Thrombin potently enhances swelling‐sensitive glutamate efflux from cultured astrocytes

Ramos‐Mandujano, Gerardo; Vázquez-Juárez, Erika; Hernández-Benítez, Reyna; Pasantes‐Morales, Herminia

doi:10.1002/glia.20513

Cited by 46 publications

(72 citation statements)

References 33 publications

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“…Another possibility is that ER-related proteins may be expressed in gliomas and may mediate the response to tamoxifen (51). Finally, especially at high doses, tamoxifen might act independently of any steroid receptor by influencing calmodulin (78), various kinases (70), or intracellular calcium (79), or through other mechanisms (80). A number of studies indicate that inhibition of cell proliferation in gliomas by tamoxifen seems to operate…”

Section: Actions Of Steroid Hormone Receptor Agonists and Antagonistsmentioning

confidence: 99%

Do Steroid Hormones Play a Role in the Etiology of Glioma?

Kabat

Etgen

Rohan

2010

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Gliomas are the most common type of primary malignant brain tumor and have a very poor prognosis. Little is known, however, about the etiology of these tumors. Evidence from a number of sources suggests that endogenous steroid hormones may play a role in the development of gliomas. First, the descriptive epidemiology of glioma suggests a relative protection of females compared with males, particularly during the premenopausal years. Second, some gliomas and glioblastomas express estrogen receptors (ER), especially ERβ, as well as aromatase, the enzyme responsible for the conversion of testosterone to estradiol, and possibly other steroid hormone receptors. Third, experimental studies indicate that glioblastomas transplanted into animals grow at a slower rate in females compared with males. Finally, experimental studies show that estradiol, 2-methoxyestradiol, and a number of selective estrogen receptor modulators inhibit proliferation of gliomas and induce cell death. These hormonal agonists and antagonists may act either through classical steroid hormone receptors or independently of such receptors. In view of these findings, further clinical, experimental, and epidemiologic studies are needed to elucidate the role of steroid hormone agonists and antagonists in the development and proliferation of glioma. If hormonal pathways are involved in gliomagenesis, this could eventually lead to the design of preventive strategies. Cancer Epidemiol Biomarkers Prev; 19(10); 2421-7. ©2010 AACR.Little is known about the etiology of brain neoplasms, which in general are highly fatal (1). Gliomas, which include astrocytomas, oligodendrogliomas, and ependymomas, are the most common type of primary malignant brain tumor, accounting for approximately 80% of cases (2). Gliomas originate from glial cells (astrocytes or oligodendrocytes). Gliobastoma multiforme, the highest grade of glioma, is the most common and most aggressive type of malignant glioma. Most cases of glioblastoma multiforme (∼90%), referred to as "primary glioblastoma multiforme," develop rapidly without detectable evidence of a less malignant precursor tumor, whereas about 10% of glioblastomas, referred to as "secondary glioblastoma multiforme," develop slowly from low-grade astrocytomas (3). The only established risk factors for gliomas are high-dose ionizing radiation and certain rare genetic conditions, which together account for only a small proportion of cases (1, 4, 5). However, evidence from a number of sources suggests a possible role of endogenous ovarian steroid hormones in the development of glioma. Given that this topic has received little attention in major reviews on brain tumor epidemiology to date (1, 4-6), we review here findings from descriptive and analytic epidemiology, clinical studies, and experimental animal and cell culture studies pertinent to the potential role of steroid hormones in the development of glioma. Descriptive EpidemiologyThe incidence rate of glioma in adulthood is 50% greater in men than in women (5, 7). For example...

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Section: Actions Of Steroid Hormone Receptor Agonists and Antagonistsmentioning

confidence: 99%

Do Steroid Hormones Play a Role in the Etiology of Glioma?

Kabat

Etgen

Rohan

2010

Cancer Epidemiology, Biomarkers &Amp; Prevention

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“…Several recent in vitro studies have found that a number ob substances, which are produced ore released in ischemia, such as reactive oxygen species H 2 O 2 , reactive nitrogen species peroxynitrite, thrombin, and ATP, all drastically increase swelling-activated glutamate release from moderately swollen astrocytes [69][70][71][72].…”

Section: Volume-regulated Anion Channels and The Reversed Mode Of Glumentioning

confidence: 99%

Disruption of ionic and cell volume homeostasis in cerebral ischemia: The perfect storm

Mongin

2007

Pathophysiology

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The mechanisms of brain tissue damage in stroke are strongly linked to the phenomenon of excitotoxicity, which is defined as damage or death of neural cells due to excessive activation of receptors for the excitatory neurotransmitters glutamate and aspartate. Under physiological conditions, ionotropic glutamate receptors mediate the processes of excitatory neurotransmission and synaptic plasticity. In ischemia, sustained pathological release of glutamate from neurons and glial cells causes prolonged activation of these receptors, resulting in massive depolarization and cytoplasmic Ca 2+ overload. The NMDA subtype of glutamate receptors is particularly important as it represents the main initial route for the Ca 2+ influx. High cytoplasmic levels of Ca 2+ activate many degradative processes that, depending on the metabolic status, cause immediate or delayed death of neural cells. This traditional view has been expanded by a number of observations that implicate Cl − channels and several types of non-channel transporter proteins, such as the Na + ,K + ,2Cl − cotransporter, Na + /H + exchanger, and Na + /Ca 2+ exchanger, in the development of glutamate toxicity. Some of these ion transporters increase tissue damage by promoting pathological cell swelling and necrotic cell death, while others contribute to a long term accumulation of cytoplasmic Ca 2+ . This brief review is aimed at illustrating how the dysregulation of various ion transport processes combine in a 'perfect storm' that disrupts neural ionic homeostasis and culminates in the irreversible damage and death of neural cells. The clinical relevance of individual transporters as targets for therapeutic intervention in stroke is also briefly discussed.

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“…In this context, we and others Kimelberg, 2002, 2005;Heacock et al, 2004Heacock et al, , 2006Cheema et al, 2005Cheema et al, , 2007Ramos-Mandujano et al, 2007) have recently demonstrated that the volume-dependent release of osmolytes from a variety of neural cells can be dramatically enhanced following activation of certain G-protein-coupled receptors. Receptor activation not only increases the extent of osmolyte release, but it also lowers the threshold osmolarity ("set-point") at which osmolytes are released, thereby permitting cells to respond to small, physiologically relevant, reductions in osmolarity.…”

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confidence: 81%

Cholesterol Regulates Volume-Sensitive Osmolyte Efflux from Human SH-SY5Y Neuroblastoma Cells following Receptor Activation

Cheema

Fisher

2007

J Pharmacol Exp Ther

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The ability of cholesterol to modulate receptor-mediated increases in the volume-dependent release of the organic osmolyte, taurine, has been examined. Depletion of cholesterol from SH-SY5Y neuroblastoma by preincubation of the cells with 5 mM methyl-␤-cyclodextrin (CD) for 10 min resulted in a 40 to 50% reduction in cholesterol and an enhancement of the ability of proteinase-activated receptor (PAR) 1, muscarinic cholinergic receptor (mAChR), and sphingosine 1-phosphate receptor to stimulate taurine efflux, when monitored under hypoosmotic conditions. Basal (swelling-induced) release of taurine was also enhanced by cholesterol depletion, but less markedly. Both basaland receptor-mediated increases in taurine efflux were mediated via a volume-sensitive organic osmolyte and anion channel in control and cholesterol-depleted cells. Studies with the PAR-1 and mAChR receptor subtypes indicated that the stimulatory effect of CD pretreatment could be reversed by incubation of the cells with either CD/cholesterol or CD/5-cholesten-3␣-ol donor complexes and that cholesterol depletion increased agonist efficacy, but not potency. The ability of cholesterol depletion to promote the PAR-1 receptor-mediated stimulation of osmolyte release was most pronounced under conditions of isotonicity or mild hypotonicity. In contrast to CD pretreatment, preincubation of the cells with cholesterol oxidase, a condition under which lipid microdomains are also disrupted, had no effect on either basal-or receptor-stimulated taurine efflux. Taken together, the results suggest that cholesterol regulates receptor-mediated osmolyte release via its effects on the biophysical properties of the plasma membrane, rather than its presence in lipid microdomains.

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Thrombin potently enhances swelling‐sensitive glutamate efflux from cultured astrocytes

Cited by 46 publications

References 33 publications

Do Steroid Hormones Play a Role in the Etiology of Glioma?

Do Steroid Hormones Play a Role in the Etiology of Glioma?

Disruption of ionic and cell volume homeostasis in cerebral ischemia: The perfect storm

Cholesterol Regulates Volume-Sensitive Osmolyte Efflux from Human SH-SY5Y Neuroblastoma Cells following Receptor Activation

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