Biomimetic 3D bacterial cellulose-graphene foam hybrid scaffold regulates neural stem cell proliferation and differentiation

Guo, Rongrong; Li, Jian; Chen, Chuntao; Xing, Miao; Liao, Menghui; Hu, Yangnan; Liu, Yun; Li, Dan; Zou, Jun; Sun, Dongping; Torre, Vincent; Zhang, Qi; Chai, Renjie; Tang, Mingliang

doi:10.1016/j.colsurfb.2021.111590

Cited by 76 publications

(52 citation statements)

References 71 publications

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“…Damages from a variety of sources can impair HC function, including genetic factors, aging, ototoxic drugs, chronic cochlear infections, and noise exposure [19,[27][28][29][30][31]. In this study, we reported the protective effect of Clusterin deficiency against age-related hearing loss and drug-induced ototoxicity, which are both due to irreversible loss of sensory HCs [32][33][34][35][36] and degeneration of the spiral ganglion neurons (SGNs) [37][38][39][40][41][42]. CLU is an extracellular chaperone protein that has been implicated in diverse physiological and pathophysiological cellular processes.…”

Section: Discussionmentioning

confidence: 97%

Deletion of Clusterin Protects Cochlear Hair Cells against Hair Cell Aging and Ototoxicity

et al. 2021

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Hearing loss is a debilitating disease that affects 10% of adults worldwide. Most sensorineural hearing loss is caused by the loss of mechanosensitive hair cells in the cochlea, often due to aging, noise, and ototoxic drugs. The identification of genes that can be targeted to slow aging and reduce the vulnerability of hair cells to insults is critical for the prevention of sensorineural hearing loss. Our previous cell-specific transcriptome analysis of adult cochlear hair cells and supporting cells showed that Clu, encoding a secreted chaperone that is involved in several basic biological events, such as cell death, tumor progression, and neurodegenerative disorders, is expressed in hair cells and supporting cells. We generated Clu-null mice (C57BL/6) to investigate its role in the organ of Corti, the sensory epithelium responsible for hearing in the mammalian cochlea. We showed that the deletion of Clu did not affect the development of hair cells and supporting cells; hair cells and supporting cells appeared normal at 1 month of age. Auditory function tests showed that Clu-null mice had hearing thresholds comparable to those of wild-type littermates before 3 months of age. Interestingly, Clu-null mice displayed less hair cell and hearing loss compared to their wildtype littermates after 3 months. Furthermore, the deletion of Clu is protected against aminoglycoside-induced hair cell loss in both in vivo and in vitro models. Our findings suggested that the inhibition of Clu expression could represent a potential therapeutic strategy for the alleviation of age-related and ototoxic drug-induced hearing loss.

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Section: Discussionmentioning

confidence: 97%

Deletion of Clusterin Protects Cochlear Hair Cells against Hair Cell Aging and Ototoxicity

et al. 2021

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“…The development of nanomedication would alter the stability and permeability of drugs, which might bring hope to the emergency of more efficacious and less toxic medication. Moreover, with the research progresses in the field of regeneration of cochlear hair cells and neural fibers [24,[204][205][206][207][208], NIHL might be curable one day in the future.…”

Section: Discussionmentioning

confidence: 99%

Noise-Induced Hearing Loss: Updates on Molecular Targets and Potential Interventions

Mao

Chen

2021

Neural Plasticity

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Noise overexposure leads to hair cell loss, synaptic ribbon reduction, and auditory nerve deterioration, resulting in transient or permanent hearing loss depending on the exposure severity. Oxidative stress, inflammation, calcium overload, glutamate excitotoxicity, and energy metabolism disturbance are the main contributors to noise-induced hearing loss (NIHL) up to now. Gene variations are also identified as NIHL related. Glucocorticoid is the only approved medication for NIHL treatment. New pharmaceuticals targeting oxidative stress, inflammation, or noise-induced neuropathy are emerging, highlighted by the nanoparticle-based drug delivery system. Given the complexity of the pathogenesis behind NIHL, deeper and more comprehensive studies still need to be fulfilled.

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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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Biomimetic 3D bacterial cellulose-graphene foam hybrid scaffold regulates neural stem cell proliferation and differentiation

Cited by 76 publications

References 71 publications

Deletion of Clusterin Protects Cochlear Hair Cells against Hair Cell Aging and Ototoxicity

Deletion of Clusterin Protects Cochlear Hair Cells against Hair Cell Aging and Ototoxicity

Noise-Induced Hearing Loss: Updates on Molecular Targets and Potential Interventions

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

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