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1.
Article in English | WPRIM | ID: wpr-915896

ABSTRACT

Objective@#Using microRNA (miR) as a biomarker has been a new way for diagnosing many diseases. Although many studies on miR-biomarker have been published, researches on miR-biomarker in ankylosing spondylitis (AS) are limited. Therefore, the objective of this study was to valiate a candidate serum miR as a novel disease-specific novel miR for AS. @*Methods@#Total RNAs were extracted from sera samples of patients with AS (n=57), patients with rheumatoid arthritis (RA) (n=37), or healthy controls (HC) (n=19). Through serum miR screening by microarray, differential levels of miR were subsequently validated by real time PCR. At the time of serum sampling, clinical values such as sex, age, disease duration, AS-disease activity score, uveitis, peripheral arthritis, enthesitis, human leukocyte antigen-B27 presence, and recent medication were evaluated. @*Results@#We found that the expression level of serum miR-3620-3p in AS was notably lower than that in RA or HC. The receiver–operator characteristics curve for determining the diagnostic accuracy showed an area under the curve of 0.919 (p<0.001) with a sensitivity of 87.1% and a specificity of 86.0%. Correlation studies showed that the expression level of miR-3620-3p was only associated with the development of uveitis (p<0.05). @*Conclusion@#Serum miR-3620-3p can be as a new biomarker for diagnosing AS.

2.
Article in English | WPRIM | ID: wpr-896885

ABSTRACT

17α-hydroxylase/17,20-lyase deficiency, caused by mutations in the cytochrome P450 family 17 subfamily A member 1 gene (CYP17A1), is an extremely rare form of congenital adrenal hyperplasia that is characterized by diverse phenotypes resulting from specific mutations. Here, we report 2 phenotypic females with 17α-hydroxylase/17,20-lyase deficiency: one with the 46,XX karyotype presenting primary amenorrhea and sexual infantilism, and the other with the 46,XY karyotype presenting a disorder of sexual development. In both cases, the serum levels of adrenocorticotropic hormone, 11-deoxycorticosterone, and gonadotropin were elevated, whereas the levels of testosterone and dehydroepiandrosterone were reduced. Next-generation sequencing revealed one patient with compound heterozygosity for p.Trp17Ter (c.51G>A) and p.His373Leu (c.1118A>T), and the other with homozygosity for p.His373Leu (c.1118A>T). This report further describes 2 cases of 17α-hydroxylase/17,20-lyase deficiency in patients who harbored a p.His373Leu substitution, commonly found in Korean individuals, and presented diverse phenotypes.

3.
Article in English | WPRIM | ID: wpr-889181

ABSTRACT

17α-hydroxylase/17,20-lyase deficiency, caused by mutations in the cytochrome P450 family 17 subfamily A member 1 gene (CYP17A1), is an extremely rare form of congenital adrenal hyperplasia that is characterized by diverse phenotypes resulting from specific mutations. Here, we report 2 phenotypic females with 17α-hydroxylase/17,20-lyase deficiency: one with the 46,XX karyotype presenting primary amenorrhea and sexual infantilism, and the other with the 46,XY karyotype presenting a disorder of sexual development. In both cases, the serum levels of adrenocorticotropic hormone, 11-deoxycorticosterone, and gonadotropin were elevated, whereas the levels of testosterone and dehydroepiandrosterone were reduced. Next-generation sequencing revealed one patient with compound heterozygosity for p.Trp17Ter (c.51G>A) and p.His373Leu (c.1118A>T), and the other with homozygosity for p.His373Leu (c.1118A>T). This report further describes 2 cases of 17α-hydroxylase/17,20-lyase deficiency in patients who harbored a p.His373Leu substitution, commonly found in Korean individuals, and presented diverse phenotypes.

4.
Article in English | WPRIM | ID: wpr-763096

ABSTRACT

Cancer and ischemic stroke (IS) are leading causes of death and disability, worldwide. It is reported that cancer increases IS incidence with various unknown mechanism. We retrospectively reviewed medical records of single tertiary medical center between January 2012 and December 2016. A total of 40,047 patients with cancer were analyzed and 63 patients (0.16%) were diagnosed of IS with underlying cancer. Lung (27.0%), gastric (14.3%) and colorectal (12.7%) cancers were the most frequent types of cancers and adenocarcinoma was the most common histologic type. We compared the clinical variables (demographic data, comorbidities, cancer stage, infarction pattern and severity) between adenocarcinoma and non-adenocarcinoma groups. And the results showed low coexistence of dyslipidemia and smoking history, and higher rate of multiple vascular territory infarct in adenocarcinoma group (p < 0.05). Six-month post stroke mortality rate was 34.6% and systemic metastasis and multi-territorial infarction were significantly relevant with the six-month mortality (p < 0.001). Also, initial National Institute of Health Stroke Scale (p < 0.05) and modified Rankin Scale scores were statistically significantly worse in mortality group (p < 0.05). In conclusion, the most frequent cancer type was lung cancer and adenocarcinoma the most common histologic type. Mortality at 6-month post stroke was high, and it was associated with stage of cancer and initial neurological severity.


Subject(s)
Adenocarcinoma , Cause of Death , Comorbidity , Dyslipidemias , Humans , Incidence , Infarction , Lung , Lung Neoplasms , Medical Records , Mortality , Neoplasm Metastasis , Retrospective Studies , Smoke , Smoking , Stroke
5.
Article in English | WPRIM | ID: wpr-727979

ABSTRACT

The caudal subnucleus of the spinal trigeminal nucleus (medullary dorsal horn; MDH) receives direct inputs from small diameter primary afferent fibers that predominantly transmit nociceptive information in the orofacial region. Recent studies indicate that reactive oxygen species (ROS) is involved in persistent pain, primarily through spinal mechanisms. In this study, we aimed to investigate the role of xanthine/xanthine oxidase (X/XO) system, a known generator of superoxide anion (O₂(·−)), on membrane excitability in the rat MDH neurons. For this, we used patch clamp recording and confocal imaging. An application of X/XO (300 µM/30 mU) induced membrane depolarization and inward currents. When slices were pretreated with ROS scavengers, such as phenyl N-tert-butylnitrone (PBN), superoxide dismutase (SOD), and catalase, X/XO-induced responses decreased. Fluorescence intensity in the DCF-DA and DHE-loaded MDH cells increased on the application of X/XO. An anion channel blocker, 4,4-diisothiocyanatostilbene-2,2-disulfonic acid (DIDS), significantly decreased X/XO-induced depolarization. X/XO elicited an inward current associated with a linear current-voltage relationship that reversed near −40 mV. X/XO-induced depolarization reduced in the presence of La³⁺, a nonselective cation channel (NSCC) blocker, and by lowering the external sodium concentration, indicating that membrane depolarization and inward current are induced by influx of Na⁺ ions. In conclusion, X/XO-induced ROS modulate the membrane excitability of MDH neurons, which was related to the activation of NSCC.


Subject(s)
Animals , Catalase , Facial Pain , Fluorescence , Ions , Membranes , Neurons , Oxidoreductases , Posterior Horn Cells , Rats , Reactive Oxygen Species , Sodium , Spinal Cord Dorsal Horn , Superoxide Dismutase , Superoxides , Trigeminal Nucleus, Spinal , Xanthine Oxidase
6.
Article in Korean | WPRIM | ID: wpr-54240

ABSTRACT

Recent studies indicate that mitochondria are an important source of reactive oxygen species (ROS) in the spinal dorsal horn. In our previous study, application of malate, a mitochondrial electron transport complex I substrate, induced a membrane depolarization, which was inhibited by pretreatment with ROS scavengers. In the present study, we used patch clamp recording in the substantia geletinosa (SG) neurons of spinal slices, to investigate the cellular mechanism of mitochondrial ROS on neuronal excitability. DNQX (an AMPA receptor antagonist) and AP5 (an NMDA receptor antagonist) decreased the malate-induced depolarization. In an external calcium free solution and addition of tetrodotoxin (TTX) for blockade of synaptic transmission, the malateinduced depolarization remained unchanged. In the presence of DNQX, AP5 and AP3 (a group I metabotropic glutamate receptor (mGluR) antagonist), glutamate depolarized the membrane potential, which was suppressed by PBN. However, oligomycin (a mitochondrial ATP synthase inhibitor) or PPADS (a P2 receptor inhibitor) did not affect the substrates-induced depolarization. These results suggest that mitochondrial substrate-induced ROS in SG neuron directly acts on the postsynaptic neuron, therefore increasing the ion influx via glutamate receptors.


Subject(s)
Animals , Calcium , Electron Transport Complex I , Glutamic Acid , Membrane Potentials , Membranes , Mitochondria , Mitochondrial Proton-Translocating ATPases , N-Methylaspartate , Neurons , Oligomycins , Rats , Reactive Oxygen Species , Receptors, AMPA , Receptors, Glutamate , Receptors, Metabotropic Glutamate , Spinal Cord Dorsal Horn , Substantia Gelatinosa , Synaptic Transmission , Tetrodotoxin
7.
Article in English | WPRIM | ID: wpr-25322

ABSTRACT

The aim of this study was to investigate prevalence and risk factors associated with spasticity at 3 months after a first-ever stroke in Korean patients. This cohort study included consecutive patients with first-ever stroke who were admitted to 9 participated hospitals in different areas of Korea. The Modified Ashworth Scale (MAS), which defines spasticity as MAS > 1 in any of the examined joints was used to assess patients 3 months after stroke occurrence. The prevalence of spasticity was 7.3% (339 of 4,658 patients), 3 months after stroke onset. Spasticity was more frequent in upper extremity (6.7%) than lower extremity (4.3%). Severity of spasticity was as follows: 63.1%: MAS I, 23.3%: MAS I+, 9.4%: MAS II, 2.6%: MAS III, and 1.4%: MAS IV. Stroke type (hemorrhagic) (p < 0.05) were identified as correlated risk factors. Patients with spasticity scored higher with National Institute of Health Stroke Scale (NIHSS) and lower with modified Rankin Scale (mRS) than non-spastic patients (p < 0.001). This study showed 7.3% prevalence of spasticity in Korean first-ever stroke patients at 3 months, and identified those who carried higher risks of developing spasticity who would particularly benefit from preventive or therapeutic strategies. It would contribute to assessing spasticity in patients with first-ever stroke in Korea.


Subject(s)
Cohort Studies , Humans , Joints , Korea , Lower Extremity , Muscle Spasticity , Prevalence , Rehabilitation , Risk Factors , Stroke , Upper Extremity
8.
Article in Korean | WPRIM | ID: wpr-104522

ABSTRACT

Growing evidence suggests that mitochondrial reactive oxygen species (ROS) are involved in various pain states. This study was performed to investigate whether ROS-induced changes in neuronal excitability in trigeminal subnucleus caudalis are related to ROS generation in mitochondria. Confocal scanning laser microscopy was used to measure ROS-induced fluorescence intensity in live rat trigeminal caudalis slices. The ROS level increased during the perfusion of malate, a mitochondrial substrate, after loading of 2',7'-dichlorofluorescin diacetate (H2DCF-DA), an indicator of the intracellular ROS; the ROS level recovered to the control condition after washout. When pre-treated with phenyl N-tert-butylnitrone (PBN) and 4-hydroxy-2,2,6,6-tetramethylpiperidene-1-oxyl (TEMPOL), malate-induced increase of ROS level was suppressed. To identify the direct relation between elevated ROS levels and mitochondria, we applied the malate after double-loading of H2DCF-DA and chloromethyl-X-rosamine (CMXRos; MitoTracker Red), which is a mitochondria-specific fluorescent probe. As a result, increase of both intracellular ROS and mitochondrial ROS were observed simultaneously. This study demonstrated that elevated ROS in trigeminal subnucleus caudalis neuron can be induced through mitochondrial-ROS pathway, primarily by the leakage of ROS from the mitochondrial electron transport chain.


Subject(s)
Animals , Electron Transport , Fluorescence , Microscopy, Confocal , Mitochondria , Neurons , Perfusion , Rats , Reactive Oxygen Species
9.
Article in English | WPRIM | ID: wpr-171620

ABSTRACT

BACKGROUND/OBJECTIVES: Inflammation is associated with various types of acute and chronic alcohol liver diseases. In this study, we examined whether umbelliferone (7-hydroxycoumarin, UF) ameliorates chronic alcohol-induced liver damage by modulating inflammatory response and the antioxidant system. METHODS: Rats were fed a Liber-Decarli liquid diet containing 5% alcohol with or without UF (0.05 g/L) for 8 weeks, while normal rats received an isocaloric carbohydrate liquid diet. RESULTS: Chronic alcohol intake significantly increased serum tumor necrosis factor-alpha (TNF-alpha) and interleukin 6 levels and decreased interleukin 10 level; however, UF supplementation reversed the cytokines related to liver damage. UF significantly suppressed hepatic lipopolysaccharide binding protein, toll-like receptor 4 (TLR4), nuclear factor kappa B, and TNF-alpha gene expression increases in response to chronic alcohol intake. Masson's trichrome staining revealed that UF improved mild hepatic fibrosis caused by alcohol, and UF also significantly increased the mRNA expressions and activities of superoxide dismutase and catalase in liver, and thus, decreased lipid peroxide and mitochondrial hydrogen peroxide levels. CONCLUSIONS: The findings of this study indicate that UF protects against alcohol-induced liver damage by inhibiting the TLR4 signaling pathway and activating the antioxidant system.


Subject(s)
Animals , Antioxidants , Carrier Proteins , Catalase , Cytokines , Diet , Fibrosis , Gene Expression , Hydrogen Peroxide , Inflammation , Interleukin-10 , Interleukin-6 , Liver , Liver Diseases , NF-kappa B , Rats , RNA, Messenger , Superoxide Dismutase , Toll-Like Receptor 4 , Tumor Necrosis Factor-alpha
10.
Article in Korean | WPRIM | ID: wpr-116979

ABSTRACT

Reactive oxygen species (ROS) and nitrogen species (RNS) are implicated in cellular signaling processes and as a cause of oxidative stress. Recent studies indicate that ROS and RNS are important signaling molecules involved in nociceptive transmission. Xanthine oxidase (XO) system is a well-known system for superoxide anions (O2(.-)) generation, and sodium nitroprusside (SNP) is a representative nitric oxide (NO) donor. Patch clamp recording in spinal slices was used to investigate the role of O2(.-) and NO on substantia gelatinosa (SG) neuronal excitability. Application of xanthine and xanthine oxidase (X/XO) compound induced membrane depolarization. Low concentration SNP (10 microM) induced depolarization of the membrane, whereas high concentration SNP (1 mM) evoked membrane hyperpolarization. These responses were significantly decreased by pretreatment with phenyl N-tert-butylnitrone (PBN; nonspecific ROS and RNS scavenger). Addition of thapsigargin to an external calcium free solution for blocking synaptic transmission, led to significantly decreased X/XO-induced responses. Additionally, X/XO and SNP-induced responses were unchanged in the presence of intracellular applied PBN, indicative of the involvement of presynaptic action. Inclusion of GDP-beta-S or suramin (G protein inhibitors) in the patch pipette decreased SNP-induced responses, whereas it failed to decrease X/XO-induced responses. Pretreatment with n-ethylmaleimide (NEM; thiol-alkylating agent) decreased the effects of SNP, suggesting that these responses were mediated by direct oxidation of channel protein, whereas X/XO-induced responses were unchanged. These data suggested that ROS and RNS play distinct roles in the regulation of the membrane excitability of SG neurons related to the pain transmission.


Subject(s)
Animals , Calcium , Ethylmaleimide , Humans , Membranes , Neurons , Nitric Oxide , Nitrogen , Nitroprusside , Oxidative Stress , Rats , Reactive Oxygen Species , Substantia Gelatinosa , Superoxides , Suramin , Synaptic Transmission , Thapsigargin , Tissue Donors , Xanthine , Xanthine Oxidase
11.
Journal of Stroke ; : 115-121, 2013.
Article in English | WPRIM | ID: wpr-14331

ABSTRACT

BACKGROUND AND PURPOSE: Variant alleles of CYP2C9 and VKORC1 account for differences in anticoagulation response. We sought to establish a warfarin dosing formula for individualized target International Normalization Ratio of Prothrombin Times (INRs) using data from single nucleotide polymorphisms (SNPs) in VKORC1 and CYP2C9 in Korean patients. METHODS: Ischemic stroke patients displaying stable target INR for at least 3 months before enrollment were analyzed. Warfarin and vitamin K levels were measured to adjust for confounders. Phenotypes were defined using the 'warfarin response index' (WRI) defined as INR divided by the daily maintenance warfarin dose. We tested SNPs in CYP2C9 (3 sites: 430C>T (rs1799853), 1075A>C (rs1057910), 1076T>C) and VKORC1 (14 sites: 381C>T, 861C>A (rs17880887), 2653G>C, 3673A>G, 5496G>T, 5808T>G (r17882154), 6009C>T, 6484T>C (rs9934438), 6853C>T (rs17886369), 7566T>C, 8767G>C, 8814T>C, 9041G>A (rs17880624), and 9071G>T) using a standard sequencing method. Multivariate linear regression analysis was applied to establish the formula for warfarin dosage. RESULTS: All 204 patients had excellent drug compliance. The mean INR was 2.22 (+0.56) and mean daily maintenance dose of warfarin was 3.92 mg (+1.54). Patients with low WRI were younger (PC, PC, 3673G>A, 6484T>C, 6853C>G. 7566C>T, 9041G>A) (r2=1). Based on these data, a warfarin dosing formula was established. CONCLUSIONS: WRI is influenced by age, body mass index and SNPs in VKORC1 and CYP2C9 in Korean stroke patients. The obtained warfarin dosing formula may be clinically applicable.


Subject(s)
Alleles , Body Mass Index , Compliance , Genotype , Heterozygote , Humans , International Normalized Ratio , Linear Models , Phenotype , Polymorphism, Single Nucleotide , Prevalence , Prothrombin Time , Stroke , Vitamin K , Warfarin
12.
Article in Korean | WPRIM | ID: wpr-102158

ABSTRACT

Recent studies indicate that reactive oxygen species (ROS) can act as modulators of neuronal activity, and are critically involved in persistent pain primarily through spinal mechanisms. In this study, we investigated the effects of NaOCl, a ROS donor, on neuronal excitability and the intracellular calcium concentration ([Ca2+]i) in spinal substantia gelatinosa (SG) neurons. In current clamp conditions, the application of NaOCl caused a membrane depolarization, which was inhibited by pretreatment with phenyl-N-tert-buthylnitrone (PBN), a ROS scavenger. The NaOCl-induced depolarization was not blocked however by pretreatment with dithiothreitol, a sulfhydryl-reducing agent. Confocal scanning laser microscopy was used to confirm whether NaOCl increases the intracellular ROS level. ROS-induced fluorescence intensity was found to be increased during perfusion of NaOCl after the loading of 2',7'-dichlorofluorescin diacetate (H2DCF-DA). NaOCl-induced depolarization was not blocked by pretreatment with external Ca2+ free solution or by the addition of nifedifine. However, when slices were pretreated with the Ca2+ ATPase inhibitor thapsigargin, NaOCl failed to induce membrane depolarization. In a calcium imaging technique using the Ca2+-sensitive fluorescence dye fura-2, the [Ca2+]i was found to be increased by NaOCl. These results indicate that NaOCl activates the excitability of SG neurons via the modulation of the intracellular calcium concentration, and suggest that ROS induces nociception through a central sensitization.


Subject(s)
Animals , Calcium , Calcium-Transporting ATPases , Central Nervous System Sensitization , Dithiothreitol , Fluoresceins , Fluorescence , Fura-2 , Humans , Membranes , Microscopy, Confocal , Neurons , Nociception , Perfusion , Rats , Reactive Oxygen Species , Substantia Gelatinosa , Thapsigargin , Tissue Donors
13.
Article in Korean | WPRIM | ID: wpr-45684

ABSTRACT

Recent studies indicate that reactive oxygen species (ROS) are critically involved in persistent pain primarily through spinal mechanisms, and that mitochondria are the main source of ROS in the spinal dorsal horn. To investigate whether mitochondrial ROS can induce changes in membrane excitability on spinal substantia gelatonosa (SG) neurons, we examined the effects of mitochondrial electron transport complex (ETC) substrates and inhibitors on the membrane potential of SG neurons in spinal slices. Application of ETC inhibitors, rotenone or antimycin A, resulted in a slowly developing and slight membrane depolarization in SG neurons. Also, application of both malate, a complex I substrate, and succinate, a complex II substrate, caused reversible membrane depolarization and enhanced firing activity. Changes in membrane potential after malate exposure were more prominent than succinate exposure. When slices were pretreated with ROS scavengers such as phenyl-N-tert-buthylnitrone (PBN), catalase and 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (TEMPOL), malate-induced depolarization was significantly decreased. Intracellular calcium above 100 microM increased malateinduced depolarization, witch was suppressed by cyclosporin A, a mitochondrial permeability transition (MPT) inhibitor. These results suggest that enhanced production of spinal mitochondrial ROS can induce nociception through central sensitization.


Subject(s)
Animals , Antimycin A , Calcium , Catalase , Central Nervous System Sensitization , Cyclosporine , Electron Transport , Fires , Horns , Malates , Membrane Potentials , Membranes , Mitochondria , Neurons , Nociception , Permeability , Rats , Reactive Oxygen Species , Rotenone , Substantia Gelatinosa , Succinic Acid
14.
Article in Korean | WPRIM | ID: wpr-9939

ABSTRACT

Using whole cell current- and voltage-clamp recording we investigated the characteristics and pharmacology of group I metabotropic glutamate receptor (mGluR)-mediated responses in rat medial vestibular nucleus (MVN) neurons. In current clamp conditions, activation of mGluR I by application of the group I mGluR agonist (R,S)-3,5-dihydroxyphenylglycine (DHPG) induced a direct excitation of MVN neurons that is characterized by depolarization and increased spontaneous firing frequency. To identify which of mGluR subtypes are responsible for the various actions of DHPG in MVN, we used two subtype-selective antagonists. (S)-(+)-alpha-amino-a-methylbenzeneacetic acid (LY367385) is a potent competitive antagonist that is selective for mGluR1, whereas 2-methyl-6-(phenylethynyl)-pyridine (MPEP) is a potent noncompetitive antagonist that is selective for mGluR5. In voltage clamp conditions, DHPG application increased the frequency of spontaneous and miniature inhibitory postsynaptic currents (IPSCs) but had no effect on amplitude distributions. Antagonism of the DHPG-induced increase of miniature IPSCs required the blockade of both mGluR1 and mGluR5. DHPG application induced an inward current, which can be enhanced under depolarized conditions. DHPG-induced current was blocked by LY367385, but not by MPEP. Both LY367385 and MPEP antagonized the DHPG-induced suppression of the calcium activated potassium current (IAHP). These data suggest that mGluR1 and mGluR5 have similar roles in the regulation of the excitability of MVN neurons, and show a little distinct. Furthermore, mGluR I, via pre- and postsynaptic actions, have the potential to modulate the functions of the MVN.


Subject(s)
Animals , Benzoates , Calcium , Fires , Glycine , Inhibitory Postsynaptic Potentials , Methoxyhydroxyphenylglycol , Neurons , Potassium , Rats , Receptors, Metabotropic Glutamate , Vestibular Nuclei
15.
Genomics & Informatics ; : 59-63, 2011.
Article in English | WPRIM | ID: wpr-98932

ABSTRACT

Obesity provokes many serious human diseases, including various cardiovascular diseases and diabetes. Body mass index (BMI) is a highly heritable trait that is broadly used to diagnose obesity. To identify genetic loci associated with obesity in Asians, we conducted a genome-wide association study (GWAS) of a population of Korean adults (n=6,742, age 40~60 years) and detected six BMI risk loci (TNR, FAM124B, RGS12, NFE2L3, MC4R and FTO) having p<1x10(-5). However, in the replication study, only melanocortin 4 receptor gene (MC4R) (rs9946888, p=4.58x10(-7)) was replicated with marginal significance (p<0.05) in the second cohort (n=5,102, age 40~60 years). This study indicates that each locus associated with BMI has very weak genetic effect.


Subject(s)
Adult , Asian Continental Ancestry Group , Body Mass Index , Cardiovascular Diseases , Cohort Studies , Genetic Loci , Genome-Wide Association Study , Humans , Obesity , Receptor, Melanocortin, Type 4
16.
Article in Korean | WPRIM | ID: wpr-191457

ABSTRACT

Recent studies have implicated reactive oxygen species (ROS) as determinants of the pathological pain caused by the activation of peripheral neurons. It has not been elucidated, however, how ROS activate the primary sensory neurons in the pain pathway. In this study, calcium imaging was performed to investigate the effects of NaOCl, a ROS donor, on the intracellular calcium concentration ([Ca2+]i) in acutely dissociated dorsal root ganglion (DRG) neurons. DRG was sequentially treated with 0.2 mg/ml of both protease and thermolysin, and single neurons were then obtained by mechanical dissociation. The administration of NaOCl then caused a reversible increase in the [Ca2+]i, which was inhibited by pretreatment with phenyl-N-tert-buthylnitrone (PBN) and isoascorbate, both ROS scavengers. The NaOCl-induced [Ca2+]i increase was suppressed both in a calcium free solution and after depletion of the intracellular Ca2+ pool by thapsigargin. Additionally, this increase was predominantly blocked by pretreatment with the transient receptor potential (TRP) antagonists, ruthenium red (50 microM) and capsazepine (10 microM). Collectively, these results suggest that an increase in the intracellular calcium concentration is produced from both extracellular fluid and the intracellular calcium store, and that TRP might be involved in the sensation of pain induced by ROS.


Subject(s)
Animals , Calcium , Capsaicin , Diagnosis-Related Groups , Dissociative Disorders , Extracellular Fluid , Ganglia, Spinal , Humans , Neurons , Rats , Reactive Oxygen Species , Ruthenium Red , Sensation , Sensory Receptor Cells , Spinal Nerve Roots , Thapsigargin , Thermolysin , Tissue Donors
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