MicroRNA-132 Potentiates Cholinergic Anti-inflammatory Signaling by Targeting Acetylcholinesterase

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

Standard

MicroRNA-132 Potentiates Cholinergic Anti-inflammatory Signaling by Targeting Acetylcholinesterase. / Shaked, Iftach; Meerson, Ari; Wolf, Yochai; Avni, Ran; Greenberg, David; Gilboa-Geffen, Adi; Soreq, Hermona.

In: Immunity, Vol. 31, No. 6, 18.12.2009, p. 965-973.

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

Harvard

Shaked, I, Meerson, A, Wolf, Y, Avni, R, Greenberg, D, Gilboa-Geffen, A & Soreq, H 2009, 'MicroRNA-132 Potentiates Cholinergic Anti-inflammatory Signaling by Targeting Acetylcholinesterase', Immunity, vol. 31, no. 6, pp. 965-973. https://doi.org/10.1016/j.immuni.2009.09.019

APA

Shaked, I., Meerson, A., Wolf, Y., Avni, R., Greenberg, D., Gilboa-Geffen, A., & Soreq, H. (2009). MicroRNA-132 Potentiates Cholinergic Anti-inflammatory Signaling by Targeting Acetylcholinesterase. Immunity, 31(6), 965-973. https://doi.org/10.1016/j.immuni.2009.09.019

Vancouver

Shaked I, Meerson A, Wolf Y, Avni R, Greenberg D, Gilboa-Geffen A et al. MicroRNA-132 Potentiates Cholinergic Anti-inflammatory Signaling by Targeting Acetylcholinesterase. Immunity. 2009 Dec 18;31(6):965-973. https://doi.org/10.1016/j.immuni.2009.09.019

Author

Shaked, Iftach ; Meerson, Ari ; Wolf, Yochai ; Avni, Ran ; Greenberg, David ; Gilboa-Geffen, Adi ; Soreq, Hermona. / MicroRNA-132 Potentiates Cholinergic Anti-inflammatory Signaling by Targeting Acetylcholinesterase. In: Immunity. 2009 ; Vol. 31, No. 6. pp. 965-973.

Bibtex

@article{b03a62bb714d4c649dd08c98a1acdf7a,
title = "MicroRNA-132 Potentiates Cholinergic Anti-inflammatory Signaling by Targeting Acetylcholinesterase",
abstract = "MicroRNAs (miRNAs) contribute to both neuronal and immune cell fate, but their involvement in intertissue communication remained unexplored. The brain, via vagal secretion of acetylcholine (ACh), suppresses peripheral inflammation by intercepting cytokine production; therefore, we predicted that microRNAs targeting acetylcholinesterase (AChE) can attenuate inflammation. Here, we report that inflammatory stimuli induced leukocyte overexpression of the AChE-targeting miR-132. Injected locked nucleic acid (LNA)-modified anti-miR-132 oligonucleotide depleted miR-132 amounts while elevating AChE in mouse circulation and tissues. In transfected cells, a mutated 3'UTR miR-132 binding site increased AChE mRNA expression, whereas cells infected with a lentivirus expressing pre-miR-132 showed suppressed AChE. Transgenic mice overexpressing 3'UTR null AChE showed excessive inflammatory mediators and impaired cholinergic anti-inflammatory regulation, in spite of substantial miR-132 upregulation in brain and bone marrow. Our findings identify the AChE mRNA-targeting miR-132 as a functional regulator of the brain-to-body resolution of inflammation, opening avenues for study and therapeutic manipulations of the neuro-immune dialog.",
keywords = "GENE-EXPRESSION, DENDRITIC CELLS, SPLICE VARIANTS, HEART-FAILURE, HOST RESPONSE, VAGUS NERVE, PATHWAY, ACTIVATION, BRAIN, INFLAMMATION",
author = "Iftach Shaked and Ari Meerson and Yochai Wolf and Ran Avni and David Greenberg and Adi Gilboa-Geffen and Hermona Soreq",
year = "2009",
month = dec,
day = "18",
doi = "10.1016/j.immuni.2009.09.019",
language = "English",
volume = "31",
pages = "965--973",
journal = "Immunity",
issn = "1074-7613",
publisher = "Cell Press",
number = "6",

}

RIS

TY - JOUR

T1 - MicroRNA-132 Potentiates Cholinergic Anti-inflammatory Signaling by Targeting Acetylcholinesterase

AU - Shaked, Iftach

AU - Meerson, Ari

AU - Wolf, Yochai

AU - Avni, Ran

AU - Greenberg, David

AU - Gilboa-Geffen, Adi

AU - Soreq, Hermona

PY - 2009/12/18

Y1 - 2009/12/18

N2 - MicroRNAs (miRNAs) contribute to both neuronal and immune cell fate, but their involvement in intertissue communication remained unexplored. The brain, via vagal secretion of acetylcholine (ACh), suppresses peripheral inflammation by intercepting cytokine production; therefore, we predicted that microRNAs targeting acetylcholinesterase (AChE) can attenuate inflammation. Here, we report that inflammatory stimuli induced leukocyte overexpression of the AChE-targeting miR-132. Injected locked nucleic acid (LNA)-modified anti-miR-132 oligonucleotide depleted miR-132 amounts while elevating AChE in mouse circulation and tissues. In transfected cells, a mutated 3'UTR miR-132 binding site increased AChE mRNA expression, whereas cells infected with a lentivirus expressing pre-miR-132 showed suppressed AChE. Transgenic mice overexpressing 3'UTR null AChE showed excessive inflammatory mediators and impaired cholinergic anti-inflammatory regulation, in spite of substantial miR-132 upregulation in brain and bone marrow. Our findings identify the AChE mRNA-targeting miR-132 as a functional regulator of the brain-to-body resolution of inflammation, opening avenues for study and therapeutic manipulations of the neuro-immune dialog.

AB - MicroRNAs (miRNAs) contribute to both neuronal and immune cell fate, but their involvement in intertissue communication remained unexplored. The brain, via vagal secretion of acetylcholine (ACh), suppresses peripheral inflammation by intercepting cytokine production; therefore, we predicted that microRNAs targeting acetylcholinesterase (AChE) can attenuate inflammation. Here, we report that inflammatory stimuli induced leukocyte overexpression of the AChE-targeting miR-132. Injected locked nucleic acid (LNA)-modified anti-miR-132 oligonucleotide depleted miR-132 amounts while elevating AChE in mouse circulation and tissues. In transfected cells, a mutated 3'UTR miR-132 binding site increased AChE mRNA expression, whereas cells infected with a lentivirus expressing pre-miR-132 showed suppressed AChE. Transgenic mice overexpressing 3'UTR null AChE showed excessive inflammatory mediators and impaired cholinergic anti-inflammatory regulation, in spite of substantial miR-132 upregulation in brain and bone marrow. Our findings identify the AChE mRNA-targeting miR-132 as a functional regulator of the brain-to-body resolution of inflammation, opening avenues for study and therapeutic manipulations of the neuro-immune dialog.

KW - GENE-EXPRESSION

KW - DENDRITIC CELLS

KW - SPLICE VARIANTS

KW - HEART-FAILURE

KW - HOST RESPONSE

KW - VAGUS NERVE

KW - PATHWAY

KW - ACTIVATION

KW - BRAIN

KW - INFLAMMATION

U2 - 10.1016/j.immuni.2009.09.019

DO - 10.1016/j.immuni.2009.09.019

M3 - Journal article

VL - 31

SP - 965

EP - 973

JO - Immunity

JF - Immunity

SN - 1074-7613

IS - 6

ER -

ID: 289310902