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Artemin transiently increases iNOS expression in primary cultured trigeminal ganglion neurons
Shang, HQ;Wang, Y;Chao, XH;Sun, GY;Bai, XH;Xu, L;Han, YC;Li, JF;Wang, HB;Fan, ZM
NEUROSCIENCE LETTERS 2017年 660卷 页码:34-38
NEUROTROPHIC FACTOR FAMILY; NITRIC-OXIDE SYNTHASE; GENE-RELATED PEPTIDE; NEUROPATHIC PAIN; SENSORY NEURONS; NERVOUS-SYSTEM; GLIAL-CELLS; RELEASE; TRPV1; OVEREXPRESSION
Artemin, a member of the glial cell line-derived neurotrophic factor family, is an important cytokine and a critical participant in trigeminal pain disorders such as tongue pain and migraine. However, the mechanisms underlying artemin's activity are largely unknown. In the present study, we used primary cultured trigeminal ganglion neurons (TGNs) to determine the effect of artemin on the expression of the inducible form of nitric oxide synthase (iNOS), which is released in response to painful and inflammatory stimuli. Following artemin treatment, western blot analysis showed that the protein level of iNOS was transiently elevated after artemin treatment for 15 min (p < 0.05). Immunofluorescence revealed that both the expressions of iNOS and GFRa3 were significantly up-regulated after artemin treatment for 15 min. In addition, iNOS expression induced by artemin was co-localized with GFRa3 and TUJ-1 in primary cultured TGNs, respectively. Our results indicate a previously unknown role of artemin in regulating iNOS expression in primary cultured TGNs, and regulation of iNOS might be involved in the mechanism through which artemin participates in the trigeminal pain pathway.
Prevalence of Mutations in Deafness-Causing Genes in Cochlear Implanted Patients with Profound Nonsyndromic Sensorineural Hearing Loss in Shandong Province, China
Luo, JF;Bai, XH;Zhang, FG;Xiao, Y;Gu, LT;Han, YC;Fan, ZM;Li, JF;Xu, L;Wang, HB
ANNALS OF HUMAN GENETICS 2017年 81卷6期 页码:258-266
ENLARGED VESTIBULAR AQUEDUCT; PENDRED-SYNDROME; GJB2 MUTATIONS; CONNEXIN-26 MUTATIONS; SLC26A4 MUTATIONS; JAPANESE; IDENTIFICATION; FREQUENCIES; POPULATION; IMPAIRMENT
The mutations of GJB2, SLC26A4, and mtDNA12SrRNA are the most common inherited causes of nonsyndromic sensorineural hearing loss (NSHL) in China, yet previous genetic screenings were mainly carried on patients with moderate-to-profound impairment. We aimed to detect the mutation frequencies in NSHL population within a more specified range of severity. Patients with profound NSHL who had undergone cochlear implantation in the Shandong Provincial Hospital (Shandong, China) were recruited. The majority (n = 472) were between 0.7 and 6 years old, and the remaining (n = 63) were between 6 and 70 years old. In total, 115 mutation alleles of the three genes were screened with SNP scan assay. Of the patients, 19.44% (104/535) were found to have GJB2 mutations, and the most common allele was c.235delC, followed by c.299_300delAT and c.109G>A. SLC26A4 mutations were detected in 13.46% patients (72/535), and the most common allele was c.919-2A>G (IVS7-2A>G), followed by c.1174A>T and c.2168A>G. Seven patients (1.31%) carried mutations in mtDNA12SrRNA, with the alleles of m.1555A>G and m.1494C>T. We found the allele frequency of c.109G>A (GJB2) was relatively lower in the profound NSHL population in comparison to the moderate-to-profound ones, and the c.1174A>T (SLC26A4) relatively higher. It suggests those mutations may be connected with the degree of deafness, which needs more observations and analyses to support.
Spag6 Mutant Mice Have Defects in Development and Function of Spiral Ganglion Neurons, Apoptosis, and Higher Sensitivity to Paclitaxel
Li, XF;Xu, L;Sun, GY;Wu, XM;Bai, XH;Li, JF;Strauss, JF;Zhang, ZB;Wang, HB
SCIENTIFIC REPORTS 2017年 7卷
MICROTUBULE-ASSOCIATED PROTEIN; MINIMAL RESIDUAL DISEASE; GROWTH; CANCER; EXPRESSION; GENES; CELLS; IDENTIFICATION; REGENERATION; MIGRATION
Mammalian Sperm Associated Antigen 6 (SPAG6) is the orthologue of Chlamydomonas PF16, a protein localized in the axoneme central apparatus. Recent studies showed that Spag6 has a role in brain neuronal proliferation and differentiation. The mammalian spiral ganglion neurons (SGNs) are specialzed bipolar neurons in the inner ear. However, the role of SPAG6 in SGN has not been elucidated. Therefore, We hypothesized that a Spag6 knockout would affect the development and function of SGNs. We utilized Spag6-deficient mice and SGN explants to define the role of SPAG6. On postnatal day 30 (P30) mutant mice had lower SGN density compared to their wild-type littermates, and more apoptosis was evident in the mutants. Increased Bax expression, a disturbed distribution of cytochrome c, and cleaved caspase-3 positive staining indicated that increased apoptosis involved a mitochondrial pathway. Transmission electron microscopy revealed abnormalities in the ultrastructure of mutant SGNs as early as P7. In vitro, lack of SPAG6 affected the growth of neurites and growth cones. Additionally, SPAG6 deficiency decreased synapse density in SGN explants. Finally, Spag6 mutant SGNs were more sensitive to the microtubule stabilizing agent, paclitaxel. These findings suggest that Spag6 plays a crucial role in SGN development and function.
Allicin protects against cisplatin-induced vestibular dysfunction by inhibiting the apoptotic pathway
Wu, XM;Cai, J;Li, XF;Li, H;Li, JF;Bai, XH;Liu, WW;Han, YC;Xu, L;Zhang, DG;Wang, HB;Fan, ZM
EUROPEAN JOURNAL OF PHARMACOLOGY 2017年 805卷 页码:108-117
GUINEA-PIGS; D-METHIONINE; CELL-DEATH; ATPASE ACTIVITIES; EPITHELIAL-CELLS; FACTOR AIF; IN-VITRO; OTOTOXICITY; INJURY; TOXICITY
Cisplatin is an anticancer drug that causes the impairment of inner ear function as side effects, including hearing loss and balance dysfunction. The purpose of this study was to investigate the effects of allicin against cisplatin-induced vestibular dysfunction in mice and to make clear the mechanism underlying the protective effects of allicin on oto-vestibulotoxicity. Mice intraperitoneally injected with cisplatin exhibited vestibular dysfunction in swimming test, which agreed with impairment in vestibule. However, these impairments were significantly prevented by pre-treatment with allicin. Allicin markedly reduced cisplatin-activated expression of cleaved-caspase-3 in hair cells and vascular layer cells of utricule, saccule and ampulla, but also decreased AIF nuclear translocation of hair cells in utricule, saccule and ampulla. These results showed that allicin played an effective role in protecting vestibular dysfunction induced by cisplatin via inhibiting caspase-dependent and caspase-independent apoptotic pathways. Therefore, allicin may be useful in preventing oto-vestibulotoxicity mediated by cisplatin.
Allicin protects auditory hair cells and spiral ganglion neurons from cisplatin - Induced apoptosis
Wu, XM;Li, XF;Song, YD;Li, H;Bai, XH;Liu, WW;Han, YC;Xu, L;Li, JF;Zhang, DG;Wang, HB;Fan, ZM
NEUROPHARMACOLOGY 2017年 116卷 页码:429-440 影响因子:4.936
INDUCED OTOTOXICITY; ANTIOXIDANT SYSTEM; OXIDATIVE STRESS; IN-VITRO; INJURY; DEATH; RAT; MECHANISMS; PATHWAY; DYSFUNCTION
Cisplatin is a broad-spectrum anticancer drug that is commonly used in the clinic. Ototoxicity is one of the major side effects of this drug, which caused irreversible sensorineural hearing loss. Allicin, the main biologically active compound derived from garlic, has been shown to exert various anti-apoptotic and anti-oxidative activities in vitro and in vivo studies. We took advantage of C57 mice intraperitoneally injected with cisplatin alone or with cisplatin and allicin combined, to investigate whether allicin plays a protective role in vivo against cisplatin ototoxicity. The result showed that C57 mice in cisplatin group exhibited increased shift in auditory brainstem response, whereas the auditory fuction of mice in allicin + cisplatin group was protected in most frequencies, which was accordance with observed damages of outer hair cells (OHCs) and spiral ganglion neurons (SGNs) in the cochlea. Allicin markedly protected SGN mitochondria from damage and releasing cytochrome c, and significantly reduced pro-apoptosis factor expressions activated by cisplatin, including Bax, cleaved-caspase-9, cleaved-caspase-3and p53. Furthermore, allicin reduced the level of Malondialdehyde (MDA), but increased the level of superoxide dismutase (SOD). All data suggested that allicin could prevent hearing loss induced by cisplatin effectively, of which allicin protected SGNs from apoptosis via mitochondria' pathway while protected OHCs and supporting cells (SCs) from apoptosis through p53 pathway. (C) 2017 Elsevier Ltd. All rights reserved.
NLRX1 accelerates cisplatin-induced ototoxity in HEI-OC1 cells via promoting generation of ROS and activation of JNK signaling pathway
Yin, HY;Sun, GY;Yang, QQ;Chen, C;Qi, Q;Wang, HB;Li, JF
SCIENTIFIC REPORTS 2017年 7卷
JUNCTIONAL INTERCELLULAR COMMUNICATION; OXYGEN SPECIES PRODUCTION; REACTIVE OXYGEN; AUDITORY CELLS; INDUCED APOPTOSIS; HAIR-CELLS; IN-VITRO; INFLAMMATORY CYTOKINES; HEARING-LOSS; C-JUN
Nucleotide-binding domain and leucine-rich-repeat-containing family member X1 (NLRX1), located in mitochondria, can recognize cytoplasmic pattern recognition receptors and is tightly related to reactive oxygen species (ROS) production, mitochondrial function, apoptosis and inflammation. The present study was designed to explore whether NLRX1 expresses in HEI-OC1 cells and, if so, to investigate the possible correlations between NLRX1 and cisplatin-induced ototoxity in vitro. Here, we report that NLRX1 was specifically localized to mitochondria in the cytoplasm of HEI-OC1 cells and its expression was increased concurrent with the increase of ROS production and occurrence of apoptosis in HEI-OC1 cells in response to cisplatin stimulus. NLRX1 overexpression led to a higher apoptosis in HEI-OC1 cells treated with cisplatin, whereas, NLRX silencing decreased cisplatin induced apoptosis. Mechanistic studies showed that NLRX1 activated mitochondrial apoptosis pathway as well as promoted ROS generation and JNK activation. Either inhibition of ROS generation or JNK signaling significantly prevented NLRX1-mediated mitochondrial apoptosis in HEI-OC1cells. In addition, NLRX1 expression was confirmed in cochlear explants. The findings from this work reveal that NLRX1 sensitizes HEI-OC1 cells to cisplatin-induced apoptosis via activation of ROS/JNK signaling pathway, suggesting that NLRX1 acts as an important regulator of the cisplatin-elicited ototoxity.
c-Myb knockdown increases the neomycin-induced damage to hair-cell-like HEI-OC1 cells in vitro
Yu, XY;Liu, WW;Fan, ZM;Qian, FP;Zhang, DG;Han, YC;Xu, L;Sun, GY;Qi, JY;Zhang, SS;Tang, ML;Li, JF;Chai, RJ;Wang, HB
SCIENTIFIC REPORTS 2017年 7卷
BREAST-CANCER CELLS; INDUCED APOPTOSIS; MYELOID-LEUKEMIA; EXPRESSION; OTOTOXICITY; ACTIVATION; DEATH; GENE; DIFFERENTIATION; PROTECTS
c-Myb is a transcription factor that plays a key role in cell proliferation, differentiation, and apoptosis. It has been reported that c-Myb is expressed within the chicken otic placode, but whether c-Myb exists in the mammalian cochlea, and how it exerts its effects, has not been explored yet. Here, we investigated the expression of c-Myb in the postnatal mouse cochlea and HEI-OC1 cells and found that c-Myb was expressed in the hair cells (HCs) of mouse cochlea as well as in cultured HEI-OC1 cells. Next, we demonstrated that c-Myb expression was decreased in response to neomycin treatment in both cochlear HCs and HEI-OC1 cells, suggesting an otoprotective role for c-Myb. We then knocked down c-Myb expression with shRNA transfection in HEI-OC1 cells and found that c-Myb knockdown decreased cell viability, increased expression of pro-apoptotic factors, and enhanced cell apoptosis after neomycin insult. Mechanistic studies revealed that c-Myb knockdown increased cellular levels of reactive oxygen species and decreased Bcl-2 expression, both of which are likely to be responsible for the increased sensitivity of c-Myb knockdown cells to neomycin. This study provides evidence that c-Myb might serve as a new target for the prevention of aminoglycoside-induced HC loss.
A Novel Nonsense Mutation of POU4F3 Gene Causes Autosomal Dominant Hearing Loss (vol 2016, 1512831, 2016)
Zhang, C;Wang, MM;Xiao, Y;Zhang, FG;Zhou, YC;Li, JF;Zheng, QY;Bai, XH;Wang, HB
NEURAL PLASTICITY 2017年
Triple semicircular canal plugging: a novel modality for the treatment of intractable Meniere's disease
Zhang, DG;Fan, ZM;Han, YC;Lv, YF;Li, YW;Wang, HB
ACTA OTO-LARYNGOLOGICA 2016年 136卷12期 页码:1230-1235
ENDOLYMPHATIC MASTOID SHUNT; LONG-TERM; OCCLUSION; EFFICACY; SURGERY
Conclusions: TSCP, which can reduce vertiginous symptoms in patients with intractable MD, represents an effective therapy for this disorder.;-;Objective: To explore the long-term efficacy of triple semicircular canal plugging (TSCP) in the treatment of intractable Meniere's disease (MD).;-;Methods: Seventy-nine patients diagnosed with unilateral MD referred to a vertigo clinic of the hospital between December 2010 and December 2013 were included in this study for retrospective analysis. TSCP was performed in the affected ear for each patient. Vertigo control and auditory function were measured. Pure tone audiometry, caloric test, and cervical vestibular evoked myogenic potential (cVEMP) were performed in 2-year follow-up. Thirty-six MD patients, who accepted endolymphatic sac decompression (ESD) operation were selected as a comparison group.;-;Results: The total control rate of vertigo in the TSCP group was 98.7% in the 2-year follow-up, with a complete control rate of 81.0% and substantial control rate of 17.7%. The rate of hearing preservation was 70.9%. The total control rate of vertigo in the ESD operation group was 72.2%. The vertigo control rate of TSCP was significantly higher than that of ESD operation. Twenty-four months after treatment, canal paresis was found in the operation side of all patients of TSCP by means of caloric test.
Novel compound heterozygous mutations in SLC26A4 gene in a Chinese Han family with enlarged vestibular aqueduct
Wang, MM;Zhang, FG;Xu, L;Xiao, Y;Li, JF;Fan, ZM;Sun, Q;Bai, XH;Wang, HB
INTERNATIONAL JOURNAL OF PEDIATRIC OTORHINOLARYNGOLOGY 2016年 90卷 页码:170-174
PENDRED-SYNDROME; HEARING-LOSS; MONDINI DYSPLASIA; UNIQUE SPECTRUM; PDS; DEAFNESS; IDENTIFICATION; PHENOTYPE; GENOTYPE; DFNB4
Objective: To identify the disease-related SLC26A4 mutants in a Chinese Han pedigree associated with Enlarged vestibular aqueduct (EVA).;-;Methods: EVA diagnosis was based on the family history, clinical examinations, systematically audiometric evaluations, high-resolution computed tomography (HRCT) of the temporal bone, and magnetic resonance imaging (MRI) of inner ear. Sanger sequencing and mutation analysis of the SLC26A4 gene were performed in all members of this family to identify the disease-related SLC26A4 mutants. Mutations in the SLC26A4 gene were compared with 200 ethnically matched control persons to exclude common polymorphism.;-;Results: All members in this family were negative for systemic and thyroid diseases. There were three subjects (I-2, II-2 and II-3) with bilateral sensorineural deafness since childhood. Temporal bone HRCT scans and inner ear MRI showed bilateral enlarged vestibular aqueduct with Mondini malformation in II-2 and II-3. A novel SLC26A4 splice-site mutation c.1001 + 5G > C was identified in compound heterozygosity with the mutation c.919-2A > G in the proband and in II-2. This novel compound heterozygote of two splice site mutations was not found in 200 normal hearing Chinese Han controls.;-;Conclusions: A novel splice site mutation of c.1001 + 5G > C was identified, and the novel compound heterozygote of two splice site mutations, c.1001 + 5G > C and c.919-2A > G, in the SLC26A4 gene has been linked to hearing impairment in EVA patients. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
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