A Polydopamine-Functionalized Carbon Microfibrous Scaffold Accelerates the Development of Neural Stem Cells

Yang, Yanru; Zhang, Yuhua; Chai, Renjie; Gu, Zhongze

doi:10.3389/fbioe.2020.00616

Cited by 14 publications

(12 citation statements)

References 39 publications

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“…In addition, vincristine, a kind of cytoskeleton protein, is closely related to local adhesion and regulates cell proliferation. The expression of vincristine in NSCs cultured with PDA was enhanced significantly, and it showed that NSCs were much more proliferative than the non-PDA treatment group (Yang et al, 2020).…”

Section: Pda and The Activity Of Neuron And Neuron-likecells Nsc Adhementioning

confidence: 95%

Applications of Polydopamine-Modified Scaffolds in the Peripheral Nerve Tissue Engineering

Yan

Liao

et al. 2020

Front. Bioeng. Biotechnol.

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Peripheral nerve injury is a common and complicated traumatic disease in clinical neurosurgery. With the rapid advancement and development of medical technologies, novel tissue engineering provides alternative therapies such as nerve conduit transplantation. It has achieved significant outcomes. The scaffold surface modification is vital to the reconstruction of a pro-healing interface. Polydopamine has high chemical activity, adhesion, hydrophilicity, hygroscopicity, stability, biocompatibility, and other properties. It is often used in the surface modification of biomaterials, especially in the peripheral nerve regeneration. The present review discusses that polydopamine can promote the adhesion, proliferation, and differentiation of neural stem cells and the growth of neuronal processes. Polydopamine is widely used in the surface modification of nerve conduits and has a potential application prospect of repairing peripheral nerve injury. Polydopamine-modified scaffolds are promising in the peripheral nerve tissue engineering.

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Section: Pda and The Activity Of Neuron And Neuron-likecells Nsc Adhementioning

confidence: 95%

Applications of Polydopamine-Modified Scaffolds in the Peripheral Nerve Tissue Engineering

Yan

Liao

et al. 2020

Front. Bioeng. Biotechnol.

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“…Spiral ganglion neurons lack the ability to regenerate after damage in the mammalian cochlea, which is a major cause of auditory neuropathy and may compromise the therapeutic effects of cochlear implants ( Guo et al, 2019 ). Extensive studies have been performed using neural stem cells for regeneration of neurons and the SGNs ( Fang et al, 2019 ; Li et al, 2019 ; Tang et al, 2019 ; Han et al, 2020 ; Xia et al, 2020 ; Yang et al, 2020 , 2021 ; Yuan et al, 2021 ). Yet, functional regeneration of SGNs from the resident glial cells may represent a novel strategy for hearing restoration caused by SGN damages.…”

Section: Discussionmentioning

confidence: 99%

Cochlear Sox2+ Glial Cells Are Potent Progenitors for Spiral Ganglion Neuron Reprogramming Induced by Small Molecules

Chen

Huang

et al. 2021

Front. Cell Dev. Biol.

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In the mammalian cochlea, spiral ganglion neurons (SGNs) relay the acoustic information to the central auditory circuits. Degeneration of SGNs is a major cause of sensorineural hearing loss and severely affects the effectiveness of cochlear implant therapy. Cochlear glial cells are able to form spheres and differentiate into neurons in vitro. However, the identity of these progenitor cells is elusive, and it is unclear how to differentiate these cells toward functional SGNs. In this study, we found that Sox2+ subpopulation of cochlear glial cells preserves high potency of neuronal differentiation. Interestingly, Sox2 expression was downregulated during neuronal differentiation and Sox2 overexpression paradoxically inhibited neuronal differentiation. Our data suggest that Sox2+ glial cells are potent SGN progenitor cells, a phenotype independent of Sox2 expression. Furthermore, we identified a combination of small molecules that not only promoted neuronal differentiation of Sox2– glial cells, but also removed glial cell identity and promoted the maturation of the induced neurons (iNs) toward SGN fate. In summary, we identified Sox2+ glial subpopulation with high neuronal potency and small molecules inducing neuronal differentiation toward SGNs.

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“…Hearing loss could be caused by genetic factors, aging, infectious diseases, ototoxic drugs, and noise exposure [1][2][3][4][5][6]. The reported mechanisms of noise-induced hair cells (HCs) and spiral ganglion neuron damage mainly include mechanical shearing forces and oxidative damage to HCs [7] and glutamate excitotoxicity to neurons [8][9][10][11]. In the past, noise exposure was considered harmful only when it causes a per-manent threshold shift (PTS) [3,[12][13][14][15][16].…”

Section: Introductionmentioning

confidence: 99%

Dose-Dependent Pattern of Cochlear Synaptic Degeneration in C57BL/6J Mice Induced by Repeated Noise Exposure

Qian

Wang

et al. 2021

Neural Plasticity

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It is widely accepted that even a single acute noise exposure at moderate intensity that induces temporary threshold shift (TTS) can result in permanent loss of ribbon synapses between inner hair cells and afferents. However, effects of repeated or chronic noise exposures on the cochlear synapses especially medial olivocochlear (MOC) efferent synapses remain elusive. Based on a weeklong repeated exposure model of bandwidth noise over 2-20 kHz for 2 hours at seven intensities (88 to 106 dB SPL with 3 dB increment per gradient) on C57BL/6J mice, we attempted to explore the dose-response mechanism of prolonged noise-induced audiological dysfunction and cochlear synaptic degeneration. In our results, mice repeatedly exposed to relatively low-intensity noise (88, 91, and 94 dB SPL) showed few changes on auditory brainstem response (ABR), ribbon synapses, or MOC efferent synapses. Notably, repeated moderate-intensity noise exposures (97 and 100 dB SPL) not only caused hearing threshold shifts and the inner hair cell ribbon synaptopathy but also impaired MOC efferent synapses, which might contribute to complex patterns of damages on cochlear function and morphology. However, repeated high-intensity (103 and 106 dB SPL) noise exposures induced PTSs mainly accompanied by damages on cochlear amplifier function of outer hair cells and the inner hair cell ribbon synaptopathy, rather than the MOC efferent synaptic degeneration. Moreover, we observed a frequency-dependent vulnerability of the repeated acoustic trauma-induced cochlear synaptic degeneration. This study provides a sight into the hypothesis that noise-induced cochlear synaptic degeneration involves both afferent (ribbon synapses) and efferent (MOC terminals) pathology. The pattern of dose-dependent pathological changes induced by repeated noise exposure at various intensities provides a possible explanation for the complicated cochlear synaptic degeneration in humans. The underlying mechanisms remain to be studied in the future.

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A Polydopamine-Functionalized Carbon Microfibrous Scaffold Accelerates the Development of Neural Stem Cells

Cited by 14 publications

References 39 publications

Applications of Polydopamine-Modified Scaffolds in the Peripheral Nerve Tissue Engineering

Applications of Polydopamine-Modified Scaffolds in the Peripheral Nerve Tissue Engineering

Cochlear Sox2+ Glial Cells Are Potent Progenitors for Spiral Ganglion Neuron Reprogramming Induced by Small Molecules

Dose-Dependent Pattern of Cochlear Synaptic Degeneration in C57BL/6J Mice Induced by Repeated Noise Exposure

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