Glutamate-Dependent Transcriptional Regulation in Bergmann Glia Cells: Involvement of p38 MAP Kinase

Zepeda, Rossana C.; Barrera, Iliana; Castelán, Francisco; Soto-Cid, Abraham; Hernández‐Kelly, Luisa C.; López-Bayghen, Esther; Ortega, Arturo

doi:10.1007/s11064-007-9580-x

Cited by 13 publications

(7 citation statements)

References 34 publications

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“…A similar mechanism has previously been proposed to account for the selective vulnerability of pallidal neurons to Mn (Spadoni et al 2000). In addition, glutamate toxicity also involves activation of several kinases including ERK1/ 2, JNK, and p38 (Grant et al 2001;Zhang et al 2006;Zepeda et al 2008;Chen et al 2009). The involvement of these kinases in the toxic action of glutamate is evidenced by the fact that inhibitors of ERK phosphorylation and p38 kinase activity prevent glutamate-induced cell death (Stanciu et al 2000;Jeon et al 2000).…”

Section: Mechanism Of Mn-induced Toxicitymentioning

confidence: 58%

Are There Common Biochemical and Molecular Mechanisms Controlling Manganism and Parkisonism

Roth

2009

Neuromol Med

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Over the past several decades there has been considerable progress in our basic knowledge as to the mechanisms and factors regulating Mn toxicity. The disorder known as manganism is associated with the preferential accumulation of Mn in the globus pallidus of the basal ganglia which is generally considered to be the major and initial site of injury. Because the area of the CNS comprising the basal ganglia is very complex and dependent on the precise function and balance of several neurotransmitters, it is not surprising that symptoms of manganism often overlap with that of Parkinson's disease. The fact that neurological symptoms and onset of Mn toxicity are quite broad and can vary unpredictably probably reflects specific genetic variance of the physiological and biochemical makeup within the basal ganglia in any individual. Differences in response to Mn overexposure are, thus, likely due to underlying genetic variability which ultimately presents in deviations in both susceptibility as well as the characteristics of the neurological lesions and symptoms expressed. Although chronic exposure to Mn is not the initial causative agent provoking Parkinsonism, there is evidence suggesting that persistent exposure can predispose an individual to acquire dystonic movements associated with Parkinson's disease. As noted in this review, there appears to be common threads between the two disorders, as mutations in the genes, parkin and ATP13A2, associated with early onset of Parkinsonism, may also predispose an individual to develop Mn toxicity. Mutations in both genes appear to effect transport of Mn into the cell. These genetic difference coupled with additional environmental or nutritional factors must also be considered as contributing to the severity and onset of manganism.

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Section: Mechanism Of Mn-induced Toxicitymentioning

confidence: 58%

Are There Common Biochemical and Molecular Mechanisms Controlling Manganism and Parkisonism

Roth

2009

Neuromol Med

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“…It is not well understood how EW provokes P38 activation. As one possible mechanism, EW-induced glutamate neurotransmission may be involved in this process based on a study in which glutamate increased P38 phosphorylation in cultured chick cerebellar glial cells [ 111 ]. Another potential mechanism is inferred from studies in which oxidative stress was attributed to P38 activation [ 112 , 113 ].…”

Section: Protein Kinasementioning

confidence: 99%

Alcohol Withdrawal and Brain Injuries: Beyond Classical Mechanisms

Jung

Metzger

2010

Molecules

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Unmanaged sudden withdrawal from the excessive consumption of alcohol (ethanol) adversely alters neuronal integrity in vulnerable brain regions such as the cerebellum, hippocampus, or cortex. In addition to well known hyperexcitatory neurotransmissions, ethanol withdrawal (EW) provokes the intense generation of reactive oxygen species (ROS) and the activation of stress-responding protein kinases, which are the focus of this review article. EW also inflicts mitochondrial membranes/membrane potential, perturbs redox balance, and suppresses mitochondrial enzymes, all of which impair a fundamental function of mitochondria. Moreover, EW acts as an age-provoking stressor. The vulnerable age to EW stress is not necessarily the oldest age and varies depending upon the target molecule of EW. A major female sex steroid, 17β-estradiol (E2), interferes with the EW-induced alteration of oxidative signaling pathways and thereby protects neurons, mitochondria, and behaviors. The current review attempts to provide integrated information at the levels of oxidative signaling mechanisms by which EW provokes brain injuries and E2 protects against it.

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“…Nuclear protein extracts were prepared as described elsewhere [ 20 ] and used to identify ERα and ERβ expression in muscles. Total protein extracts were prepared to measure Glut4 relative expression as previously reported [ 21 ].…”

Section: Methodsmentioning

confidence: 99%

High Estradiol Differentially Affects the Expression of the Glucose Transporter Type 4 in Pelvic Floor Muscles of Rats

et al. 2018

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PurposeTo characterize the relationship between serum estradiol levels and the expression of glucose transporter type 4 (Glut4) in the pubococcygeus and iliococcygeus muscles in female rats.MethodsThe muscles were excised from virgin rats during the metestrus and proestrus stages of the estrous cycle, and from sham and ovariectomized rats implanted with empty or estradiol benzoate–filled capsules. The expression of estrogen receptors (ERs) was inspected in the muscles at metestrus and proestrus. Relative Glut4 expression, glycogen content, and serum glucose levels were measured. Appropriate statistical tests were done to identify significant differences (P≤0.05).ResultsThe pubococcygeus and iliococcygeus muscles expressed ERα and ERβ. Glut4 expression and glycogen content in the pubococcygeus muscle were higher at proestrus than at metestrus. No significant changes were observed in the iliococcygeus muscle. In ovariectomized rats, the administration of estradiol benzoate increased Glut4 expression and glycogen content in the pubococcygeus muscle alone.ConclusionsHigh serum estradiol levels increased Glut4 expression and glycogen content in the pubococcygeus muscle, but not in the iliococcygeus muscle.

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Glutamate-Dependent Transcriptional Regulation in Bergmann Glia Cells: Involvement of p38 MAP Kinase

Cited by 13 publications

References 34 publications

Are There Common Biochemical and Molecular Mechanisms Controlling Manganism and Parkisonism

Are There Common Biochemical and Molecular Mechanisms Controlling Manganism and Parkisonism

Alcohol Withdrawal and Brain Injuries: Beyond Classical Mechanisms

High Estradiol Differentially Affects the Expression of the Glucose Transporter Type 4 in Pelvic Floor Muscles of Rats

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