Nitric oxide-induced calcium release

Kakizawa, Sho; Yamazawa, Toshiko; Iino, Masamitsu

doi:10.4161/chan.22555

Cited by 26 publications

(10 citation statements)

References 25 publications

(23 reference statements)

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“…Sperm pellet was obtained by centrifugation at 6,000 RPM for 5 min. Mature sperm from Rohu fish ( Labeo rohita) were collected as described before ( Majhi et al, 2013 ). In all cases, extreme care was taken to minimize the sufferings and the number of animals used.…”

Section: Methodsmentioning

confidence: 99%

Expression of temperature-sensitive ion channel TRPM8 in sperm cells correlates with vertebrate evolution

Majhi

Saha

Kumar

et al. 2015

PeerJ

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Transient Receptor Potential cation channel, subfamily Melastatin, member 8 (TRPM8) is involved in detection of cold temperature, different noxious compounds and in execution of thermo- as well as chemo-sensitive responses at cellular levels. Here we explored the molecular evolution of TRPM8 by analyzing sequences from various species. We elucidate that several regions of TRPM8 had different levels of selection pressure but the 4th–5th transmembrane regions remain highly conserved. Analysis of synteny suggests that since vertebrate origin, TRPM8 gene is linked with SPP2, a bone morphogen. TRPM8, especially the N-terminal region of it, seems to be highly variable in human population. We found 16,656 TRPM8 variants in 1092 human genomes with top variations being SNPs, insertions and deletions. A total of 692 missense mutations are also mapped to human TRPM8 protein of which 509 seem to be delateroiours in nature as supported by Polyphen V2, SIFT and Grantham deviation score. Using a highly specific antibody, we demonstrate that TRPM8 is expressed endogenously in the testis of rat and sperm cells of different vertebrates ranging from fish to higher mammals. We hypothesize that TRPM8 had emerged during vertebrate evolution (ca 450 MYA). We propose that expression of TRPM8 in sperm cell and its role in regulating sperm function are important factors that have guided its molecular evolution, and that these understandings may have medical importance.

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Section: Methodsmentioning

confidence: 99%

Expression of temperature-sensitive ion channel TRPM8 in sperm cells correlates with vertebrate evolution

Majhi

Saha

Kumar

et al. 2015

PeerJ

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“…During early stages in 3xTg FAD mice, it is thought that a mixture of NMDA-R dependent and independent mechanisms [30] and enhanced NO signaling boosts postsynaptic RyR-mediated Ca 2+ signaling and compensates against enhancement of LTD by other mechanisms [14,23,70,86,154]. In older (8 month) AD Tg mice, LTP is reduced compared to age-matched non-transgenic mice due in part to a reduction in the NMDA-R independent mechanisms [30].…”

Section: Ca2+ and Long And Short Term Plasticity Defects In Admentioning

confidence: 99%

Emerging pathways driving early synaptic pathology in Alzheimer's disease

Briggs

Chakroborty

Stutzmann

2017

Biochemical and Biophysical Research Communications

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The current state of the AD research field is highly dynamic is some respects, while seemingly stagnant in others. Regarding the former, our current lack of understanding of initiating disease mechanisms, the absence of effective treatment options, and the looming escalation of AD patients is energizing new research directions including a much-needed re-focusing on early pathogenic mechanisms, validating novel targets, and investigating relevant biomarkers, among other exciting new efforts to curb disease progression and foremost, preserve memory function. With regard to the latter, the recent disappointing series of failed Phase III clinical trials targeting Aβ and APP processing, in concert with poor association between brain Aβ levels and cognitive function, have led many to call for a re-evaluation of the primacy of the amyloid cascade hypothesis. In this review, we integrate new insights into one of the earliest described signaling abnormalities in AD pathogenesis, namely intracellular Ca2+ signaling disruptions, and focus on its role in driving synaptic deficits – which is the feature that does correlate with AD-associated memory loss. Excess Ca2+release from intracellular stores such as the endoplasmic reticulum (ER) has been well-described in cellular and animal models of AD, as well as human patients, and here we expand upon recent developments in ER-localized release channels such as the IP3R and RyR, and the recent emphasis on RyR2. Consistent with ER Ca2+ mishandling in AD are recent findings implicating aspects of SOCE, such as STIM2 function, and TRPC3 and TRPC6 levels. Other Ca2+-regulated organelles important in signaling and protein handling are brought into the discussion, with new perspectives on lysosomal regulation. These early signaling abnormalities are discussed in the context of synaptic pathophysiology and disruptions in synaptic plasticity with a particular emphasis on short-term plasticity deficits. Overall, we aim to update and expand the list of early neuronal signaling abnormalities implicated in AD pathogenesis, identify specific channels and organelles involved, and link these to proximal synaptic impairments driving the memory loss in AD. This is all within the broader goal of identifying novel therapeutic targets to preserve cognitive function in AD.

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“…Further, RyR1 is also expressed in the brain, where we recently identified another mode of intracellular Ca 2+ mobilization mediated by RyR: the NO-induced Ca 2+ release (NICR), which is dependent on the S -nitrosylation of RyR1 at cysteine 3635 [108]. In Purkinje cells in acute cerebellar slices, NICR is induced by physiological patterns of neuronal activity, and is essential for the induction of cerebellar LTP, which is the reverse process of cerebellar long-term depression (LTD) [108,109]…”

Section: Neuronal Cell Death By Nomentioning

confidence: 99%

Essential Roles of Natural Products and Gaseous Mediators on Neuronal Cell Death or Survival

Mikami

Kakizawa

Yamazawa

2016

IJMS

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Although precise cellular and molecular mechanisms underlying neurodegeneration still remain enigmatic, key factors associated with degenerative disorders, such as glutamate toxicity and oxidative stress, have been recently identified. Accordingly, there has been growing interest in examining the effects of exogenous and endogenous molecules on neuroprotection and neurodegeneration. In this paper, we review recent studies on neuroprotective and/or neurodegenerative effects of natural products, such as caffeic acid and chlorogenic acid, and gaseous mediators, including hydrogen sulfide and nitric oxide. Furthermore, possible molecular mechanisms of these molecules in relation to glutamate signals are discussed. Insight into the pathophysiological role of these molecules will make progress in our understanding of molecular mechanisms underlying neurodegenerative diseases, and is expected to lead to potential therapeutic approaches.

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Nitric oxide-induced calcium release

Cited by 26 publications

References 25 publications

Expression of temperature-sensitive ion channel TRPM8 in sperm cells correlates with vertebrate evolution

Expression of temperature-sensitive ion channel TRPM8 in sperm cells correlates with vertebrate evolution

Emerging pathways driving early synaptic pathology in Alzheimer's disease

Essential Roles of Natural Products and Gaseous Mediators on Neuronal Cell Death or Survival

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