Modulation of Intracellular Ca2+ Concentration by Vitamin B12 in Rat Thymocytes

Sukocheva, Olga; Abramov, Andrey Y.; Levitskaya, JO; Gagel’gans, A. I.; Carpenter, David O.

doi:10.1006/bcmd.2001.0450

Cited by 6 publications

(6 citation statements)

References 44 publications

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“…The observation that Cbl was able to exert its full protective action when added well after NaHS suggests strongly that it was able to enter cells and scavenge sulfide within them, as well as remove it from the incubation medium. Additional in vitro studies [24,25] using cyanocobalamin at supraphysiological levels (10–1000 µM) comparable to the concentration we used in our experiments (300 µM) also suggest strongly that this form of vitamin B 12 is able to cross the plasmalemma and impact cell function in the absence of TC II. In both cases, cyanocobalamin raised the intracellular Ca 2+ concentration; in thymocytes this was shown to be due mainly to inhibition of Ca 2+ uptake by the endoplasmic reticulum [24], whilst in synaptosomes it appeared that the rise in [Ca 2+ ] i was mostly dependent on activation of N/P/Q type Ca 2+ channels via a PKC-dependent mechanism [25].…”

Section: Discussionsupporting

confidence: 68%

“…Additional in vitro studies [24,25] using cyanocobalamin at supraphysiological levels (10–1000 µM) comparable to the concentration we used in our experiments (300 µM) also suggest strongly that this form of vitamin B 12 is able to cross the plasmalemma and impact cell function in the absence of TC II. In both cases, cyanocobalamin raised the intracellular Ca 2+ concentration; in thymocytes this was shown to be due mainly to inhibition of Ca 2+ uptake by the endoplasmic reticulum [24], whilst in synaptosomes it appeared that the rise in [Ca 2+ ] i was mostly dependent on activation of N/P/Q type Ca 2+ channels via a PKC-dependent mechanism [25]. In contrast, we did not observe a Cbl-induced rise in [Ca 2+ ] i in CB chemoreceptor cells (Figure 5A), and Cbl did not cause a rise in catecholamine release, as would be predicted to occur if it was elevating [Ca 2+ ] i.…”

Section: Discussionsupporting

confidence: 68%

“…Hall et al (1979) also showed that HeLa cells were able to take up free vitamin B 12 in the absence of transcobalamin and that this led to the synthesis of both methyl- and 5′-deoxyadenosyl-cobalamin, suggesting that the vitamin B 12 had entered both the cytoplasm and the mitochondria [23]. More recently, studies carried out in thymocytes [24] and synaptosomes [25] provide evidence that cyanocobalamin, which has a similar structure to hydroxycobalamin, is able to cross the plasmalemma in the absence of TC II when applied in vitro at supraphysiological concentrations.…”

Section: Introductionmentioning

confidence: 99%

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Hydroxycobalamin Reveals the Involvement of Hydrogen Sulfide in the Hypoxic Responses of Rat Carotid Body Chemoreceptor Cells

et al. 2019

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Carotid body (CB) chemoreceptor cells sense arterial blood PO2, generating a neurosecretory response proportional to the intensity of hypoxia. Hydrogen sulfide (H2S) is a physiological gaseous messenger that is proposed to act as an oxygen sensor in CBs, although this concept remains controversial. In the present study we have used the H2S scavenger and vitamin B12 analog hydroxycobalamin (Cbl) as a new tool to investigate the involvement of endogenous H2S in CB oxygen sensing. We observed that the slow-release sulfide donor GYY4137 elicited catecholamine release from isolated whole carotid bodies, and that Cbl prevented this response. Cbl also abolished the rise in [Ca2+]i evoked by 50 µM NaHS in enzymatically dispersed CB glomus cells. Moreover, Cbl markedly inhibited the catecholamine release and [Ca2+]i rise caused by hypoxia in isolated CBs and dispersed glomus cells, respectively, whereas it did not alter these responses when they were evoked by high [K+]e. The L-type Ca2+ channel blocker nifedipine slightly inhibited the rise in CB chemoreceptor cells [Ca2+]i elicited by sulfide, whilst causing a somewhat larger attenuation of the hypoxia-induced Ca2+ signal. We conclude that Cbl is a useful and specific tool for studying the function of H2S in cells. Based on its effects on the CB chemoreceptor cells we propose that endogenous H2S is an amplifier of the hypoxic transduction cascade which acts mainly by stimulating non-L-type Ca2+ channels.

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Section: Discussionsupporting

confidence: 68%

Section: Discussionsupporting

confidence: 68%

Section: Introductionmentioning

confidence: 99%

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Hydroxycobalamin Reveals the Involvement of Hydrogen Sulfide in the Hypoxic Responses of Rat Carotid Body Chemoreceptor Cells

et al. 2019

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“…Our previous study indicated that ER stress inhibition significantly protected against neuronal apoptosis after spinal cord injury (He et al, 2017), but the role of ER stress in TBI is still unclear. An increasing number of studies suggested that vitamin B 12 regulated ER homeostasis (Sukocheva et al, 2001; Ghemrawi et al, 2013). Furthermore, it was reported that vitamin B 12 deficiency activated ER stress pathways by increasing the phosphorylation of PERK and IRE1α and the expression of ATF6 (Ghemrawi et al, 2013).…”

Section: Introductionsmentioning

confidence: 99%

Vitamin B12 Enhances Nerve Repair and Improves Functional Recovery After Traumatic Brain Injury by Inhibiting ER Stress-Induced Neuron Injury

Liu

et al. 2019

Front. Pharmacol.

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Traumatic brain injury (TBI) is one of the most common causes of neurological damage in young human populations. Vitamin B 12 has been reported to promote axon growth of neuronal cells after peripheral nerve injury, which is currently used for the treatment of peripheral nerve damage in the clinical trial. Thus, we hypothesized that TBI can be attenuated by vitaminB 12 treatment through its beneficial role on axon regeneration after nerve injury. To confirm it, the biological function of vitaminB 12 was characterized using hematoxylin and eosin (H&E) staining, Luxol fast blue (LFB) staining, western blot analysis, and immunohistochemistry staining. The results showed that the neurological functional recovery was improved in the VitaminB 12 -treated group after TBI, which may be due to downregulation of the endoplasmic reticulum stress-related apoptosis signaling pathway. Moreover, the microtubule stabilization, remyelination and myelin reparation were rescued by vitamin B 12 , which was consistent with the treatment of 4-phenylbutyric acid (4-PBA), an endoplasmic reticulum stress inhibitor. The study suggests that vitamin B 12 may be useful as a novel neuroprotective drug for TBI.

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“…In this respect, it is interesting to note that vitamin B12 may serve as a modulator of the immune response. Tamura et al found that vitamin B12 is related to CD8+ cells and NK cells [ 66 ], and Sukocheva et al reported that vitamin B12 can regulate Ca 2+ spikes in immune cells over a wide range of concentrations, possibly giving rise to physiological changes [ 67 ]. Thus, the role of vitamin B12 in inflammation and immune function may serve as an indirect link to EAC.…”

Section: Discussionmentioning

confidence: 99%

Intake of Dietary One-Carbon Metabolism-Related B Vitamins and the Risk of Esophageal Cancer: A Dose-Response Meta-Analysis

Qiang

Xin

et al. 2018

Nutrients

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Several B vitamins are essential in the one-carbon metabolism pathway, which is central to DNA methylation, synthesis, and repair. Moreover, an imbalance in this pathway has been linked to certain types of cancers. Here, we performed a meta-analysis in order to investigate the relationship between the intake of four dietary one-carbon metabolism-related B vitamins (B2, B6, folate, and B12) and the risk of esophageal cancer (EC). We searched PubMed, Web of Science, and Embase for relevant studies published through 1 March 2018. The odds ratio (OR) with 95% confidence interval (CI) for the highest versus the lowest level of each dietary B vitamin was then calculated. From 21 articles reporting 26 studies including 6404 EC cases and 504,550 controls, we found an inverse correlation between the consumption of vitamin B6 and folate and the risk of EC; this association was specific to the US, Europe, and Australia, but was not found in Asia. A dose-response analysis revealed that each 100 μg/day increase in folate intake reduced the risk of EC by 12%. Moreover, each 1 mg/day increase in vitamin B6 intake decreased the risk of EC by 16%. Surprisingly, we found that each 1 μg/day increase in vitamin B12 intake increased the risk of esophageal adenocarcinoma by 2%, particularly in the US and Europe, suggesting both geographic and histological differences. Together, our results suggest that an increased intake of one-carbon metabolism-related B vitamins may protect against EC, with the exception of vitamin B12, which should be consumed in moderation.

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Modulation of Intracellular Ca2+ Concentration by Vitamin B12 in Rat Thymocytes

Cited by 6 publications

References 44 publications

Hydroxycobalamin Reveals the Involvement of Hydrogen Sulfide in the Hypoxic Responses of Rat Carotid Body Chemoreceptor Cells

Hydroxycobalamin Reveals the Involvement of Hydrogen Sulfide in the Hypoxic Responses of Rat Carotid Body Chemoreceptor Cells

Vitamin B12 Enhances Nerve Repair and Improves Functional Recovery After Traumatic Brain Injury by Inhibiting ER Stress-Induced Neuron Injury

Intake of Dietary One-Carbon Metabolism-Related B Vitamins and the Risk of Esophageal Cancer: A Dose-Response Meta-Analysis

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