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1.
Journal of Chinese Physician ; (12): 1266-1269, 2021.
Article in Chinese | WPRIM | ID: wpr-909693

ABSTRACT

In most non-excited cells, voltage-gated T-type calcium channels present three properties of activation, inactivation and slow inactivation, thus contribute to cellular calcium signaling and membrane potential. By which T-type calcium channels play an important role in many cancer cellular processes such as cell proliferation, differentiation, apoptosis, invasion, and metastasis. Inhibiting T-type calcium channels by drugs or genetic tools can change the related cellular currents and the intracellular Ca 2+ , thereby regulating the biological tumorigenesis. This article reviews the electrophysiological of T-type calcium channels during tumor progression, aims to provide a scientific basis for the study and treatment in cancer.

2.
J. venom. anim. toxins incl. trop. dis ; 27: e20210001, 2021. tab, graf, ilus
Article in English | LILACS, VETINDEX | ID: biblio-1351017

ABSTRACT

Phα1ß is a neurotoxin purified from spider venom that acts as a high-voltage-activated (HVA) calcium channel blocker. This spider peptide has shown a high selectivity for N-type HVA calcium channels (NVACC) and an analgesic effect in several animal models of pain. Its activity was associated with a reduction in calcium transients, glutamate release, and reactive oxygen species production from the spinal cord tissue and dorsal ganglia root (DRG) in rats and mice. It has been reported that intrathecal (i.t.) administration of Phα1ß to treat chronic pain reverted opioid tolerance with a safer profile than ω-conotoxin MVIIA, a highly selective NVACC blocker. Following a recent development of recombinant Phα1ß (CTK 01512-2), a new molecular target, TRPA1, the structural arrangement of disulphide bridges, and an effect on glial plasticity have been identified. CTK 01512-2 reproduced the antinociceptive effects of the native toxin not only after the intrathecal but also after the intravenous administration. Herein, we review the Phα1ß antinociceptive activity in the most relevant pain models and its mechanisms of action, highlighting the impact of CTK 01512-2 synthesis and its potential for multimodal analgesia.


Subject(s)
Pain , Peptides/isolation & purification , Reactive Oxygen Species , Analgesics/adverse effects , Neurotoxins/isolation & purification
3.
Article | IMSEAR | ID: sea-215974

ABSTRACT

Introduction:Obesity is closely associated with various types of illness, primarily caused by more calorie intake than body burn. In adipocytes, Calcium (Ca2+) is an important second messenger involved in theregulation of many physiological functions which are essential for survival. In the present research, we have investigated the role of Ca2+ions in obesity by manipulating cytosolic Ca2+ion concentration by selective blocking/advancing the Ca2+ions through the voltage-gated calcium channels. Voltage-gated calcium channel (vCa) plays a key role in regulating intracellular and extracellular Ca2+concentration.Cytoplasmic level of Ca2+was manipulated by supplying calcium carbonateand by using vCa blockers i.e. nifedipine-(N-type-vCa-CCB) and ethosuximide (T-type, vCa-CCB).Methods:Obesity was induced by progesterone in female mice and test drugs were co-administered with progesterone whereas sibutramine was used as standard. The treatment was carried out for 28 days, during and afterthetreatment periodvarious parameters were studied viz food consumption, change in body weight and temperature, the effect on WAT (white adipose tissue, adiposity index, histology of fat pad) and fecal lipid content.Results:Calcium carbonate treated group has shown promising effects in the decrease in body weight by increasing fecal lipid content and lipolysis which was reflected by an increase in body temperature. Ethosuximide also offered significant protection by decreasing the food intake but has not shown any notable effect on fecal fat content, whereas nifedipine has not offered any protection against the obesity induced by neurosteroid.Conclusion:Calcium carbonate has significant anti-obesity activity by including thermogenesis, and increasing fecal lipid content

4.
European J Med Plants ; 2019 Oct; 29(3): 1-11
Article | IMSEAR | ID: sea-189501

ABSTRACT

Aims: We aimed in this study to investigate the mechanisms of the vasorelaxation effect caused by the anthocyanins-enriched extract of Odontonema strictum flowers. Study Design: Anthocyanins-enriched extract of Odontonema strictum flowers and vasorelaxantes activities of mice aortic rings. Place and Duration of Study: The flowers of Odontonema strictum (Nees) Kuntze (Acanthaceae) were collected in January 2015 at the “Institut de Recherche en Sciences de la Santé (IRSS)” experimental station in Ouagadougou. The experiments were conducted in October - November 2018 at the department of Medicine and Traditional Pharmacopeia-Pharmacy (MEPHATRA-PH)/IRSS. Methodology: The extract was enriched in anthocyanins using Amberlite XAD-7 non-ionic resin column. The vasorelaxant activity of anthocyanins-enriched extract of O. strictum flowers (OSF) was tested using isolated organ-chamber technique with mice aorta rings. Results: OSF showed concentration-dependent relaxant effects on mice endothelium intact or denuded aortic rings pre-contracted with U46619 (10-7 M) and KCl (80 mM). OSF induced relaxation in the mice aortic rings by stimulating smooth muscle cells. The vasorelaxant effect of OSF (10-1000 µg/mL) was similar in endothelium-intact and endothelium-denuded aortic rings. The maximum relaxant effect was 93.78 ± 4.69% and 92.30 ± 3.19% for endothelium-intact and endothelium-denuded aortic rings, respectively. Moreover, after incubation of the aorta rings with OSF (400 µg/mL) or vehicle (0.02% of DMSO) in PSS, OSF blocked the contraction through mechanism involving inhibition of CaCl2 and U46619 effect. Conclusions: The present study provides a pharmacological evidence for the antihypertensive medicinal use of Odontonema strictum by highlighting its vasorelaxant activity.

5.
Experimental Neurobiology ; : 568-577, 2019.
Article in English | WPRIM | ID: wpr-763789

ABSTRACT

The thalamus is a brain structure known to modulate sensory information before relaying to the cortex. The unique ability of a thalamocortical (TC) neuron to switch between the high frequency burst firing and single spike tonic firing has been implicated to have a key role in sensory modulation including pain. Of the two firing modes, burst firing, especially maintaining certain burst firing properties, was suggested to be critical in controlling nociceptive behaviors. Therefore, understanding the factors that influence burst firing properties would offer important insight into understanding sensory modulation. Using computational modeling, we investigated how the balance of excitatory and inhibitory inputs into a TC neuron influence TC bursting properties. We found that intensity of inhibitory inputs and the timing of excitatory input delivery control the dynamics of bursting properties. Then, to reflect a more realistic model, excitatory inputs delivered at different dendritic locations—proximal, intermediate, or distal—of a TC neuron were also investigated. Interestingly, excitatory input delivered into a distal dendrite, despite the furthest distance, had the strongest influence in shaping burst firing properties, suggesting that not all inputs equally contribute to modulating TC bursting properties. Overall, the results provide computational insights in understanding the detailed mechanism of the factors influencing temporal pattern of thalamic bursts.


Subject(s)
Brain , Calcium Channels, T-Type , Computational Biology , Dendrites , Fires , Neurons , Sensory Gating , Thalamus
6.
Chinese Journal of Cardiology ; (12): 640-646, 2019.
Article in Chinese | WPRIM | ID: wpr-805712

ABSTRACT

Objective@#To investigate the impact of n-3 polyunsaturated fatty acid (n-3 PUFA) on function and expression of store-operated calcium channels (SOCC) in coronary artery smooth muscle cells (SMC) derived from diabetic rat.@*Methods@#A total of 180 healthy male Sprague-Dawley (SD) rats were randomly divided into normal group (N, n=45), placebo-treated diabetic group (D, n=45), lose dose n-3 PUFA treated diabetic group (DL, n=45) and high dose n-3 PUFAs treated diabetic group (DH, n=45). Streptozotocin-induced diabetic rat animal model was established by two consecutive intraperitoneal injections. After modeling, rats in group DL and DH were treated with 10 mg·kg-1·d-1 and 50 mg·kg-1·d-1 n-3 PUFAs respectively per gavage for eight weeks. After eight weeks, rat coronary artery SMC was isolated by enzyme digestion. Changes of cytosolic calcium concentration in coronary artery SMC were examined by calcium fluorescence imaging technique, coronary artery tension was detected by myograph system, and protein expressions of SOCC on coronary artery SMC were measured by Western blot.@*Results@#SOCC induced ΔF340/F380 of group N, D, DL and DH were 0.425±0.023, 0.838±0.037, 0.342±0.052 and 0.364±0.045 respectively, which was significantly lower in group N, DL, DH than in group D (P<0.05). SOCC induced changes of tensions were 0.94±0.09, 1.95±0.18, 1.35±0.24 and 1.01±0.18 in the group N, D, DL and DH, respectively, which was significantly lower in group N and DH than in group D (P<0.05). Protein expressions of STIM1, Orai1 and TRPC1 were significantly higher in diabetic rat coronary SMC than in group N (P<0.05). STIM1 protein expressions were significantly lower in group DL and DH than in group D, and Orai1 and TRPC1 protein expressions were similar among group.@*Conclusions@#Coronary artery tension, cytosolic calcium concentration and protein expressions of SOCC are higher in diabetic rat coronary artery SMC when compared with normal rats. n-3 PUFA intervention could downregulate the protein expression of SOCC, reduce cytosolic calcium concentration and coronary artery tension, and is protective to the diabetic injury in coronary artery.

7.
Chinese Journal of Cardiology ; (12): 608-613, 2019.
Article in Chinese | WPRIM | ID: wpr-805707

ABSTRACT

Objective@#To investigate the effects and mechanism of digoxin on atrium electrical remodeling and susceptibility of atrial fibrillation (AF) in aged rabbits.@*Methods@#Twenty aged male New Zealand rabbits were divided into aged group and aged plus digoxin group (n=10 each). Electrical parameters including heart rate (HR), RR and QT interval, ST segment and P wave dispersion from normal Ⅱ electrocardiogram, and the maximum upstroke velocity (Maxdv/dt), plateau potential (plateau P), action potential duration of 10%, 20% and 90% (APD10, APD20, APD90) from recording of monophasic action potential (MAP), as well as atrial effective refractory period (AERP200) and dispersion (dERP200) with 200 ms of basic cycle length (BCL), and frequency self adaptation of AERP with 300 ms and 150 ms of BCLs (fERP) were recorded and compared between the 2 groups. BCLs and inducibility of AF post programmed electrical stimulation and Burst-pacing in left atrium tissue of rabbits in vivo were also analyzed. The L-type calcium current (ICa-L) in 2 groups were recorded via whole-cell patch clamp technique, and the fluorescence intensity of intracellular free Ca2+ was detected with Flup-3/AM loading by the laser scanning confocal microscope in enzymatically dissociated single rabbit atrial myocytes.@*Results@#Compared with aged group, the heart rate was faster, RR and QT interval were obvious shorter, ST segment was raised and P wave dispersion was significantly increased in aged plus digoxin group (all P<0.05). Moreover, compared with aged group, the Maxdv/dt and plateau P were obviously increased, APD10 and APD20 were significantly prolongated, and APD90 was significantly shorter in aged plus digoxin group (all P<0.01). Otherwise, the fERP was markedly increased (0.81±0.15 vs. 0.67±0.05), and the induced rate of AF was obviously higher in aged plus digoxin group than in aged group (6/8 vs. 4/9) (all P<0.01). With voltage clamp model, digoxin significantly increased ICa-L of atrial myocytes of aged rabbits, When command potential was 10 mV, the current densities of ICa-L were significantly higher in digoxin group than that in aged group ((15.45±2.38) pA/pF vs. (7.03±1.69) pA/pF, P<0.01). Otherwise, the I-V curve of ICa-L was downward shifted of all I-V curves in digoxin perfused aged atrial cells of rabbits. Moreover, the fluorescence intensities of intracellular free Ca2+ was significantly higher in aged plus digoxin group than in aged group ((1 748±173) μmol/L vs. (478.13±87.63) μmol/L, P<0.01).@*Conclusion@#Digoxin could aggravate the atrial electrical remodeling in atrium of aged rabbits, facilitate susceptibility of atrial fibrillation in aged rabbit, increased current density of ICa-L and concentration of intracellular free Ca2+, followed Ca2+ overload and oscillations might be part of the underlying mechanisms.

8.
Article in Chinese | WPRIM | ID: wpr-861829

ABSTRACT

Background: Obesity is associated with many functional gastrointestinal disorders, such as gastrointestinal motility disorder. Previous studies showed that adipose tissue-derived adipokine visfatin (VF), which increased in obesity, might impair myometrial contractility and cause vascular smooth muscle relaxation. Aims: To investigate the effect of VF on contractility of colonic smooth muscle in rats and its underlying mechanism. Methods: Segments of distal colon from normal Sprague-Dawley (SD) rats were dissected into strips (0.3 cm × 0.8 cm), and the effect of VF on contractility of muscle strips was measured by biological signal collection system. In in vitro study, colonic smooth muscle cells (SMCs) from neonatal SD rats were cultured and treated with VF; phosphorylation of myoglobulin light chain (MLC) and expression of calcium channel protein Cav1.2 (α1 subunit) were assessed by Western blotting. Cultured in buffer solution with or without calcium, the acetylcholine-stimulated intracellular Ca2+ level in SMCs was detected by confocal laser scanning microscopy. Results: In muscle strip contractility assay, VF (200 ng/mL) significantly inhibited the contractility of colonic smooth muscle strip from normal adult rats (P<0.05). In cultured colonic SMCs, VF (200 ng/mL) down-regulated the calcium channel protein Cav1.2 expression and reduced the intracellular Ca2+ level and MLC phosphorylation (P<0.05). Conclusions: VF may down-regulate the expression of calcium channel protein Cav1.2 on the membrane of colonic SMCs and cause colonic dysmotility by interfering with Ca2+ signaling and smooth muscle contractility.

9.
Article in Chinese | WPRIM | ID: wpr-861795

ABSTRACT

Irritable bowel syndrome (IBS) is a common functional gastrointestinal disorder, mainly manifested as recurrent abdominal pain, abdominal discomfort and/or changes of defecation habits and stool character, its pathogenesis has not been fully clarified. The pathophysiology is characterized by visceral hypersensitivity, abnormal intestinal motility, and so on. Abnormality of ion channels may be in involved in the pathophysiological mechanism of IBS. This article reviewed the progress in study on ion channels and pathogenesis of IBS.

10.
Article in English | WPRIM | ID: wpr-761801

ABSTRACT

Docosahexaenoic acid (DHA), an omega-3-fatty acid, modulates multiple cellular functions. In this study, we addressed the effects of DHA on human umbilical vein endothelial cell calcium transient and endothelial nitric oxide synthase (eNOS) phosphorylation under control and adenosine triphosphate (ATP, 100 µM) stimulated conditions. Cells were treated for 48 h with DHA concentrations from 3 to 50 µM. Calcium transient was measured using the fluorescent dye Fura-2-AM and eNOS phosphorylation was addressed by western blot. DHA dose-dependently reduced the ATP stimulated Ca²⁺-transient. This effect was preserved in the presence of BAPTA (10 and 20 µM) which chelated the intracellular calcium, but eliminated after withdrawal of extracellular calcium, application of 2-aminoethoxy-diphenylborane (75 µM) to inhibit store-operated calcium channel or thapsigargin (2 µM) to delete calcium store. In addition, DHA (12 µM) increased ser1177/thr495 phosphorylation of eNOS under baseline conditions but had no significant effect on this ratio under conditions of ATP stimulation. In conclusion, DHA dose-dependently inhibited the ATP-induced calcium transient, probably via store-operated calcium channels. Furthermore, DHA changed eNOS phosphorylation suggesting activation of the enzyme. Hence, DHA may shift the regulation of eNOS away from a Ca²⁺ activated mode to a preferentially controlled phosphorylation mode.


Subject(s)
Adenosine Triphosphate , Adenosine , Blotting, Western , Calcium Channels , Calcium , Endothelial Cells , Humans , Nitric Oxide Synthase Type III , Phosphorylation , Thapsigargin , Umbilical Veins
11.
Article in Chinese | WPRIM | ID: wpr-790193

ABSTRACT

Objective: To evaluate spasmolytic mechanisms of aqueous and methanolic extracts from Distemonanthus benthamianus trunk-bark. Methods: Spasmolytic activities of extracts were evaluated in vitro on spontaneous and potassium chloride-induced jejunum contractions, or against cholinergic [acetylcholine (0.3μmol/L)] stimulations. High performance liquid chromatography analysis of both extracts was performed in reference to standard compounds. Results: Extracts developed concentration-dependent inhibitory activities. The methanolic extract, which revealed better activity, produced spasmolytic and myorelaxant effects at concentrations of 0.01-0.30 mg/mL with EC50 of 0.06 and 0.09 mg/mL (95% CI: 0.03-0.3 mg/mL), respectively. Its anticholinergic effect was obtained at the same concentrations with EC50 of 0.11 mg/mL (95% CI:0.03-0.3 mg/mL). Chromatograms showed the presence of gallic acid in both extracts, rutin being only detected in the aqueous extract. Conclusions: Distemonanthus benthamianus extracts exhibit verapamil and atropine-like activities, thus highlighting calcium channels and muscarinic receptors blocking potentials, which may be conveyed by some phenolic compounds. These results confirm the antidiarrheal activity of Distemonanthus benthamianus extracts.

12.
Article in Chinese | WPRIM | ID: wpr-790158

ABSTRACT

:Vascular endothelial cells are the barrier of blood vessels .Endothelial injury will lead to occurrence of multiple diseases ,whose mechanism is related to intracellular calcium signal pool regulation .Ca2+ is a secondary messenger for information delivery inside and outside cells ,it initiates endothelial cell signals and plays an important role in controlling vascular tension and endothelial permeability .Study on mechanism of vascular endothelial cell in‐jury has become a hot topic in recent years ,and calcium homeostasis imbalance is the key factor ,whose mechanism is still not clear .The present article reviewed regulating mechanisms of vascular endothelial cytoplasmic membrane calcium transport and intracellular calcium pool regulation , aimed at providing new thinking for prevention and treatment of calcium regulation related diseases .

13.
Article in Chinese | WPRIM | ID: wpr-841615

ABSTRACT

Objective: To observe the effect of 17β-estradiol (17β-E2) on the calcium (Ca2) channels during the osteogenic differentiation of rat bone marrow mesenchymal stem cells (MSCs), and to elucidate the mechanism of 17β-E2 in the osteogenic differentiation of MSCs. Methods: The MSCs were separated by density gradient centrifugation and adherent screening, and passaged for 3 times continuously to induce osteoblast differentiation. The MSCs were divided into control group [cultivated in osteoblast culture medium alone (OBM)] and different doses of 17β-E2 groups (added with 0. 1, 1.0, 10. 0, and 100. 0 pmol · L-1 17β-E2 in OBM, respectively). On the 14th day of osteogenic induction, the cells in each group were stained with Fluo-3/AM, and the Ca2 levels were determinated by laser scanning confocal microscope; the mean fluorescence intensity (MFD was used to respresent the level of Ca2. Whole-cell Ca2 currents were recorded using whole-cell patch clamp technique under different conditions. Results: The MSCs with fibroblast-like cells, oval nuclei and visible nucleoli were successfully isolated by density gradient centrifugation and adherent screening. The subcultured MSCs grew vigorously and maintained the morphological characteristics of primary cells. Following the increase of 17β-E2 concentration, the Fluo-3 fluorescence staining intensity of Ca2 in each group was also gradually increased, especially in 100. 0 pmol · L-1 17β-E2 group. Compared with control group, the MFI of Ca' and the current peak values of Ca' in 10. 0 and 100. 0 pmol · L-1 17β-E2 groups were increased (P0. 05). Conclusion: The cells isolated by density gradient and adherent screening method are the rat MScs. 17β-E2 plays a role in promoting osteogenesis by enhancing the opening of Ca' channels in the MSCs and the inward current of calcium ions in a dose-dependent manner.

14.
Braz. j. med. biol. res ; 51(4): e7124, 2018. graf
Article in English | LILACS | ID: biblio-889061

ABSTRACT

Marasmius androsaceus is a medicinal fungus mainly used to treat various forms of pain in China. This study investigated the analgesic effects of an ethanol extract of M. androsaceus (MAE) and its potential molecular mechanisms. Oral administration of MAE (50, 200, and 1000 mg/kg) had significant analgesic effects in an acid-induced writhing test, a formalin test, and a hot-plate test, with effectiveness similar to tramadol (the positive control drug). The autonomic activity test showed that MAE had no harmful effects on the central nervous system in mice. MAE resulted in significantly enhanced levels of noradrenalin and 5-hydroxytryptamine in serum but suppressed both of these neurotransmitters in the hypothalamus after 30 s of hot-plate stimulation. Co-administration with nimodipine (10 mg/kg; a Ca2+ channel blocker) strongly enhanced the analgesic effect in the hot-plate test compared to MAE alone. Moreover, MAE down-regulated the expression of calmodulin-dependent protein kinase II (CaMKII) in the hypothalamus after a 30-s thermal stimulus. These results suggested that the analgesic ability of MAE is related to the regulation of metabolism by monoamine neurotransmitters and Ca2+/CaMKII-mediated signaling, which can potentially aid the development of peripheral neuropathic pain treatments obtained from M. androsaceus.


Subject(s)
Animals , Male , Mice , Pain/drug therapy , Tramadol/pharmacology , Plant Extracts/pharmacology , Marasmius/chemistry , Analgesics/pharmacology , Pain Measurement/drug effects , Disease Models, Animal
15.
Article in English | WPRIM | ID: wpr-715249

ABSTRACT

BACKGROUND/OBJECTIVE: This study was designed to investigate how a Portulaca oleracea L. extract (POE) stimulates insulin secretion in INS-1 pancreatic β-cells. MATERIALS/METHOD: INS-1 pancreatic β-cells were incubated in the presence of various glucose concentrations: 1.1 or 5.6, 16.7 mM glucose. The cells were treated with insulin secretagogues or insulin secretion inhibitor for insulin secretion assay using an insulin ELISA kit. In order to quantify intracellular influx of Ca2+ caused by POE treatment, the effect of POE on intracellular Ca2+ in INS-1 pancreatic β-cells was examined using Fluo-2 AM dye. RESULTS: POE at 10 to 200 µg/mL significantly increased insulin secretion dose-dependently as compared to the control. Experiments at three glucose concentrations (1.1, 5.6, and 16.7 mM) confirmed that POE significantly stimulated insulin secretion on its own as well as in a glucose-dependent manner. POE also exerted synergistic effects on insulin secretion with secretagogues, such as L-alanine, 3-isobutyl-1-methylxanthine, and especially tolbutamide, and at a depolarizing concentration of KCl. The insulin secretion caused by POE was significantly attenuated by treatment with diazoxide, an opener of the K+ ATP channel (blocking insulin secretion) and by verapamil (a Ca2+ channel blocker). The insulinotropic effect of POE was not observed under Ca2+-free conditions in INS-1 pancreatic β-cells. When the cells were preincubated with a Ca2+ fluorescent dye, Fluo-2 (acetoxymethyl ester), the cells treated with POE showed changes in fluorescence in red, green, and blue tones, indicating a significant increase in intracellular Ca2+, which closely correlated with increases in the levels of insulin secretion. CONCLUSIONS: These findings indicate that POE stimulates insulin secretion via a K+ ATP channel-dependent pathway in INS-1 pancreatic β-cells.


Subject(s)
1-Methyl-3-isobutylxanthine , Adenosine Triphosphate , Alanine , Calcium Channels , Diabetes Mellitus , Diazoxide , Enzyme-Linked Immunosorbent Assay , Fluorescence , Glucose , Insulin , Portulaca , Tolbutamide , Verapamil
16.
Chinese Journal of Orthopaedics ; (12): 1458-1465, 2018.
Article in Chinese | WPRIM | ID: wpr-734396

ABSTRACT

Objective To investigate the regulatory effects of stromal interaction molecule-2 (STIM2) on Ca2+ release activated Ca2+ (CRAC) channel of chondrocytes using STIM2 overexpression model.Methods Chondrocytes were harvested from degenerative (osteoarthritic chondrocytes) or normal regions (normal chondrocytes) of articular cartilage during total knee arthroplasty.CRAC channel function of chondrocytes was tested with Real-time calcium imaging.The protein expression level of STIM2 was examined with Western Blot.The STIM2 overexpression plasmid was constructed and transfected into chondrocytes.The transfect efficiency was verified by cell fluorescence,Real-time PCR,and Western Blot.Results Compared with normal chondrocytes (2.87±0.32 folds,231.96±17.82 s),osteoarthritic chondrocytes (2.13±0.12 folds,336.85±15.88 s) demonstrated lower peak intensity of calcium signal in the presence of thapsigargin,and required longer duration to reach saturated calcium concentration after exogenous calcium addition.STIM2 expression level was increased in osteoarthritic chondrocytes.After plasmid transfection,the fluorescence intensity,gene expression and protein level of STIM2 in chondrocytes were increased.Compared with chondrocytes in control group (4.58±0.28 folds,4.34±0.33 folds),chondrocytes of STIM2 overexpression group (2.60±0.19 folds,2.24±0.19 folds) showed decreased calcium signal peak intensity upon either thapsigargin stimulation or exogenous calcium addition.Conclusion STIM2 negatively regulates CRAC channel function and decreases stored-Ca2+ in chondrocytes.

17.
Chinese Journal of Pathophysiology ; (12): 996-1001, 2018.
Article in Chinese | WPRIM | ID: wpr-701229

ABSTRACT

AIM:To observe the effect of thyroxine on the expression of T-type calcium channels Cav3. 1, Cav3. 2 and Cav3. 3 in rat myocardium, and to explore the possible biological mechanism between the changes of the ex-pression of T-type calcium channels and the arrhythmia in hyperthyroid heart disease. METHODS:Healthy SD rats (n=20) were randomly divided into normal control group (n=10) and hyperthyroid heart disease group (n=10). The animal model was established by intraperitoneal injection of levothyroxine for 35 d. The contents of T3 and T4 in serum, the heart-to-body weight ratio, the diameter of cardiac myocytes and electrocardiograph were measured to evaluate hyperthyroid heart disease. Moreover, the mRNA and protein expression levels of T-type calcium channels in the myocardium were measured by RT-PCR, immunohistochemistry and Western blot. RESULTS:After intraperitoneal injection of levothyroxine for 35 d, compared with the normal control group, the serum contents of T3 and T4, the heart-to-body weight ratio and the diameter of cardiac myocytes were significantly increased in hyperthyroid heart disease group (P<0.05), and arrhythmia occurred in hyperthyroid heart disease group. By immunohistochemistry and Western blot, the protein expression of Cav3. 1 in-creased significantly (P<0.05), while the protein expression of Cav3.2 decreased significantly (P<0.01). However, no change of the Cav3. 3 protein was observed. The results of RT-PCR were the same as immunohistochemistry and Western blot. CONCLUSION:Thyroxine promotes the expression of Cav3. 1 in the myocardium but inhibits the expression of Cav3. 2 at mRNA and protein levels, which might be involved in arrhythmia in hyperthyroid heart disease.

18.
Tianjin Medical Journal ; (12): 657-660, 2018.
Article in Chinese | WPRIM | ID: wpr-698088

ABSTRACT

Studies have shown that stromal interaction molecule 1(STIM1) is closely related to the development of tumors, and which is involved in the regulation of apoptosis, proliferation, migration and invasion in many human cancers. Blocking or knockdown of STIM1 can significantly inhibit the proliferation and migration of cancer cells. Elucidation of the regulatory mechanism of STIM1 in cancer cells will be helpful for the identification of new therapeutic targets. This paper reviews the mechanism of STIM1 molecule in different tumors and its clinical application.

19.
Article in English | WPRIM | ID: wpr-728614

ABSTRACT

The exponential increase in the use of mobile communication has triggered public concerns about the potential adverse effects of radiofrequency electromagnetic fields (RF-EMF) emitted by mobile phones on the central nervous system (CNS). In this study, we explored the relationship between calcium channels and apoptosis or autophagy in the hippocampus of C57BL/6 mice after RF-EMF exposure with a specific absorption rate (SAR) of 4.0 W/kg for 4 weeks. Firstly, the expression level of voltage-gated calcium channels (VGCCs), a key regulator of the entry of calcium ions into the cell, was confirmed by immunoblots. We investigated and confirmed that pan-calcium channel expression in hippocampal neurons were significantly decreased after exposure to RF-EMF. With the observed accumulation of autolysosomes in hippocampal neurons via TEM, the expressions of autophagy-related genes and proteins (e.g., LC3B-II) had significantly increased. However, down-regulation of the apoptotic pathway may contribute to the decrease in calcium channel expression, and thus lower levels of calcium in hippocampal neurons. These results suggested that exposure of RF-EMF could alter intracellular calcium homeostasis by decreasing calcium channel expression in the hippocampus; presumably by activating the autophagy pathway, while inhibiting apoptotic regulation as an adaptation process for 835 MHz RF-EMF exposure.


Subject(s)
Absorption , Animals , Apoptosis , Autophagy , Calcium Channels , Calcium , Cell Phone , Central Nervous System , Down-Regulation , Electromagnetic Fields , Hippocampus , Homeostasis , Ions , Mice , Neurons
20.
Article in English | WPRIM | ID: wpr-218945

ABSTRACT

Diabetes mellitus (DM) is becoming a lifestyle-related pandemic disease. Diabetic patients frequently develop electrolyte disorders, especially diabetic ketoacidosis or nonketotic hyperglycemic hyperosmolar syndrome. Such patients show characteristic potassium, magnesium, phosphate, and calcium depletion. In this review, we discuss a homeostatic mechanism that links calcium and DM. We also provide a synthesis of the evidence in favor or against this linking mechanism by presenting recent clinical indications, mainly from veterinary research. There are consistent results supporting the use of calcium and vitamin D supplementation to reduce the risk of DM. Clinical trials support a marginal reduction in circulating lipids, and some meta-analyses support an increase in insulin sensitivity, following vitamin D supplementation. This review provides an overview of the calcium and vitamin D disturbances occurring in DM and describes the underlying mechanisms. Such elucidation will help indicate potential pathophysiology-based precautionary and therapeutic approaches and contribute to lowering the incidence of DM.


Subject(s)
Calcium Channels , Calcium , Diabetes Mellitus , Diabetic Ketoacidosis , Homeostasis , Humans , Incidence , Insulin Resistance , Magnesium , Pandemics , Potassium , Vitamin D
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