Inhibitory gene expression of the Cav3.1 T-type calcium channel to improve neuronal injury induced by lidocaine hydrochloride

Wen, Xianjie; Xu, Shiyuan; Zhang, Qingguo; Li, Xiaohong; Liu, Hua; Yang, Chonglin; Wang, Hanbing; Liu, Hongzhen

doi:10.1016/j.ejphar.2016.02.019

Cited by 15 publications

(16 citation statements)

References 23 publications

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“…This would trigger the phenomena called calcium-induced calcium release, giving rise to more calcium release from cellular calcium storage organelle -the endoplasmic reticulum. The resultant intracellular calcium overload leads ultimately to cell apoptosis [8]. In the present study, 1 mM bupivacaine treatment effectively activated Cav3.1 expression and significantly increased intracellular calcium ion concentration.…”

Section: Discussionmentioning

confidence: 65%

“…Wen et al found that the expression of Cav3.1 (the main sub-unit of T-type calcium channel) was up-regulated by lidocaine [8]. The elevated calcium channel expression mediates calcium ion influx, resulting in increased intracellular calcium ion concentration.…”

Section: Discussionmentioning

confidence: 99%

“…It was found that T-type calcium channels might be involved in neuronal apoptosis caused by local anesthetic related toxicity and certain specific T-type calcium channel blocker such as NNC 55-0396 dihydrochloride could suppress the toxicity [8,9]. The present study demonstrated that an herbal medicine called quercetin, at 50 μM concentration, protected SH-SY5Y cells from bupivacaine-induced cellular death, and was as effective as mibefradil, one T-type calcium channel blocker, at 10 μM concentration.…”

Section: Discussionmentioning

confidence: 99%

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Protective effect of quercetin on bupivacaine-induced neurotoxicity via T-type calcium channel inhibition

Chen¹,

Wu²,

Tang³

et al. 2017

Trop. J. Pharm Res

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Section: Discussionmentioning

confidence: 65%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Protective effect of quercetin on bupivacaine-induced neurotoxicity via T-type calcium channel inhibition

Chen¹,

Wu²,

Tang³

et al. 2017

Trop. J. Pharm Res

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“…Our previous study demonstrated that ropivacaine hydrochloride induced the up-regulation of mRNA expression of all four CaMK II subtypes in rat dorsal root ganglion (DRG) neurons 21 . We also found that low-voltage-dependent calcium channels, namely, T-type calcium channels, were intimately involved with local anesthetic neurotoxicity 22, 23 . T-type calcium channels act as pacemakers to regulate intracellular calcium ion levels, which control CaMKII activity 17 .…”

Section: Introductionmentioning

confidence: 73%

CaMK II γ down regulation protects dorsal root ganglion neurons from ropivacaine hydrochloride neurotoxicity

Wen

Li³

et al. 2017

Sci Rep

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T-type calcium channels are intimately involved in the local anesthetics neurotoxicity. Does CaMKIIγ regulate T-type calcium currents in local anesthetics neurotoxicity? This study generated pAd-CaMKIIγ and pAd-shRNA adenovirus vectors to up-and down-regulate CaMKIIγ mRNA expression in dorsal root ganglion neurons (DRG). Normal DRG (Normal group), empty vector DRG (Empty vector group), pAdCaMKIIγ DRG (pAd-CaMKIIγ group) and pAd-shRNA DRG (pAd-shRNA group) were treated or untreated with 3 mM ropivacaine hydrochloride for 4 h. Cell viability, apoptosis rate, CaMKIIγ, pCaMKIIγ, Cav3.2, and Cav3.3 expression were detected. Ultrastructural changes in DRG were observed under a transmission electron microscope. The results demonstrated that the cell viability of DRG treated with ropivacaine hydrochloride decreased markedly, the apoptosis rate, CaMKIIγ, pCaMKIIγ, Cav3.2, Cav3.3 expression increased significantly. CaMKIIγ up-regulation aggravated ropivacaine hydrochlorideinduced cell damage and increased Cav3.2 and Cav3.3 expression. In conclusion, CaMKIIγ regulated Cav3.2 and Cav3.3 expression in DRG, which was involved with ropivacaine hydrochloride-induced cell injury.Ropivacaine hydrochloride is a widely used local anesthetic in clinical anesthesia and pain management because of good separation of the sensory and motor nerve block, few systemic reactions and lower cardiac toxicity 1-4 . However, high concentrations or long exposure times of local anesthetics to neurons also results in neuronal damage 5,6 . Ropivacaine hydrochloride is commonly used in peripheral nerve block or spinal analgesia with a long exposure time, but it also causes nerve damage and abnormal sensations similar to other local anesthetics 7,8 . A multicenter study reported that the occurrence rate of local anesthetic-induced transient neurological syndrome (TNS) was 8.1% 9 . TNS is reversible, but it causes patient discomfort with spastic and radioactive burning pain. The precise mechanism of local anesthetic neurotoxicity is not clear; it generally involves the physicochemical properties of the anesthetic, intracellular calcium concentration, cell apoptosis, inflammation and neurotrophic factors [10][11][12][13] . Intracellular calcium overload is an important factor in local anesthetic neurotoxicity. Gold et al. found that local anesthetics increased calcium ion concentrations of DRG neurons, which resulted in nerve injury 14 . Extracellular calcium chelating agents improved local anesthetic-induced nerve injury 14 . These data demonstrate that calcium influx is closely related to local anesthetic injury.Calcium/calmodulin-dependent protein kinase II (CaMKII) is a multifunctional protease with multiple phosphorylation sites. CaMKII is the primary component of the postsynaptic density (PSD), and it is widely distributed in muscle, nerve and immune tissue [15][16][17] . CaMKII is divided into four subtypes: α, β, γ, and δ. CaMKII phosphorylation is associated with numerous physiological and pathological processes [18][19][20] . Our previous study...

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“…For example, the T-type calcium channel regulates the release of neurotransmitter, hormone secretion and neuronal excitability [5][6]. T-type calcium channels are closely related with neuropathic pain and spinal cord injury induced by local anaesthetics [7][8][9][10][11]. There are three T-type calcium channel subtypes: Cav3.1, Cav3.2 and Cav3.3.…”

Section: Introductionmentioning

confidence: 99%

One-cell model for inhibiting Cav3.3 mRNA expression by RNA interference

Peng

Wang

et al. 2017

Biotechnology & Biotechnological Equipment

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To gain insights into the function of Cav3.3 T-type calcium channel in dorsal root ganglion neurons, we designed a one-cell model in dorsal root ganglion neurons that specifically inhibits the expression of Cav3.3 mRNA. We designed three different shRNA sequences and then connected them to pYr-1.1 plasmid and labelled them as pYr-1.1-Cav3.3 shRNA1, pYr-1.1-Cav3.3 shRNA2 and pYr-1.1-Cav3.3 shRNA3, respectively. The correct sequence vector (pYr-1.1-Cav3.3 shRNA3) was then recombined with the pAd/PL-DEST vector into pAd-Cav3.3 shRNA the adenovirus vector. The dorsal root ganglion neurons were infected with the pAd-Cav3.3 shRNA adenovirus vector. After detecting the expression of Cav3.3 mRNA and protein, the pAd-Cav3.3 shRNA adenovirus vector was verified by digestion and sequencing. These results showed that the constructed pAd-Cav3.3 shRNA adenovirus vector could infect dorsal root ganglion cells and inhibit the expression of Cav3.3 mRNA or protein. These results established a one-cell model for further functional study of Cav3.3.

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Inhibitory gene expression of the Cav3.1 T-type calcium channel to improve neuronal injury induced by lidocaine hydrochloride

Cited by 15 publications

References 23 publications

Protective effect of quercetin on bupivacaine-induced neurotoxicity via T-type calcium channel inhibition

Protective effect of quercetin on bupivacaine-induced neurotoxicity via T-type calcium channel inhibition

CaMK II γ down regulation protects dorsal root ganglion neurons from ropivacaine hydrochloride neurotoxicity

One-cell model for inhibiting Cav3.3 mRNA expression by RNA interference

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