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ZBTB20 regulates nociception and pain sensation by modulating TRP channel expression in nociceptive sensory neurons

An-Jing Ren, Kai Wang, Huan Zhang, Anjun Liu, Xianhua Ma, Qing Liang, Dongmei Cao, John N. Wood, David Z. He, Yu-Qiang Ding, Wen-Jun Yuan, Zhifang Xie () and Weiping J. Zhang ()
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An-Jing Ren: Second Military Medical University
Kai Wang: Second Military Medical University
Huan Zhang: Second Military Medical University
Anjun Liu: Second Military Medical University
Xianhua Ma: Second Military Medical University
Qing Liang: Second Military Medical University
Dongmei Cao: Second Military Medical University
John N. Wood: University College London
David Z. He: Creighton University School of Medicine
Yu-Qiang Ding: Tongji University School of Medicine
Wen-Jun Yuan: Key Lab of Ministry of Education in Fertility Preservation and Maintenance, Ningxia Medical University
Zhifang Xie: Second Military Medical University
Weiping J. Zhang: Second Military Medical University

Nature Communications, 2014, vol. 5, issue 1, 1-14

Abstract: Abstract In mammals, pain sensation is initiated by the detection of noxious stimuli through specialized transduction ion channels and receptors in nociceptive sensory neurons. Transient receptor potential (TRP) channels are the key sensory transducers that confer nociceptors distinct sensory modalities. However, the regulatory mechanisms about their expression are poorly defined. Here we show that the zinc-finger protein ZBTB20 regulates TRP channels expression in nociceptors. ZBTB20 is highly expressed in nociceptive sensory neurons of dorsal root ganglia. Disruption of ZBTB20 in nociceptors led to a marked decrease in the expression levels of TRPV1, TRPA1 and TRPM8 and the response of calcium flux and whole-cell currents evoked by their respective specific agonists. Phenotypically, the mice lacking ZBTB20 specifically in nociceptors showed a defect in nociception and pain sensation in response to thermal, mechanical and inflammatory stimulation. Our findings point to ZBTB20 as a critical regulator of nociception and pain sensation by modulating TRP channels expression in nociceptors.

Date: 2014
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms5984

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DOI: 10.1038/ncomms5984

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