Topics on the Na+/Ca2+ Exchanger: Responses of Na+/Ca2+ Exchanger to Interferon-γ and Nitric Oxide in Cultured Microglia

Matsuda, Takehisa; Nagano, Tadayoshi; Takemura, Masashi; Baba, Akemichi

doi:10.1254/jphs.fmj06002x4

Cited by 27 publications

(15 citation statements)

References 37 publications

(22 reference statements)

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“…ASK1 is activated by various stimuli, including calcium influx, ER stress, oxidative stress, lipopolysaccharide (LPS), and receptor-mediated signaling through tumor necrosis factor receptor (TNFR) and Toll-like receptor 4 (TLR4), TLR7, and TLR8 (11,12). Notably, IFN-␥ has been reported to cause Ca 2ϩ influx and ER and oxidative stress in a variety of cell lines (27,28). Activated ASK1 further stimulates the downstream p38 and JNK pathways for driving various cellular responses.…”

Section: Discussionmentioning

confidence: 99%

Regulation of the Death-Associated Protein Kinase 1 Expression and Autophagy via ATF6 Requires Apoptosis Signal-Regulating Kinase 1

Gade

Manjegowda

Nallar

et al. 2014

Molecular and Cellular Biology

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Section: Discussionmentioning

confidence: 99%

Regulation of the Death-Associated Protein Kinase 1 Expression and Autophagy via ATF6 Requires Apoptosis Signal-Regulating Kinase 1

Gade

Manjegowda

Nallar

et al. 2014

Molecular and Cellular Biology

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“…This may be attributed to phosphorylation of NCX, because PKC can phosphorylate NCX, and most, but not all, studies have reported PKC-mediated increase in NCX activity (Vigne et al, 1988;Iwamoto et al, 1996b). The involvement of PKC and tyrosine kinase in controlling NCX activity in microglia has previously been reported by Matsuda et al (2006). PI3K is also involved in reverse mode of NCX activity, as observed in neonatal cardiomyocytes (McDowell et al, 2004).…”

Section: The Signal Cascade Of B 1 Receptor Activationmentioning

confidence: 92%

“…Another interesting observation was the involvement of NCX operating in reverse mode leading to Ca 2ϩ influx. Although the physiological function of NCX is assumed to be Ca 2ϩ extrusion, Matsuda et al (2006) provide evidence that Ca 2ϩ uptake via NCX operating in reverse mode may play a role for microglial function under pathological conditions. The signaling cascade of BK and its coupling to NCX might be quite distinct in microglia compared with other cell types.…”

Section: Distinct Mechanisms Of Microglial Migration Induced By Bk Anmentioning

confidence: 96%

“…(Quednau et al, 1997;He et al, 1998), and microglia (Nagano et al, 2004). In pathological conditions such as interferon-␥ (IFN-␥) or nitric oxide exposure, the activity and expression of NCX increased in microglia, causing Na ϩ -dependent Ca 2ϩ uptake (Matsuda et al, 2006). These results imply that NCX-induced Ca 2ϩ influx plays a key role in microglial function.…”

Section: Activation Of Intermediate-conductance Camentioning

confidence: 99%

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Bradykinin-Induced Microglial Migration Mediated by B₁-Bradykinin Receptors Depends on Ca²⁺Influx via Reverse-Mode Activity of the Na⁺/Ca²⁺Exchanger

et al. 2007

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Bradykinin (BK) is produced and acts at the site of injury and inflammation. In the CNS, migration of microglia toward the lesion site plays an important role pathologically. In the present study, we investigated the effect of BK on microglial migration. Increased motility of cultured microglia was mimicked by B 1 receptor agonists and markedly inhibited by a B 1 antagonist , but not by a B 2 receptor antagonist. BK induced chemotaxis in microglia isolated from wild-type and B 2 -knock-out mice but not from B 1 -knock-out mice. BK-induced motility was not blocked by pertussis toxin but was blocked by chelating intracellular Ca 2ϩ or by low extracellular Ca 2ϩ , implying that Ca 2ϩ influx is prerequisite. Blocking the reverse mode of Na ϩ /Ca 2ϩ exchanger (NCX) completely inhibited BK-induced migration. The involvement of NCX was further confirmed by using NCX ϩ/Ϫ mice; B 1 -agonist-induced motility and chemotaxis was decreased compared with that in NCX ϩ/ϩ mice. Activation of NCX seemed to be dependent on protein kinase C and phosphoinositide 3-kinase, and resultant activation of intermediate-conductance (IK-type) Ca 2ϩ -dependent K ϩ currents (I K(Ca) ) was activated. Despite these effects, BK did not activate microglia, as judged from OX6 staining. Using in vivo lesion models and pharmacological injection to the brain, it was shown that microglial accumulation around the lesion was also dependent on B 1 receptors and I K(Ca) . These observations support the view that BK functions as a chemoattractant by using the distinct signal pathways in the brain and, thus, attracts microglia to the lesion site in vivo.

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“…2,3) Recently, a potent and selective NCX enzyme inhibitor, 2-[4-[(2,5)-difluoro-phenyl]methoxy]-5-ethoxyaniline (SEA0400) has been developed, 4) and has been reported to provide protection in models of cerebral ischemia and reperfusion injury after ischemia. 5,6) However, the effect of NCX on epilepsy has not been reported.…”

mentioning

confidence: 99%

Involvement of Na+/Ca2+ Exchanger in Pentylenetetrazol-Induced Convulsion by Use of Na+/Ca2+ Exchanger Knockout Mice

Saito

Kaneko

Tanaka

et al. 2009

Biological & Pharmaceutical Bulletin

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Epilepsy is a common psychiatric disorder, and in the last decade, genetic abnormalities of genes encoding ion channels expressed in the brain have been identified as the cause of twenty idiopathic epilepsy syndromes. We have already reported that nicotinic acetylcholine receptor mutation exhibit the nocturnal frontal lobe epilepsy phenotype in rats. 1)Experimentally, numerous studies also suggest that ion channels, in particular Ca 2ϩ or K ϩ channels, are involved in epilepsy; however, the detailed mechanisms are unclear. The Na ϩ /Ca 2ϩ exchanger (NCX) is a cell-membrane ion transporter which plays an important role in regulation of intracellular Ca 2ϩ levels. In the central nervous system (CNS), NCX has been classified into three types of isoforms; NCX1, NCX2, and NCX3. NCX1 is expressed at high levels in the brain, the heart, and the kidney, while NCX2 and NCX3 are mainly expressed at high levels in the brain and in skeletal muscles.2,3) Recently, a potent and selective NCX enzyme inhibitor, 2-[4-[(2,5)-difluoro-phenyl]methoxy]-5-ethoxyaniline (SEA0400) has been developed, 4) and has been reported to provide protection in models of cerebral ischemia and reperfusion injury after ischemia. 5,6) However, the effect of NCX on epilepsy has not been reported.In the present study, therefore, we examined the involvement of NCX in drug-induced convulsions in mice using either the NCX inhibitor SEA0400 or NCX knockout mice.In the present study, ddY-male mice weighing 25-35 g were used. The animals were maintained at 24Ϯ2°C with a 12 h light-dark cycle, and were given free access to commercial food and tap water. The NCX inhibitor SEA0400 (2 mg/kg, per os (p.o.); SEA0400 group) or vehicle (20% soy bean oil; control group) was administered to mice at 45 min prior to either pentylenetetrazol (PTZ 60 mg/kg, intraperitoneally (i.p.); nϭ7 and 6, respectively; Sigma), bicuculline (5 mg/kg, i.p.; nϭ8 and 9, respectively; Sigma), nicotine (6 mg/kg, i.p.; nϭ5 and 3, respectively; Wako), or 4-aminopyridine (10 mg/kg, i.p.; nϭ5 for both groups; Sigma) for induction of different types of seizures. The appropriate dose of each drug was examined by checking dosage dependence in advance, ensuring that it was not a lethal dose but an adequate one to cause convulsions. However, the convulsions induced by each drug were not in the same way. Therefore, we examined tail reaction, clonic convulsion, tonic flexion, tonic extension convulsion, and the reaction in the case of PTZ, bicuculline, and 4-aminopyridine. In the case of nicotine, appearance, latency and duration of wild running were added. Clonic convulsions were determined by the occurrence of rhythmical repeated muscle contractions of the limbs of the mice, and the disappearance of the righting reflex for more than 3 s.NCX1 knockout mice were prepared as previously described, 7) and housed as for ddY-male mice. These mice received pentylenetetrazol (PTZ 40 mg/kg, i.p.), bicuculline (5 mg/kg, i.p.), nicotine (6 mg/kg, i.p.), or 4-aminopyridine (10 mg/kg, i.p.) for induction of seizu...

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Topics on the Na+/Ca2+ Exchanger: Responses of Na+/Ca2+ Exchanger to Interferon-γ and Nitric Oxide in Cultured Microglia

Cited by 27 publications

References 37 publications

Regulation of the Death-Associated Protein Kinase 1 Expression and Autophagy via ATF6 Requires Apoptosis Signal-Regulating Kinase 1

Regulation of the Death-Associated Protein Kinase 1 Expression and Autophagy via ATF6 Requires Apoptosis Signal-Regulating Kinase 1

Bradykinin-Induced Microglial Migration Mediated by B₁-Bradykinin Receptors Depends on Ca²⁺Influx via Reverse-Mode Activity of the Na⁺/Ca²⁺Exchanger

Involvement of Na+/Ca2+ Exchanger in Pentylenetetrazol-Induced Convulsion by Use of Na+/Ca2+ Exchanger Knockout Mice

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Topics on the Na+/Ca2+ Exchanger: Responses of Na+/Ca2+ Exchanger to Interferon-γ and Nitric Oxide in Cultured Microglia

Cited by 27 publications

References 37 publications

Regulation of the Death-Associated Protein Kinase 1 Expression and Autophagy via ATF6 Requires Apoptosis Signal-Regulating Kinase 1

Regulation of the Death-Associated Protein Kinase 1 Expression and Autophagy via ATF6 Requires Apoptosis Signal-Regulating Kinase 1

Bradykinin-Induced Microglial Migration Mediated by B1-Bradykinin Receptors Depends on Ca2+Influx via Reverse-Mode Activity of the Na+/Ca2+Exchanger

Involvement of Na+/Ca2+ Exchanger in Pentylenetetrazol-Induced Convulsion by Use of Na+/Ca2+ Exchanger Knockout Mice

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Bradykinin-Induced Microglial Migration Mediated by B₁-Bradykinin Receptors Depends on Ca²⁺Influx via Reverse-Mode Activity of the Na⁺/Ca²⁺Exchanger