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Pivotal role for neuronal Toll-like receptors in ischemic brain injury and functional deficits.

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Pivotal role for neuronal Toll-like receptors in ischemic brain injury and functional deficits. / Tang, Sung-Chun; Arumugam, Thiruma V; Xu, Xiangru; Cheng, Aiwu; Mughal, Mohamed R; Jo, Dong Gyu; Lathia, Justin D; Siler, Dominic A; Chigurupati, Srinivasulu; Ouyang, Xin; Magnus, Tim; Camandola, Simonetta; Mattson, Mark P.

In: P NATL ACAD SCI USA, Vol. 104, No. 34, 34, 2007, p. 13798-13803.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Tang, S-C, Arumugam, TV, Xu, X, Cheng, A, Mughal, MR, Jo, DG, Lathia, JD, Siler, DA, Chigurupati, S, Ouyang, X, Magnus, T, Camandola, S & Mattson, MP 2007, 'Pivotal role for neuronal Toll-like receptors in ischemic brain injury and functional deficits.', P NATL ACAD SCI USA, vol. 104, no. 34, 34, pp. 13798-13803. <http://www.ncbi.nlm.nih.gov/pubmed/17693552?dopt=Citation>

APA

Tang, S-C., Arumugam, T. V., Xu, X., Cheng, A., Mughal, M. R., Jo, D. G., Lathia, J. D., Siler, D. A., Chigurupati, S., Ouyang, X., Magnus, T., Camandola, S., & Mattson, M. P. (2007). Pivotal role for neuronal Toll-like receptors in ischemic brain injury and functional deficits. P NATL ACAD SCI USA, 104(34), 13798-13803. [34]. http://www.ncbi.nlm.nih.gov/pubmed/17693552?dopt=Citation

Vancouver

Tang S-C, Arumugam TV, Xu X, Cheng A, Mughal MR, Jo DG et al. Pivotal role for neuronal Toll-like receptors in ischemic brain injury and functional deficits. P NATL ACAD SCI USA. 2007;104(34):13798-13803. 34.

Bibtex

@article{8e99172f909440aaa1efaa3efa31b69d,
title = "Pivotal role for neuronal Toll-like receptors in ischemic brain injury and functional deficits.",
abstract = "The innate immune system senses the invasion of pathogenic microorganisms and tissue injury through Toll-like receptors (TLR), a mechanism thought to be limited to immune cells. We now report that neurons express several TLRs, and that the levels of TLR2 and -4 are increased in neurons in response to IFN-gamma stimulation and energy deprivation. Neurons from both TLR2 knockout and -4 mutant mice were protected against energy deprivation-induced cell death, which was associated with decreased activation of a proapoptotic signaling cascade involving jun N-terminal kinase and the transcription factor AP-1. TLR2 and -4 expression was increased in cerebral cortical neurons in response to ischemia/reperfusion injury, and the amount of brain damage and neurological deficits caused by a stroke were significantly less in mice deficient in TLR2 or -4 compared with WT control mice. Our findings establish a proapoptotic signaling pathway for TLR2 and -4 in neurons that may render them vulnerable to ischemic death.",
author = "Sung-Chun Tang and Arumugam, {Thiruma V} and Xiangru Xu and Aiwu Cheng and Mughal, {Mohamed R} and Jo, {Dong Gyu} and Lathia, {Justin D} and Siler, {Dominic A} and Srinivasulu Chigurupati and Xin Ouyang and Tim Magnus and Simonetta Camandola and Mattson, {Mark P}",
year = "2007",
language = "Deutsch",
volume = "104",
pages = "13798--13803",
journal = "P NATL ACAD SCI USA",
issn = "0027-8424",
publisher = "National Academy of Sciences",
number = "34",

}

RIS

TY - JOUR

T1 - Pivotal role for neuronal Toll-like receptors in ischemic brain injury and functional deficits.

AU - Tang, Sung-Chun

AU - Arumugam, Thiruma V

AU - Xu, Xiangru

AU - Cheng, Aiwu

AU - Mughal, Mohamed R

AU - Jo, Dong Gyu

AU - Lathia, Justin D

AU - Siler, Dominic A

AU - Chigurupati, Srinivasulu

AU - Ouyang, Xin

AU - Magnus, Tim

AU - Camandola, Simonetta

AU - Mattson, Mark P

PY - 2007

Y1 - 2007

N2 - The innate immune system senses the invasion of pathogenic microorganisms and tissue injury through Toll-like receptors (TLR), a mechanism thought to be limited to immune cells. We now report that neurons express several TLRs, and that the levels of TLR2 and -4 are increased in neurons in response to IFN-gamma stimulation and energy deprivation. Neurons from both TLR2 knockout and -4 mutant mice were protected against energy deprivation-induced cell death, which was associated with decreased activation of a proapoptotic signaling cascade involving jun N-terminal kinase and the transcription factor AP-1. TLR2 and -4 expression was increased in cerebral cortical neurons in response to ischemia/reperfusion injury, and the amount of brain damage and neurological deficits caused by a stroke were significantly less in mice deficient in TLR2 or -4 compared with WT control mice. Our findings establish a proapoptotic signaling pathway for TLR2 and -4 in neurons that may render them vulnerable to ischemic death.

AB - The innate immune system senses the invasion of pathogenic microorganisms and tissue injury through Toll-like receptors (TLR), a mechanism thought to be limited to immune cells. We now report that neurons express several TLRs, and that the levels of TLR2 and -4 are increased in neurons in response to IFN-gamma stimulation and energy deprivation. Neurons from both TLR2 knockout and -4 mutant mice were protected against energy deprivation-induced cell death, which was associated with decreased activation of a proapoptotic signaling cascade involving jun N-terminal kinase and the transcription factor AP-1. TLR2 and -4 expression was increased in cerebral cortical neurons in response to ischemia/reperfusion injury, and the amount of brain damage and neurological deficits caused by a stroke were significantly less in mice deficient in TLR2 or -4 compared with WT control mice. Our findings establish a proapoptotic signaling pathway for TLR2 and -4 in neurons that may render them vulnerable to ischemic death.

M3 - SCORING: Zeitschriftenaufsatz

VL - 104

SP - 13798

EP - 13803

JO - P NATL ACAD SCI USA

JF - P NATL ACAD SCI USA

SN - 0027-8424

IS - 34

M1 - 34

ER -