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gap junction communication involved in brain protection following focal ischemia and reperfusion in rats

Neural Regeneration Research 2009年第9期4卷 677-682页

作者： Fei Wang Jian Hai Yuhong Jing Department of Neurosurgery Tongji Hospital of Tongji University Shanghai 200065 China School of Basic Medical Sciences Lanzhou University Lanzhou 730000 Gansu Province China

BACKGROUND： Studies have suggested that gap junctions not only modulate the fate of the neocortex, but are also involved in maintaining homeostasis in the mature brain. However, the neuroprotective effects of gap junction communication following brain ischemic injury remain poorly understood. OBJECTIVE： To investigate the neuroprotective effects and possible mechanisms of gap junction communication following focal ischemia and reperfusion. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the School of Basic Medical Sciences of Lanzhou University between June 2007 and May 2008. MATERIALS： Rabbit polyclonal anti-connexin 43 （Cx43） and gap junction blocking agent octanol were purchased from Sigma, USA; mouse monoclonal anti-rat glial fibrillary acidic protein （GFAP） was provided by Santa Cruz, USA; mouse monoclonal anti-rat CD11 b was produced by Abcam, England. METHODS： A total of 52 adult, male, Sprague Dawley rats were randomly assigned to three groups： sham-operated （n = 12）, vehicle control （n = 20）, and octanol-treated （n = 20）. Brain ischemia and reperfusion were induced by transient middle cerebral artery occlusion （MCAO） in vehicle control and octanol-treated groups, while no MCAO was administered to the sham-operated group. In the octanol-treated group, 5 mmol/kg octanol was dissolved in dimethyl sulfoxide （0.005% v/v） and was intraperitoneally injected 30 minutes prior to ischemic onset. Sham-operated and vehicle groups received equivalent volumes of dimethyl sulfoxide. MAIN OUTCOME MEASURES： Infarct volumes in ipsilateral striatum after MCAO were measured using cresyl violet dye; GFAP, CD11 b, and Cx43 expression in the ipsilateral striatum following MCAO were detected by immunohistochemistry; Western blot analysis was employed to determine Cx43 and GFAP expression. RESULTS： At 1 and 3 days following MCAO and reperfusion, ipsilateral striatum infarct volumes in the octanol group were significantly greater than in the vehicle group （P 〈 0.05）. There was no

关键词： gap junction brain ischemia astrocytes microglia rats

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The gap junction blocker carbenoxolone enhances propofol and sevoflurane-induced loss of consciousness

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Neural Regeneration Research 2012年第7期7卷 492-495页

作者： Zhigang Liu Yongfang Liu Bo Zhao Li Du Zhongyuan Xia Xiangdong Chen Tao Luo Department of Anesthesiology Renmin Hospital of Wuhan University Wuhan 430060 Hubei Province China Department of Anesthesiology Wuhan First Hospital Wuhan 430022 Hubei Province China

General anesthetics induce loss of consciousness by inhibiting ascending arousal pathways, and they interfere with gap junction electrical coupling. The present study aimed to determine whether inhibition of gap junction-mediated signaling could influence general anesthetic-induced loss of consciousness. The general anesthetics sevoflurane and propofol were used. Intracerebroventricular administration of carbenoxolone, a gap junction blocker, significantly decreased the time to loss of the righting reflex （P 0.05）, but prolonged the time to recovery of the reflex （P 0.05）. Moreover, intracerebroventricular administration of carbenoxolone increased the sensitivity to sevoflurane, with a leftward shift of the loss of righting reflex dose-response curve, and decreased the 50% effective concentration of sevoflurane. These results suggest that the gap junction blocker carbenoxolone enhances propofol and sevoflurane-mediated general anesthesia.

关键词： gap junction blocker propofol sevoflurane general anesthesia nerve block neuropharmacology

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The synchronization of FitzHugh-Nagumo neuron network coupled by gap junction

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Chinese Physics B 2008年第6期17卷 2297-2303页

作者：展永张素花赵同军安海龙张振东韩英荣柳辉张玉红 School of Sciences Hebei University of Technology

It is well known that the strong coupling can synchronize a network of nonlinear oscillators. Synchronization provides the basis of the remarkable computational performance of the brain. In this paper the FitzHugh-Nagumo neuron network is constructed. The dependence of the synchronization on the coupling strength, the noise intensity and the size of the neuron network has been discussed. The results indicate that the coupling among neurons works to improve the synchronization, and noise increases the neuron random dynamics and the local fluctuations; the larger the size of network, the worse the synchronization. The dependence of the synchronization on the strength of the electric synapse coupling and chemical synapse coupling has also been discussed, which proves that electric synapse coupling can enhance the synchronization of the neuron network largely.

关键词： synchronization gap junction FitzHugh-Nagumo model

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The impact of radicals in cold atmospheric plasma on the structural modification of gap junction:a reactive molecular dynamics study

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International Journal of Smart and Nano Materials 2019年第2期10卷 144-155页

作者： Rong-Guang Xu Zhitong Chen Michael Keidar Yongsheng Leng Department of Mechanical and Aerospace Engineering The George Washington UniversityWashingtonDCUSA

Cold atmospheric plasmas are currently gaining increasing attention for cancer therapy.However,very limited studies regarding the interaction mechanisms between plasma species and tissues are available.We report the interaction of plasma produced species(^(*)OH and HO_(2)^(*))with gap junction by employing reactive molecular dynamics simulations.Our results indicate ^(*)OH and HO_(2)^(*) radicals can chemically react with N-terminal of gap junction resulting in its structural damage.There are two breaking mechanisms being identified:C-N peptide bonds and C-C bonds can be damaged by ^(*)OH and HO_(2)^(*) radicals,respectively.Our findings could be particularly important for understanding the plasma-generated reactive species triggering bystander effect based on gap junction intercellular communication.

关键词： Cold atmospheric plasma reactive species molecular dynamics bystander effect gap junction

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EFFECT OF ANTIBODIES AGAINST THE gap junction PROTEIN ON DIFFERENTIATION OF INDUCED EMBRYONIC CELLS

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Science China Chemistry 1988年第11期31卷 1315-1318页

作者：曾弥白陈艳华 Shanghai Institute of Cell Biology Academia Sinica

Microinjections of antibodies against gap junction prorein to early blastomcres of Xenopus laevis were succeeded by the treatments of mesodermal inductor. It was found that induction was not affected by the injection of the antibodies but the differentiation of notochord and muscle was impeded at different degrees. Cell interactions via gap junction communication seem to be involved in the differentiation of the induced cells.

关键词： gap junction cell differentiation embryonic induction.

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Effect of zymosan on the expression and function of the gap-junction protein connexin 43 in human corneal fibroblasts

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International Journal of Ophthalmology(English edition) 2021年第3期14卷 341-348页

作者： Xiao-Shuo Zheng Hui Zheng Dan Xu Ping-Ping Liu Bing Li Zi-Mu Cao Yang Liu Ye Liu Department of Ophthalmology the Fith Affiliated HospitalSun Yat-sen UniversityZhuhai 5190001 Guangzhou ProvinceChina Institute of Enironmental Systems Biology Environmental Science and Enginecring CollegeDalian Maritime UniversityDalian 116027Liaoning ProvinceChina Department of Pathology the Fifth Affiliated HospitalSun Yat-sen UniversityZhuhai 519000Guangzhou ProvinceChina

AIM:To study the effect of zymosan,a ligand found on the surface of fungi,on gap junctional intercellular communication(GJIC)in cultured human corneal fibroblasts(HCFs).METHODS:Zymosan was added to the medium of cultured HCFs with or without the administration of mitogenactivated protein kinase(MAPK)inhibitors or the inhibitor kappa B kinase 2(IKK2)inhibitor IV.The protein and m RNA levels of connexin 43(Cx43)in HCFs were measured by Western blot,immunofluorescence,and quantitative reverse transcription-polymerase chain reaction(q RT-PCR)analyses.The GJIC activity was tested using a dye-coupling assay.RESULTS:The reduction of Cx43 protein and m RNA levels as well as a significant decrease in GJIC activity were observed in cultured HCFs when zymosan was added into the culture medium.Compared with controls(no zymosan),the protein level of Cx43 was reduced by 45%and 54%in the presence of zymosan at 200 and 600μg/m L,respectively(P<0.05);and it was reduced by 45%,48%,and 75%in the presence of zymosan(600μg/m L)for 24,36,and 48 h,respectively(P<0.05).The m RNA expression of Cx43 was reduced by 98%in the presence of zymosan(P<0.05).The effects of zymosan on Cx43 expression and GJIC activity were attenuated by the administration of PD98059[an extracellular signal-regulated kinase(ERK)signaling inhibitor](P<0.05),c-Jun NH2-terminal kinase(JNK)inhibitor II(P<0.05),and IKK2 inhibitor IV(P<0.05).CONCLUSION:Zymosan inhibits the activity of GJIC in cultured HCFs.This effect is likely regulated via the nuclear factor-κB(NF-κB),MAPK/ERK,and JNK signaling pathways.The inhibitory effects of zymosan on Cx43 expression and GJIC activity in HCFs may induce damage of corneal stroma during corneal fungal infection.

关键词： corneal fibroblast zymosan gap junction connexin 43 MAPKs

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Role of gap junction and connexin-43 in hypoxic-ischemic brain damage

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Neural Regeneration Research 2006年第6期1卷 560-562页

作者： Jieying Lin Niyang Lin Department of Pediatrica First Hospital Affiliated to Medical College of Shantou University Shantou 515041 Guangdong Province China

OBJEETIVE ： gap junction （GJ） is the structural basis tor direct intercellular communication OT nerve CellS. Connexin （Cx） is the protein subunit for constructing GJ channel. Among them, Cx43 is closely related with nervous system. Both Cx43 and nervous system play an important role in the pathophysiological development of hypoxic-ischemic injury. We are in attempt to investigate G J, Cx43 and their correlations with hypoxic-ischemic brain damage by research. DATA SOURCES ： Using the terms ＂ brain gap junction＂ in English and ＂gap junction＂ in Chinese, we searched the Medline database and Chinese BioMedical Literature Database as well as China Hospital Knowledge Database to identify the articles published from 1996 to 2006 about GJ and brain hypoxic-ischemic injury. STUDY SELECTION ： The articles were selected firstly and abstracts of 250 articles were read through. Articles in which the experimental design met randomized controlled principle were included, and study articles and case reports with repetitive contents were excluded. DATA EXTRACTION ： Among 53 included correlative articles, 23 were excluded for repetitive contents and the other 30 were analyzed. DATA SYNTHESIS： GJ, widely existing in nervous system, plays a key role in maintaining normal differentiation and development as well as physiological function of brain tissue. GJ channel is a hydrophilic, Iow-selectivity and lowohmic channel, which can provide direct channel for intercellular substance transmission and information communication. It plays an important role in the differentiation and development of nerve cells and regulation of physiological function. The functions of GJ channel are regulated by many factors, which involved intracellular pH value, Ca^2＋ concentration, ATP concentration, phosphorylation of Cx, transchannel pressure, some neurohormonal factors, regulatory factors of protein and so on. Cx43 is the main component of GJ channel in the brain tissues. Its expression in the brain tissue of mammal is the strongest, mainly in

关键词： brain damage nervous system diseases physiological function information communication gap junction nerve cells intracellular Ph value experimental design Knowledge Database

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Effect of the gap junction blocker 1-heptanol on chondrogenic differentiation of mouse bone marrow mesenchymal stem cells in vitro

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Journal of Nanjing Medical University 2009年第2期23卷 117-121页

作者： Liu Ou-yang Yukun Zhang Shuhua Yang Shunan Ye Weihua Xu Department of Orthopedics the Affiliated Union Hospital of Tongji Medical College of Huazhong Science and Technology University Wuhan 430022 China

Objective：To investigate the effect of the gap junction blocker 1-heptanol on the in vitro chondrogenic differentiation of mouse bone marrow mesenchymal stem cells（MSCs） following induction by GDF-5. Methods：MSCs were isolated from mouse bone marrow and cultured in vitro. After 3 passages cells were induced to undergo chondrogenic differentiation with recombinant human GDF-5（100 ng/ml）, with or without 1-heptanol（2.5 la mol/L）. The effect of 1-heptanol on MSCs proliferation was investigated using the MTT assay. Type II collagen mRNA and protein were examined by RT-PCR and immunocytochemistry respectively, and the sulfate glycosaminoglycan was assessed by Alcian blue dye staining. Connexin43（Cx43） protein was examined by western blotting. Results：GDF-5 induced proliferation and chondrogenic differentiation of MSCs. While 1-heptanol treatment had no effect on this proliferation, it inhibited the expression of both type II collagen mRNA and protein. The Alcian blue staining revealed that 1-heptanol also inhibited the deposition of the typical cartilage extracellular matrix promoted by recombinant GDF-5. Western blotting demonstrated that 1-heptanol had no effect on the expression of Cx43. Conclusion：These results suggest that mouse bone marrow MSCs can be differentiated into a chondrogenic phenotype by GDF- 5 administration in vitro. While the gap junction blocker, 1-heptanol, did not reduce gap junction Cx43, these intercellular communication pathways clearly played an important functional role in GDF-5-induced cartilage differentiation.

关键词： growth differentiation factor-5 gap junction cartilage mouse bone marrow mesenchymal stem cells.

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gap junction dysfunction in the prefrontal cortex induces depressive-like behaviors in rats

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中国药理学与毒理学杂志 2012年第3期 463-463页

作者：孙建栋 Department of Pharmacology Institute of Materia MedicaChinese Academy of Medical Sciences & Peking University

Growing evidence has implicated glial anomalies in the pathophysiology of major depression disorder(MDD).gap junctional communication is a main determinant of astrocytic function.However,it is unclear whether gap junction dysfunction is involved in MDD development.This study investigates changes in the function of astrocyte gap junction occurring in the rat prefrontal cortex(PFC) after chronic unpredictable stress(CUS),a rodent model of depression.Animals exposed to CUS and showing behavioral deficits in sucrose preference test(SPT) and novelty suppressed feeding test(NSFT) exhibited significant decreases in diffusion of gap junction channel-permeable dye and expression of connexin 43(Cx43),a major component of astrocyte gap junction,and abnormal gap junctional ultrastructure in the PFC.Furthermore,we analyzed the effects of typical antidepressants fluoxetine and duloxetine and glucocorticoid receptor(GR) antagonist mifepristone on CUS-induced gap junctional dysfunction and depressive-like behaviors.The cellular and behavioral alterations induced by CUS were reversed and/or blocked by treatment with typical antidepressants or mifepristone,indicating the mechanism of their antidepressant action may involve the amelioration of gap junction dysfunction and the the cellular changes may be related to GR activation.We then investigated the effects of pharmacological gap junction blockade in the PFC on depressive-like behaviors.The results demonstrate that carbenoxolone(CBX) infusions induced anhedonia in SPT,and anxiety in NSFT,and Cx43 mimetic peptides gap27 and gap26 also induced anhedonia,a core symptom of depression.Together,this study supports the hypothesis that gap junction dysfunction contributes to the pathophysiology of depression.

关键词： gap junction depression connexin 43 chronic unpredictable stress antidepressant glucocorticoid receptor

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Effects of Angiotensin II on Expression of the gap junction Channel Protein Connexin 43 in Neonatal Rat Ventricular Myocytes

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South China Journal of Cardiology 2007年第4期8卷 206-211页

作者： Jun Yang Wei Wu Department of Cardiology The First Affiliated Hospital of Nanhua University Hengyang Hunan 421001 China Department of Cardiology The Second Affiliated Hospital of Sun Yat-sen University Guangzhou 510120 China

Objectives To study the effects of angiotensin Ⅱ, as a mediator of cardiac hypertrophy, on expression of connexin 43 （Cx43） in cultured neonatal rat ventricular myocytes and correlation of expression of Cx43 and cardiomyocyte hypertrophy. Methods Cardiomyocytes were isolated from newborn SD rats. Angiotensin Ⅱwas added into the media to induce myocyte hypertrophy. Cultures were exposed to 10 ～ 6 mol/L angiotensin Ⅱ for 72 h, Cx43 expression was characterized by RT-PCR and Immunofluorescence methods. Results Immunofluorescence analysis revealed decreased Cx43 immunoreactivity in cells treated for 72 h with angiotensin Ⅱ. RT-PCR analysis demonstrated there was an obvious decrease of Cx43 mRNA level in cells exposed to angiotensin U for 72 h. The changes of expression of connexin 43 were related to its entrance into S phase of the cell cycle. Cultured neonatal rat cardiomyocytes were exposed for 72 h to increase concentrations of angiotensin II （ 1.0 × 10^ -9 ～ 1.0 × 10^ -6mol/L）, resulting in significantly decreased Cx43 expression. Conclusions Angiotensin/I leads to a concentration-dependent decrease in Cx43 protein in cultured neonatal rat ventricular myocytes by decreasing Cx43 mRNA synthesis. Signal transduction pathways activated by angiotensin II under pathophysiologic conditions of cardiac hypertrophy could initiate remodeling of gap junctions.

关键词： angiotensin Ⅱ cardiomyocyte hypertrophy connexin 43 gap junction

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