Caspase-2 and microRNA34a/c regulate lidocaine-induced dorsal root ganglia apoptosis in vitro

Li, Yandong; Jia, Zhi; Zhang, Laizhu; Wang, Jianguo; Yin, Guangming

doi:10.1016/j.ejphar.2015.10.008

Cited by 16 publications

(13 citation statements)

References 12 publications

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“…We also demonstrated that AM facilitated DRG neuronal regeneration after lidocaine-induced neurotoxicity through the activation of TrkA-signaling pathway. In a recent study, Li et al 24 reported that caspase proteins, including caspase-2 and caspase-3, were actively involved in lidocaine-induced DRG apoptosis. It is not clear whether TrkA activation is directly interacting with caspase-signaling pathways in lidocaine-injured DRG.…”

Section: Discussionmentioning

confidence: 99%

Amitriptyline Activates TrkA to Aid Neuronal Growth and Attenuate Anesthesia-Induced Neurodegeneration in Rat Dorsal Root Ganglion Neurons

et al. 2016

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Tricyclic antidepressant amitriptyline (AM) has been shown to exert neurotrophic activity on neurons. We thus explored whether AM may aid the neuronal development and protect anesthesia-induced neuro-injury in young spinal cord dorsal root ganglion (DRG) neurons.The DRG explants were prepared from 1-day-old rats. The effect of AM on aiding DRG neural development was examined by immunohistochemistry at dose-dependent manner. AM-induced changes in gene and protein expressions, and also phosphorylation states of tyrosine kinases receptor A (TrkA) and B (TrkB) in DRG, were examined by quantitative real-time polymerase chain reaction and western blot. The effect of AM on attenuating lidocaine-induced DRG neurodegeneration was examined by immunohistochemistry, and small interfering RNA (siRNA)-mediated TrkA/B down-regulation.Amitriptyline stimulated DRG neuronal development in dose-dependent manner, but exerted toxic effect at concentrations higher than 10 M. AM activated TrkA in DRG through phosphorylation, whereas it had little effect on TrkB-signaling pathway. AM reduced lidocaine-induced DRG neurodegeneration by regenerating neurites and growth cones. Moreover, the neuroprotection of AM on lidocaine-injured neurodegeneration was blocked by siRNA-mediated TrkA down-regulation, but not by TrkB down-regulation.Amitriptyline facilitated neuronal development and had protective effect on lidocaine-induced neurodegeneration, very likely through the activation of TrkA-signaling pathway in DRG.

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Section: Discussionmentioning

confidence: 99%

Amitriptyline Activates TrkA to Aid Neuronal Growth and Attenuate Anesthesia-Induced Neurodegeneration in Rat Dorsal Root Ganglion Neurons

et al. 2016

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“… 6 , 41 These observations point to an enormous potential for miRNA-mediated regulation of pain pathology and an immediate need to investigate miRNA-mediated mechanisms in pain modulation in general and in cancer pain states in particular. miR-34c-5p is one of the widely investigated miRNAs in cancer conditions 1 , 21 , 22 , 42 , 63 as well as in neurological conditions 30 , 37 , 66 and development. 4 , 32 , 48 We recently reported that bone metastatic tumor leads to massive changes in the miRNA expression repertoire in peripheral sensory neurons, and these changes are more pronounced in the hyperalgesia maintenance phase than in the establishing phase.…”

Section: Introductionmentioning

confidence: 99%

miR-34c-5p functions as pronociceptive microRNA in cancer pain by targeting Cav2.3 containing calcium channels

Gandla

Lomada

et al. 2017

Pain

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“…Cytochrome c can activate the Apaf-1-caspase-9 apoptosis system, and thus activates downstream caspases, including caspase-3, caspase-2, caspase-6, caspase-8 and caspase-10; among these, caspase-8 can cut Bid to form tBid and activates tBid. tBid recruits Bax to embed into the mitochondria after transposition to the mitochondrial membrane and forms the transmembrane channel, which promotes cytochrome c to be further released from the mitochondria, forming a positive feedback pathway, and eventually inducing cell apoptosis (23,24).…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…The caspase family is the initiator and executor of cell apoptosis in mammals, among which, caspase-3 is the most crucial apoptotic protease in the downstream of the caspase cascade reactions (24). Bcl-2 blocks the activation of the upstream caspase protease by interfering with the release of cytochrome c, thus inhibiting cell apoptosis (24). As a composition of the ion channel on the mitochondrial membrane, Bax protein allows cytochrome c to pass through the mitochondrial membrane, activating caspase-9, and further activating caspase-3, thus resulting in cell apoptosis (9).…”

Section: Discussionmentioning

confidence: 99%

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Iodine-131 induces apoptosis in human cardiac muscle cells through the p53/Bax/caspase-3 and PIDD/caspase-2/t-BID/cytochrome c/caspase-3 signaling pathway

et al. 2017

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The aim of this study was to elucidate the effects of iodine-131 on the induction of apoptosis in human cardiac muscle cells and the underlying molecular mechanisms. We found that iodine-131 reduced cell proliferation, induced apoptosis, induced p53, PIDD, t-BID (mitochondria) protein expression, suppressed cytochrome c (mitochondria) protein expression, and increased Bax protein expression, and promoted caspase-2, -3 and -9 expression levels in human cardiac muscle cells. Meanwhile, si-p53 inhibited the effects of iodine-131 on the reduction in cell proliferation and induction of apoptosis in human cardiac muscle cells through regulation of Bax/cytochrome c/caspase-3 and PIDD/caspase‑2/t-BID/cytochrome c/caspase-3 signaling pathway. After si-Bax reduced the effects of iodine-131, it reduced cell proliferation and induced apoptosis in human cardiac muscle cells through the cytochrome c/caspase-3 signaling pathway. However, si-caspase-2 also reduced the effects of iodine-131 on the reduction of cell proliferation and induction of apoptosis in human cardiac muscle cells through the t-BID/cytochrome c/caspase-3 signaling pathway. These findings demonstrated that iodine-131 induces apoptosis in human cardiac muscle cells through the p53/Bax/caspase-3 and PIDD/caspase-2/t-BID/cytochrome c/caspase-3 signaling pathway.

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Caspase-2 and microRNA34a/c regulate lidocaine-induced dorsal root ganglia apoptosis in vitro

Cited by 16 publications

References 12 publications

Amitriptyline Activates TrkA to Aid Neuronal Growth and Attenuate Anesthesia-Induced Neurodegeneration in Rat Dorsal Root Ganglion Neurons

Amitriptyline Activates TrkA to Aid Neuronal Growth and Attenuate Anesthesia-Induced Neurodegeneration in Rat Dorsal Root Ganglion Neurons

miR-34c-5p functions as pronociceptive microRNA in cancer pain by targeting Cav2.3 containing calcium channels

Iodine-131 induces apoptosis in human cardiac muscle cells through the p53/Bax/caspase-3 and PIDD/caspase-2/t-BID/cytochrome c/caspase-3 signaling pathway

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