (SGNs) are the main structures of sound transmission in the cochlea [6][7][8][9][10][11]. The auditory sensory HCs are located in the organ of Corti and include a row of inner hair cells (IHCs), three rows of outer hair cells (OHCs), and supporting cells.…”

Section: Introductionmentioning

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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“…In the inner ear, the mechanical vibration of sound wave was transformed into the electric signals by cochlear hair cells ( Wang et al, 2017 ; Liu Y. et al, 2019 ; Qi et al, 2019 , 2020 ; Zhang Y. et al, 2020 ); while spiral ganglion neurons mainly function as the neural auditory transduction cells ( Sun et al, 2016 ; Guo et al, 2019 , 2021 ; Liu W. et al, 2019b ; Zhao et al, 2019 ). Noise induced hearing loss includes damage of cochlear hair cells ( Liu et al, 2016 ; He et al, 2017 , 2021 ; Zhou et al, 2020 ; Cheng et al, 2021 ; Fu et al, 2021 ), cochlear supporting cells ( Lu et al, 2017 ; Cheng et al, 2019 ; Tan et al, 2019 ; Zhang S. et al, 2019 , 2020 ; Zhang Y. et al, 2020 ; Chen et al, 2021 ), spiral ganglion neurons ( Guo et al, 2016 , 2020 , 2021 ; Sun et al, 2016 ; Liu et al, 2021 ) and ribbon synaptopathy ( Furman et al, 2013 ; Shi et al, 2013 ; Kujawa and Liberman, 2015 ; Liberman et al, 2015 ; Bakay et al, 2018 ; Fernandez et al, 2020 ; Kohrman et al, 2020 ; Tserga et al, 2020a ; Wei et al, 2020 ; Song et al, 2021 ). It has been reported that the wave I amplitude of the auditory brainstem response (ABR) is permanently reduced and ribbon synapses between inner hair cells (IHCs) and spiral ganglion nerves are damaged after exposure to short-duration medium intensity noise ( Liberman et al, 2015 ; Fernandez et al, 2020 ; Wei et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

Disruption of Glutamate Release and Uptake-Related Protein Expression After Noise-Induced Synaptopathy in the Cochlea

Ma¹,

Zhang²,

She³

et al. 2021

Front. Cell Dev. Biol.

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High-intensity noise can cause permanent hearing loss; however, short-duration medium-intensity noise only induces a temporary threshold shift (TTS) and damages synapses formed by inner hair cells (IHCs) and spiral ganglion nerves. Synaptopathy is generally thought to be caused by glutamate excitotoxicity. In this study, we investigated the expression levels of vesicle transporter protein 3 (Vglut3), responsible for the release of glutamate; glutamate/aspartate transporter protein (GLAST), responsible for the uptake of glutamate; and Na+/K+-ATPase α1 coupled with GLAST, in the process of synaptopathy in the cochlea. The results of the auditory brainstem response (ABR) and CtBP2 immunofluorescence revealed that synaptopathy was induced on day 30 after 100 dB SPL noise exposure in C57BL/6J mice. We found that GLAST and Na+/K+-ATPase α1 were co-localized in the cochlea, mainly in the stria vascularis, spiral ligament, and spiral ganglion cells. Furthermore, Vglut3, GLAST, and Na+/K+-ATPase α1 expression were disrupted after noise exposure. These results indicate that disruption of glutamate release and uptake-related protein expression may exacerbate the occurrence of synaptopathy.

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2D Ti3C2TxMXene couples electrical stimulation to promote proliferation and neural differentiation of neural stem cells

Cited by 95 publications

References 65 publications

Next-Generation Sequencing Identifies Pathogenic Variants in HGF, POU3F4, TECTA, and MYO7A in Consanguineous Pakistani Deaf Families

Next-Generation Sequencing Identifies Pathogenic Variants in HGF, POU3F4, TECTA, and MYO7A in Consanguineous Pakistani Deaf Families

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

Disruption of Glutamate Release and Uptake-Related Protein Expression After Noise-Induced Synaptopathy in the Cochlea

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