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https://doi.org/10.1186/2040-7378-2-15
Title: | Evidence that adiponectin receptor 1 activation exacerbates ischemic neuronal death | Authors: | Thundyil, J Tang, S.-C Okun, E Shah, K Karamyan, V.T Li, Y.-I Woodruff, T.M Taylor, S.M Jo, D.-G Mattson, M.P Arumugam, T.V |
Keywords: | adiponectin receptor 1 adiponectin receptor 2 carbon dioxide glucose hydroxymethylglutaryl coenzyme A reductase kinase mitogen activated protein kinase p38 oxygen adult animal cell animal cell culture animal experiment animal model animal tissue article atmosphere brain cell brain ischemia brain tissue case report controlled study disease exacerbation embryo human human experiment immunoblotting immunochemistry in vitro study in vivo study incubation time male middle cerebral artery occlusion mouse neocortex nerve cell necrosis nonhuman pathogenesis priority journal reperfusion injury reverse transcription polymerase chain reaction |
Issue Date: | 2010 | Citation: | Thundyil, J, Tang, S.-C, Okun, E, Shah, K, Karamyan, V.T, Li, Y.-I, Woodruff, T.M, Taylor, S.M, Jo, D.-G, Mattson, M.P, Arumugam, T.V (2010). Evidence that adiponectin receptor 1 activation exacerbates ischemic neuronal death. Experimental and Translational Stroke Medicine 2 (1) : 15. ScholarBank@NUS Repository. https://doi.org/10.1186/2040-7378-2-15 | Rights: | Attribution 4.0 International | Abstract: | Background-: Adiponectin is a hormone produced in and released from adipose cells, which has been shown to have anti-diabetic and anti-inflammatory actions in peripheral cells. Two cell surface adiponectin receptors (ADRs) mediate the majority of the known biological actions of adiponectin. Thus far, ADR expression in the brain has been demonstrated in the arcuate and the paraventricular nucleus of hypothalamus, where its activation affects food intake. Recent findings suggest that levels of circulating adiponectin increase after an ischemic stroke, but the role of adiponectin receptor activation in stroke pathogenesis and its functional outcome is unclear.Methods-: Ischemic stroke was induced in C57BL/6 mice by middle cerebral artery occlusion (MCAO) for 1 h, followed by reperfusion. Primary cortical neuronal cultures were established from individual embryonic neocortex. For glucose deprivation (GD), cultured neurons were incubated in glucose-free Locke's medium for 6, 12 or 24 h. For combined oxygen and glucose deprivation (OGD), neurons were incubated in glucose-free Locke's medium in an oxygen-free chamber with 95% N2/5% CO2atmosphere for either 3, 6, 9, 12 or 24 h. Primary neurons and brain tissues were analysed for Adiponectin and ADRs using reverse transcriptase polymerase chain reaction (RT-PCR), immunoblot and immunochemistry methods.Results-: Cortical neurons express ADR1 and ADR2, and that the levels of ADR1 are increased in neurons in response to in vitro or in vivo ischemic conditions. Neurons treated with either globular or trimeric adiponectin exhibited increased vulnerability to oxygen and glucose deprivation which was associated with increased activation of a pro-apoptotic signaling cascade involving p38 mitogen-activated protein kinase (p38MAPK) and AMP-activated protein kinase (AMPK).Conclusions-: This study reveals a novel pathogenic role for adiponectin and adiponectin receptor activation in ischemic stroke. We show that cortical neurons express ADRs and reveal a pro-apoptotic role for ADR1 activation in neurons, which may render them vulnerable to ischemic death. © 2010 Thundyil et al; licensee BioMed Central Ltd. | Source Title: | Experimental and Translational Stroke Medicine | URI: | https://scholarbank.nus.edu.sg/handle/10635/177791 | ISSN: | 20407378 | DOI: | 10.1186/2040-7378-2-15 | Rights: | Attribution 4.0 International |
Appears in Collections: | Staff Publications Elements |
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