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Recent advances in the application of MXenes for neural tissue engineering and regeneration

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Neural Regeneration Research 2024年第2期19卷 258-263页

作者： Menghui Liao Qingyue Cui Yangnan Hu Jiayue Xing Danqi Wu Shasha Zheng Yu Zhao Yafeng Yu Jingwu Sun Renjie Chai State Key Laboratory of Digital Medical Engineering Department of Otolaryngology Head and Neck SurgeryZhongda HospitalSchool of Life Sciences and TechnologyAdvanced Institute for Life and HealthJiangsu Province High-Tech Key Laboratory for Bio-Medical ResearchSoutheast UniversityNanjingJiangsu ProvinceChina Co-Innovation Center of Neuroregeneration Nantong UniversityNantongJiangsu ProvinceChina Department of Oto-Rhino-Laryngology West China HospitalSichuan UniversityChengduSichuan ProvinceChina First Affiliated Hospital of Soochow University SuzhouJiangsu ProvinceChina Department of Otolaryngology-Head and Neck Surgery The First Affiliated Hospital of USTCDivision of Life Sciences and MedicineUniversity of Science and Technology of ChinaHefeiAnhui ProvinceChina Department of Otolaryngology Head and Neck Surgery Sichuan Provincial People’s HospitalUniversity of Electronic Science and Technology of ChinaChengduSichuan ProvinceChina Institute for Stem Cell and Regeneration Chinese Academy of SciencesBeijingChina Beijing Key Laboratory of Neural Regeneration and Repair Capital Medical UniversityBeijingChina

Transition metal carbides and nitrides(MXenes)are crystal nanomaterials with a number of surface functional groups such as fluorine,hydroxyl,and oxygen,which can be used as carriers for proteins and drugs.MXenes have excellent biocompatibility,electrical conductivity,surface hydrophilicity,mechanical properties and easy surface modification.However,at present,the stability of most MXenes needs to be improved,and more synthesis methods need to be explored.MXenes are good substrates for nerve cell regeneration and nerve reconstruction,which have broad application prospects in the repair of nervous system injury.Regarding the application of MXenes in neuroscience,mainly at the cellular level,the long-term in vivo biosafety and effects also need to be further explored.This review focuses on the progress of using MXenes in nerve regeneration over the last few years;discussing preparation of MXenes and their biocompatibility with different cells as well as the regulation by MXenes of nerve cell regeneration in two-dimensional and three-dimensional environments in vitro.MXenes have great potential in regulating the proliferation,differentiation,and maturation of nerve cells and in promoting regeneration and recovery after nerve injury.In addition,this review also presents the main challenges during optimization processes,such as the preparation of stable MXenes and long-term in vivo biosafety,and further discusses future directions in neural tissue engineering.

关键词： hydrogels MXenes nerve regeneration neural cells neural stem cells organoids spiral ganglion neurons

Salicylate enhances expression and function of NMDA receptors in cochlear spiral ganglion neurons

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Journal of Otology 2012年第1期7卷 9-14页

作者： GAO Meng FANG Xiu-you FENG Shuang WANG Ren-jun DENG Li-li SU Ji-ping Department of Otolaryngology Head and Neck Surgery Guangxi Medical UniversityNanningGuangxi 530021 Department of Otolaryngology Head and Neck Surgery Binzhou People HospitalBinzhouShandong 256600 Department of 4^(th)Surgery Ganyu People HospitalLianyugangJiangsu 222100

Objective To study the effect of salicylate on the expression and function of NMDA receptors in spiral ganglion neurons （SGNs）. Methods The mRNA of NR1 subunit of NMDA receptor in modiolus tissues were detected by Real time fluorescence quantitative PCR （FQ-PCR）. NMDA receptor whole-cell currents were recorded using patch clamp in acute isolated SGNs. Results Compared with the control group, salicylate significantly increased the mRNA level of NR1 subunit in SGNs. NMDA of concentrations ranging from 0.1 mM to 10 mM evoked no current in SGNs. NMDA （0. 1mM and 0.5 mM） applied with salicylate （5 mM）, however, induced inward currents （212.6±15.2pA, n=5; 607.9±44.3pA, n=5） in a dose-dependent manner, which could be inhibited by APV. Salicylate alone did not produce any current in SGNs. Conclusion Salicylate increases the expression of NMDA receptors and facilitates the currents mediated by NMDA receptors in SGNs.

关键词： Salicylate NMDA receptor spiral ganglion neurons NR1 subunit

Inhibiting DNA methylation alleviates cisplatininduced hearing loss by decreasing oxidative stress-induced mitochondria-dependent apoptosis via the LRP1-PI3K/AKT pathway

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Acta Pharmaceutica Sinica B 2022年第3期12卷 1305-1321页

作者： Yingzi He Zhiwei Zheng Chang Liu Wen Li Liping Zhao Guohui Nie Huawei Li ENT Institute and Otorhinolaryngology Department of Eye&ENT Hospital State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain ScienceFudan UniversityShanghai 200031China NHC Key Laboratory of Hearing Medicine(Fudan University) Shanghai 200031China Department of Otolaryngology and Institute of Translational Medicine Shenzhen Second People’s Hospital/the First Affiliated Hospital of Shenzhen University Health Science CenterShanghai 200032China Institutes of Biomedical Sciences Fudan UniversityShanghai 200032China The Institutes of Brain Science and the Collaborative Innovation Center for Brain Science Fudan UniversityShenzhen 518035China

Cisplatin-related ototoxicity is a critical side effect of chemotherapy and can lead to irreversible hearing loss.This study aimed to assess the potential effect of the DNA methyltransferase(DNMT)inhibitor RG108 on cisplatin-induced ototoxicity.Immunohistochemistry,apoptosis assay,and auditory brainstem response(ABR)were employed to determine the impacts of RG108 on cisplatin-induced injury in murine hair cells(HCs)and spiral ganglion neurons(SGNs).Rhodamine 123 and TMRM were utilized for mitochondrial membrane potential(MMP)assessment.Reactive oxygen species(ROS)amounts were evaluated by Cellrox green and Mitosox-red probes.Mitochondrial respiratory function evaluation was performed by determining oxygen consumption rates(OCRs).The results showed that RG108 can markedly reduce cisplatin induced damage in HCs and SGNs,and alleviate apoptotic rate by protecting mitochondrial function through preventing ROS accumulation.Furthermore,RG108 upregulated BCL-2 and downregulated APAF1,BAX,and BAD in HEI-OC1 cells,and triggered the PI3K/AKT pathway.Decreased expression of low-density lipoprotein receptor-related protein 1(LRP1)and high methylation of the LRP1 promoter were observed after cisplatin treatment.RG108 treatment can increase LRP1expression and decrease LRP1 promoter methylation.In conclusion,RG108 might represent a new potential agent for preventing hearing loss induced by cisplatin via activating the LRP1-PI3K/AKT pathway.

关键词： Cisplatin DNMT Apoptosis Hair cell spiral ganglion neurons RG108 Mitochondrial dysfunction ROS

Stem cell-based approaches: Possible route to hearing restoration?

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World Journal of Stem Cells 2020年第6期12卷 422-437页

作者： María Beatriz Durán-Alonso Institute of Biology and Molecular Genetics University of ValladolidValladolid 47003Spain

Disabling hearing loss is the most common sensorineural disability worldwide.It affects around 466 million people and its incidence is expected to rise to around 900 million people by 2050,according to World Health Organization estimates.Most cases of hearing impairment are due to the degeneration of hair cells(HCs)in the cochlea,mechano-receptors that transduce incoming sound information into electrical signals that are sent to the brain.Damage to these cells is mainly caused by exposure to aminoglycoside antibiotics and to some anti-cancer drugs such as cisplatin,loud sounds,age,infections and genetic mutations.Hearing deficits may also result from damage to the spiral ganglion neurons that innervate cochlear HCs.Differently from what is observed in avian and nonmammalian species,there is no regeneration of missing sensory cell types in the adult mammalian cochlea,what makes hearing loss an irreversible process.This review summarizes the research that has been conducted with the aim of developing cell-based strategies that lead to sensory cell replacement in the adult cochlea and,ultimately,to hearing restoration.Two main lines of research are discussed,one directed toward the transplantation of exogenous replacement cells into the damaged tissue,and another that aims at reactivating the regenerative potential of putative progenitor cells in the adult inner ear.Results from some of the studies that have been conducted are presented and the advantages and drawbacks of the various approaches discussed.

关键词： Hearing loss Cochlear hair cells spiral ganglion neurons Cell regeneration Adult stem cells Cell transplantation

Trimethyltin-induced cochlear degeneration in rat

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Journal of Otology 2016年第3期11卷 118-126页

作者： Jintao Yu Dalian Ding Hong Sun Richard Salvi Jerome A.Roth Department of Otolaryngology Union HospitalTongji Medical CollegeHuazhong University of Science and Technology Center for Hearing and Deafness University at Buffalo Department of Otolaryngology Head and Neck Surgery Xiangya HospitalCentral South University Department of Pharmacology and Toxicology University at Buffalo

Trimethyltin(TMT) is an occupational and environmental health hazard behaving as a potent neurotoxin known to affect the central nervous system as well as the peripheral auditory system.However,the mechanisms underlying TMT-induced ototoxicity are poorly understood.To elucidate the effects of TMT on the cochlea,a single injection of 4 or 8 mg/kg TMT was administered intraperitoneally to adult rats.The compound action potential(CAP) threshold was used to assess the functional status of the cochlea and histological techniques were used to assess the condition of the hair cells and auditory nerve fibers.TMT at 4 mg/kg produced a temporary CAP threshold elevation of 25-60 dB that recovered by 28 d post-treatment.Although there was no hair cell loss with the 4 mg/kg dose,there was a noticeable loss of auditory nerve fibers particularly beneath the inner hair cells.TMT at 8 mg/kg produced a large permanent CAP threshold shift that was greatest at the high frequencies.The CAP threshold shift was associated with the loss of outer hair cells and inner hair cells in the basal,high-frequency region of the cochlea,considerable loss of auditory nerve fibers and a significant loss of spiral ganglion neurons in the basal turn.spiral ganglion neurons showed evidence of soma shrinkage and nuclear condensation and fragmentation,morphological features of apoptotic cell death.TMT-induced damage was greatest in the high-frequency,basal region of the cochlea and the nerve fibers beneath the inner hair cells were the most vulnerable structures.

关键词： Trimethyltin Ototoxicity Hair cells Nerve fibers spiral ganglion neurons

Detection of apoptosis by RT-PCR array in mefloquine-induced cochlear damage

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Journal of Otology 2011年第1期6卷 1-9页

作者： DING Da-lian Someya Shinichi JIANG Hai-yan QI Wei-dong YU Dong-zhen Center for Hearing and Deafness State University of New York at Buffalo Departments of Aging and Geriatric Research Division of Biology of Aging University of Florida Department of Otolaryngology Head and Neck Surgery Huashan Hospital Affiliated Fudan University Department of Otolaryngology Head and Neck Surgery Six People＇s Hospital of Shanghai Jiao Tong University Graduate School of Agricultural and Life Sciences University of Tokyo Department of Otolaryngology Head and Neck Surgery Xiangya Hospital of Central South University

Objective To investigate the occurrence and possible mechanisms of apoptosis in cochlear epithelium and spiral ganglion neurons after mefloquine treatment. Methods We used quantitative RT-PCR apoptosis-focused gene arrays （96-well, 84 apoptosis related genes） to assess changes of gene expression in the cochlear basilar membrane （hair cells-supporting cells） and spiral ganglion neurons of rat cochlear organotypic cultures treated with 100 IxM mefloquine for 3 h. Results Significant up-or down-regulation in gene expression was detected in 23 genes in the cochlear basilar membrane, and in 32 genes in the spiral ganglion neurons compared with time-matched controls. The responding genes could be classified as pro-or anti-apoptotic, and were mainly implicated in the Bcl-2, Caspase, Card, IAP, TNF ligand / TNF receptor, Death domain / Death effector domain, DNA damage / p53, and NF-kappa B families. Synthetic analysis suggested that these families could be revised to two major pathways mainly involved in t]he death receptor-mediated signaling pathway and apoptotic mitochondrial pathway. In addition, it was found that numerous anti-apoptotic genes such as Bcl2al, Birclb, Birc3, Birc4, Bnipl, Cflar, II10, Lhx4, Mcll, Nfkbl, Prlr, Prok2, and TNF were greatly up-regulated in the cochlear tissue, which might imply the co-existence of protective response in the ceils at the early stage of mefloquine-induced damage.

关键词： mefloquine ototoxicity apoptosis cochlea spiral ganglion neurons hair cells gene expression

Hidden hearing loss:current perspectives and potential therapies

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Journal of Bio-X Research 2019年第2期2卷 62-67页

作者： Diyan Chen Gaogan Jia Yusu Ni Yan Chen ENT Institute and Otorhinolaryngology Department Affiliated Eye and ENT Hospital of Fudan University Key Laboratory of Hearing Medicine of National Health and Family Planning Commission ShanghaiChina

Hidden hearing loss(HHL),an auditory dysfunction that has gained much recent attention,has the hallmarks of speech discrimination and intelligibility deficits with normal or near-normal hearing thresholds.The pathological mechanisms of HHL are complicated and are not yet fully understood.HHL can be resulted from disorders of the central nervous system such as auditory cortex,and/or pathological changes of inner ear.Thus far,2 pathological phenomena,synaptopathy and auditory nerve demyelination,have been reported as underlying causes of otogenic HHL.Here,we review the clinical and physiological characteristics of HHL as well as the molecular pathological mechanisms of otogenic HHL and aim to allude to potential therapy targets for clinical applications in the future.

关键词： auditory cochlear hair cells demyelination hearing loss hidden hearing loss Schwann cells spiral ganglion neurons synapse synaptopathy

Gene expression in cisplatin ototoxicity and protection with p53 inhibitor

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Journal of Otology 2009年第2期4卷 61-70页

作者： Donald Coling Richard Salvi Center for Hearing & Deafness 137 Cary HallUniversity at Buffalo

Cisplatin damages cochlear hair cells and spiral ganglion neurons through cell death signaling pathways that are not fully understood. We used focused apoptosis gene microarrays to study early changes in gene expres- sion in cochlear cultures from P3 neonatal rats treated with cisplatin (0.2 mM). After 12 hours of cisplatin treat- ment, more than 50% of the 96 genes on the array showed a significant decrease in expression, consistent with widespread cell death. However, after 3 hours of cisplatin treatment, 10 genes showed significant increase in ex- pression in total cochlear tissue. In experiments with subsets of cochlear tissues, at 3h, cisplatin induced increased expression of 12 genes in the cochlear sensory epithelium (basilar membrane) and 11 genes in the spiral ganglion (tissue of Rosenthal’s canal, containing the spiral ganglion). These included pro- and anti-apoptotic genes in- volved in the p53 signaling pathway, TNF receptor family, NF-kappaB pathway, death domain family, death effec- tor domain family, Bcl-2 family, CARD family, TRAF family, and GTP signal transduction. Although the changes in gene expression showed an overlap between basilar membrane and spiral ganglion, other changes, which may reflect the unique response of each tissue, were also observed. Pifithrin-α blocked cisplatin-induced up-regulation of genes in the p53 signaling pathway when assayed by both superarray and real time PCR. The data add to our understanding of the involvement of p53 in cisplatin-induced ototoxicity and otoprotection, conferred by the p53 inhibitor Pifithrin-α.

关键词： cisplatin p53 Pifithrin-α gene expression ototoxicity cochlea hair cells spiral ganglion neurons

Basic flbroblast growth factor protects auditory neurons and hair cells from noise exposure and glutamate neurotoxicity

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中华耳科学杂志 2003年第1期1卷 1-7页

作者：翟所强王大君王嘉陵 Han Dongyi YANG Weiyan Institute of ORL Chinese PLA General Hospital 28 Fuxing Road Beijing 100853 P.R. China

The purpose of the present study was to determine protectivie effects of basic fibroblast growth factor (bFGF) on cochlear neurons and hair cells in vitro and in vivo. In experiment I, cultured spiral ganglion neurons (SGNs) prepared from P3 mice were exposed to 20mM glutamate for 2 hours before the culture medium was replaced with fresh medium containing 0, 25, 50, and 100 ng/ml bFGF, respectively. Fourteen days later, all cultures were fixed with 4% paraformaldehyde, and stained with 1% toluidine blue. The number of surviving SGNs were counted and the length of SGNs neurites were measured. Exposure to 20 mM glutamate for 24 hours resulted in an inhibition on neurite outgrowth of SGNs and elevated cell death. Treatment of the cultures with bFGF led to promotion of neurite outgrowth and elevated number of surviving SGNs. Effects of bFGF were dose dependent with the highest potency at 100 ng/ml. In experiment Ⅱ, in vivo studies were carried out with guinea pigs in which bFGF or artificial perilymph was perfused into the cochlea to assess possible protective effects of bFGF on cochlear hair cells and compound action potentials(CAP). The CAPs were measured before, immediatly and 48 hours after exposure to noise. Significant differences in CAP were observed (p＜0. 05 ) among the bFGF perfused group, control group(t =3. 896 ) and artificial perilymph perfused group (t =2. 520) at 48 hours after noise exposure, Cochleae were removed and hair cell Loss was analyzed in surface preparations prepared from all experimental animals. Acoustic trauma caused loss of 651 and 687 inner hair cells in the control and artificial perilymph perfused group, respectively. In sharp contrast, only 31 inner hair cells were lost in the bFGF perfused ears. Similarly, more outer hair cells died in the control and perilymph perfuesed group (41830 and 41968, respectively) than in the group treated with bFGF (34258). Our results demonstrate that bFGF protected SGNs against glutmate neurotoxicity in vitro. In addition, treatment with bFGF also pro

关键词： Basic fibroblast growth factor Cochlea spiral ganglion neurons excitotoxicity, acoustic trau- ma, hair cells