Swelling-activated and arachidonic acid-induced currents are TREK-1 in rat bladder smooth muscle cells

Fukasaku, Mitsuko; Kimura, Junko; Yamaguchi, Osamu

doi:10.5387/fms.2015-20

Cited by 7 publications

(6 citation statements)

References 45 publications

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“…Sevoflurane, as a commonly used anesthetic, is frequently used in animal experiments and clinical practice due to its effectiveness and safety profile. Studies have shown that sevoflurane can activate TREK-1 pathway through an indirect pathway at the cellular level, thereby preventing cell damage caused by ischemia and hypoxia ( 19 , 20 ).…”

Section: Discussionmentioning

confidence: 99%

Effects of sevoflurane on rats with ischemic brain injury and the role of the TREK-1 channel

Pan

Yang

Lü

et al. 2017

Experimental and Therapeutic Medicine

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The purpose of this investigation was to determine the effects of sevoflurane on rats with ischemic brain injury and to determine the potential role of the TREK-1 channel in this process. Normal rats were randomly divided into three groups: Sham operation, sevoflurane anesthesia or chloral hydrate anesthesia group, an additional group of TREK-1 knockout rats were also studied. Semi-quantitative PCR and western blot analysis confirmed the lack of TREK-1 expression in the brain of TREK-1 knockout rats. The thread-tie method was used to establish middle cerebral artery occlusion (MCAO) model to induce cerebral ischemic brain injury. All rates were treated for 4 days prior to ischemia (for 2 h) followed by a 24 h reperfusion period. Physiological indexes of rats in each group both prior to and after surgery showed no statistical difference (P>0.05). Neurological function was scored both before (no statistical difference) and after surgery where it was found to be significantly better (lower score) in the sevoflurane anesthesia group than in chloral hydrate anesthesia and TREK-1 knockout groups (P<0.01). The area of cerebral infarction was measured by triphenyl tetrazolium chloride staining and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay to detect the apoptosis of brain cells. TTC staining showed different degrees of cerebral infarction in the various groups; the area of cerebral infarction in sevoflurane anesthesia group was significantly lower than that in chloral hydrate anesthesia and TREK-1 knockout groups (P<0.01). TUNEL assay showed that the number of TUNEL-positive cells was significantly lower in sevoflurane anesthesia group than in TREK-1 knockout and chloral hydrate anesthesia groups (P<0.01). In conclusion, results from this investigation showed that sevoflurane can protect the nerve function of rats with cerebral ischemic brain injury possibly by affecting the expression of proteins involved in the TREK-1 signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Effects of sevoflurane on rats with ischemic brain injury and the role of the TREK-1 channel

Pan

Yang

Lü

et al. 2017

Experimental and Therapeutic Medicine

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“…Although the effect of GdCl 3 on CVI(F3) was statistically insignificant, the reagent showed a similar tendency of decrease the CVI(F3) in the LCC. These results may be owing to the diverse pharmacological properties of LaCl 3 and GdCl 3 , which have been reported to block two‐P K + channels at the same concentration as that which blocks TRPC (Alshuaib & Mathew, ; Fukasaku, Kimura, & Yamaguchi, ). The significant depression of CVI(F3) by LaCl 3 can be ascribed to the blocking on volume sensitive two‐P K + channels.…”

Section: Discussionmentioning

confidence: 99%

Different characteristics of cell volume and intracellular calcium ion concentration dynamics between the hippocampal CA1 and lateral cerebral cortex of male mouse brain slices during exposure to hypotonic stress

Takahashi

Omi

Uchino

et al. 2017

J of Neuroscience Research

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The mechanism of brain edema is complex and still remains unclear. Our aim was to investigate the | I N TR ODU C TI ONBrain edema is frequently observed in clinical practice, and is induced by traumatic injury, ischemic insult, epilepsy, blood ion imbalance (after infusion), and abnormal liver and kidney functions (Rungta et al., 2015;Butterworth, 2015). As the brain is housed in a limited space surrounded by hard cranial bones, an increase in the brain volume, due to edema, causes an increase in the intra-cranial pressure. As a result, small vessels in the brain are compressed, leading to a decrease in blood flow, which in turn causes an irreversible impairment of nerve function and, at worst, death (Michinaga & Koyama, 2015). It is therefore important to have evidence on the pathophysiological features

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“…The hypotonic challenge causes regulatory compensation and the signaling pathways may also influence the mechanosensitive channel independently of the direct action of the membrane tension. The TREK-1 current was shown to be reduced by hyperosmotic solution in Xenopus oocytes [29], and was suggested to be activated by the extracellular hypoosmotic environment in isolated rat bladder smooth muscle cells [78]. The TRAAK K + current is also activated by the hypotonic challenge [66].…”

Section: Mechanosensitive Properties Of K 2p Channels As Reflected By the Currently Available Methodsmentioning

confidence: 99%

Negative Influence by the Force: Mechanically Induced Hyperpolarization via K2P Background Potassium Channels

Lengyel

Enyedi

Czirják

2021

IJMS

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The two-pore domain K2P subunits form background (leak) potassium channels, which are characterized by constitutive, although not necessarily constant activity, at all membrane potential values. Among the fifteen pore-forming K2P subunits encoded by the KCNK genes, the three members of the TREK subfamily, TREK-1, TREK-2, and TRAAK are mechanosensitive ion channels. Mechanically induced opening of these channels generally results in outward K+ current under physiological conditions, with consequent hyperpolarization and inhibition of membrane potential-dependent cellular functions. In the past decade, great advances have been made in the investigation of the molecular determinants of mechanosensation, and members of the TREK subfamily have emerged among the best-understood examples of mammalian ion channels directly influenced by the tension of the phospholipid bilayer. In parallel, the crucial contribution of mechano-gated TREK channels to the regulation of membrane potential in several cell types has been reported. In this review, we summarize the general principles underlying the mechanical activation of K2P channels, and focus on the physiological roles of mechanically induced hyperpolarization.

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Swelling-activated and arachidonic acid-induced currents are TREK-1 in rat bladder smooth muscle cells

Cited by 7 publications

References 45 publications

Effects of sevoflurane on rats with ischemic brain injury and the role of the TREK-1 channel

Effects of sevoflurane on rats with ischemic brain injury and the role of the TREK-1 channel

Different characteristics of cell volume and intracellular calcium ion concentration dynamics between the hippocampal CA1 and lateral cerebral cortex of male mouse brain slices during exposure to hypotonic stress

Negative Influence by the Force: Mechanically Induced Hyperpolarization via K2P Background Potassium Channels

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