Hypoxia Induces an Increase in Intracellular Magnesium via Transient Receptor Potential Melastatin 7 (TRPM7) Channels in Rat Hippocampal Neurons in Vitro

Zhang, Jing; Zhao, Fengbo; Zhao, Yin; Wang, Jing; Pei, Lei; Sun, Ning; Shi, Jing

doi:10.1074/jbc.m110.148494

Cited by 37 publications

(33 citation statements)

References 61 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This has been demonstrated through the use of at least three different experimental models of ischemia (OGD, 4-vessel occlusion and chemically-induced) encompassing both in vitro and in vivo settings, indicating the ubiquitous nature of TRPM7 involvement. [41][42][43][44][45][46][47] However, a number of important questions still linger in this regard. While TRPM7 channel activity has proven essential for neuronal demise, a defined role for the kinase region has yet to be determined.…”

Section: Trpm7 and The Cytoskeletonmentioning

confidence: 99%

“…This review takes a new look at neuronal cell death including roles for both excitotoxic and non-excitotoxic processes (see Table 1). We will highlight recent insights into the function of the TRPM7 cation channel which has been implicated in ischemia-related neuronal death, [41][42][43][44][45][46][47] and elaborate on the multiple mechanistic pathways that TRPM7 may utilize in contributing to the cell death process, including regulation of the cellular cytoskeleton.…”

Section: Non-excitotoxic Cell Deathmentioning

confidence: 99%

“…following OGD in primary cultures 46,47 suggests the involvement of distinct downstream signaling pathways from those normally associated with NMDA-receptor mediated excitotoxicity and Ca…”

Section: +mentioning

confidence: 99%

“…For these purposes, the utilization of preexisting knockout mice for the cofilin regulator LIMK and its upstream mediators may prove fruitful. 126,139,140 Interestingly, modifications in the level of intracellular Ca 2+ ions are observed during both TRPM7-mediated cell injury [41][42][43][44][45][46][47] and disruption of the cytoskeleton [19][20][21] respectively. Therefore, a more detailed examination of factors associated with this second messenger pathway may yield additional evidence in the intriguing relationship between TRPM7 and the cytoskeleton.…”

Section: Trpm7-dependent Ischemic Cell Death: Lingering Questions Andmentioning

confidence: 99%

See 3 more Smart Citations

TRPM7, the cytoskeleton and neuronal death

Asrar

Aarts

2013

Channels

View full text Add to dashboard Cite

Section: Trpm7 and The Cytoskeletonmentioning

confidence: 99%

Section: Non-excitotoxic Cell Deathmentioning

confidence: 99%

“…following OGD in primary cultures 46,47 suggests the involvement of distinct downstream signaling pathways from those normally associated with NMDA-receptor mediated excitotoxicity and Ca…”

Section: +mentioning

confidence: 99%

Section: Trpm7-dependent Ischemic Cell Death: Lingering Questions Andmentioning

confidence: 99%

See 2 more Smart Citations

TRPM7, the cytoskeleton and neuronal death

Asrar

Aarts

2013

Channels

View full text Add to dashboard Cite

“…This cation is involved in cognition [11] appetite regulation [12] cortical plasticity [13] and other functions. Both cations have selective transporters in brain [14,15]. Both magnesium and zinc modulate the presynaptic transmitters release, the agonist induced response at the level of some receptors [16] and also several ion-gated ion channels [10].…”

Section: Introductionmentioning

confidence: 99%

Magnesium and Zinc Involvement in Tobacco Addiction

Nechifor¹

2012

J Addict Res Ther

View full text Add to dashboard Cite

This paper is a review regarding magnesium and zinc influence on smoking and tobacco addiction. Magnesium and zinc are two very important bivalent cations involved in different functions of central nervous system. There are different mechanisms by which magnesium can decrease the nicotine addiction. Magnesium decrease the dopamine release and the NMDA receptor stimulation by glutamate (two essential steps in the devolopment of nicotine addiction). This cation also inhibits the synthesis of substance P and nitric oxide, others important neurotransmiters involved in addiction. Magnesium may decrease the nicotine effect on GABA synthesis and could reduce also NPY involvement in nicotine addiction. Zinc also reduces the glutamatergic brain systems activity and modulates the nicotinic receptors activity from brain. The hypomagnesemia favorises the development of tobacco addiction .The magnesium treatment can be beneficial for reducing the smoking and nicotine addiction in heavy smokers. By increasing the magnesium concentration we can moderately improve the stimulation of the reward system and can reduce the needs of stimulation by nicotine or by others addictive substances. The treatment of intracellular and plasma magnesium deficit could be way to minimize the development of tobacco smoking and nicotine addiction.

show abstract

MicroRNA‐135a alleviates oxygen‐glucose deprivation and reoxygenation‐induced injury in neurons through regulation of GSK‐3β/Nrf2 signaling

Liu

Hou

et al. 2018

J Biochem & Molecular Tox

View full text Add to dashboard Cite

MicroRNAs (miRNAs) have been suggested as pivotal regulators in the pathological process of cerebral ischemia and reperfusion injury. In this study, we aimed to investigate the role of miR-135a in regulating neuronal survival in cerebral ischemia and reperfusion injury using an in vitro cellular model induced by oxygen-glucose deprivation and reoxygenation (OGD/R). Our results showed that miR-135a expression was significantly decreased in neurons with OGD/R treatment. Overexpression of miR-135a significantly alleviated OGD/R-induced cell injury and oxidative stress, whereas inhibition of miR-135a showed the opposite effects. Glycogen synthase kinase-3β (GSK-3β) was identified as a potential target gene of miR-135a. miR-135a was found to inhibit GSK-3β expression, but promote the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and downstream signaling. However, overexpression of GSK-3β significantly reversed miR-135a-induced neuroprotective effect. Overall, our results suggest that miR-135a protects neurons against OGD/R-induced injury through downregulation of GSK-3β and upregulation of Nrf2 signaling.

show abstract

Hypoxia Induces an Increase in Intracellular Magnesium via Transient Receptor Potential Melastatin 7 (TRPM7) Channels in Rat Hippocampal Neurons in Vitro

Cited by 37 publications

References 61 publications

TRPM7, the cytoskeleton and neuronal death

TRPM7, the cytoskeleton and neuronal death

Magnesium and Zinc Involvement in Tobacco Addiction

MicroRNA‐135a alleviates oxygen‐glucose deprivation and reoxygenation‐induced injury in neurons through regulation of GSK‐3β/Nrf2 signaling

Contact Info

Product

Resources

About