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Responsible editor | Enzyme beauty pain is an unpleasant sensory experience.
Certain noxious stimuli, such as thermal, mechanical or chemical stimuli, can cause pain and escape reactions in the body, thereby protecting the body from harm.
It is generally believed that different types of stimuli activate different ion channels on the cell membranes of sensory neurons, thereby converting stimulus signals into electrical signals and transmitting these signals to the brain to make the body perceive different sensations.
The team of Associate Researcher Zhang Xiaolong of the Medical Research Center of Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences) has been committed to the study of the mechanism of the relationship between abnormal ion channel membrane translocation and chronic pain.
The previous study revealed the Nav1.
6 and ClC-3 channel membrane translocation The underlying mechanism of abnormal induction of chronic pain [1,2].
Recent studies have shown that TRPM3 channel is a non-selective cation channel, which is highly expressed in the cell membrane of sensory neurons [3], and mainly senses heat noxious stimuli [4].
How the TRPM3 channel translocates from the cytoplasm of neurons to the cell membrane is still unclear.
Recently, Associate Professor Zhang Xiaolong of the Medical Research Center of Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences) and Professor Liu Xianguo of the Pain Research Center of Sun Yat-sen University jointly published a research paper entitled ATF4 selectively regulates heat nociception and contributes to kinesin-mediated TRPM3 trafficking in Nature Communications It was found that ATF4 binds to ion channel TRPM3 and kinesin KIF17, and the three form a complex.
Through the transport of kinesin KIF17, it promotes the translocation of sensory neuron TRPM3 membrane, thereby mediating heat conduction and nociceptive stimulation.Activating Transcription Factor 4 (Activating Transcription Factor 4) is highly expressed in the nervous system, and its deletion can impair the synaptic plasticity and memory formation of hippocampal neurons [5, 6].
The role of ATF4 in pain is still unclear.
The study found that knocking down and knocking out ATF4 significantly reduced the sensitivity of mice to heat noxious stimuli, but did not affect the sensitivity of mice to mechanical and cold stimuli.
In addition, in mouse sensory neurons ATF4 binds to the heat-sensitive ion channel TRPM3, and it is interesting that knocking out ATF4 significantly reduces the expression of TRPM3 on the neuronal cell membrane and increases the expression of TRPM3 in the cytoplasm without affecting the total TRPM3 Expression, suggesting that ATF4 can mediate TRPM3 membrane translocation.
It is further found that ATF4 binds to kinesin KIF17, knocking down KIF17 inhibits TRPM3 membrane translocation, and ATF4, TRPM3, and KIF17 are co-localized in sensory neurons.
In summary, ATF4 binds to TRPM3 and KIF17, and the three form a complex.
Under the transport of kinesin KIF17, it promotes the translocation of the sensory neuron TRPM3 membrane, thereby mediating the thermal pain response.
Xie Manxiu, Zeng Wei'an and Lai Renchun, Department of Anesthesiology, Sun Yat-sen University Cancer Center, and Cao Xianying, School of Food Science and Technology, Hainan University, are the co-first authors, and Zhang Xiaolong and Liu Xianguo are the co-corresponding authors.
Original link: Platemaker: 11 References 1.
Zhang, XL, Ding, HH, Xu, T.
, Liu, M.
, Ma , C.
, Wu, SL, Wei, JY, Liu, CC, Zhang, SB, and Xin, WJ (2018).
Palmitoylation of delta-catenin promotes kinesin-mediated membrane trafficking of Nav1.
6 in sensory neurons to promote neuropathic pain .
Science signaling 11.
2.
Zhang, XL, Zhang, JJ, Chen, ZH, Yang, KB, Zhang, X.
, Xiao, YB, Lei, Y.
, Cao, XY, and Xie, MX (2021).
Difference of pain vulnerability in adult and juvenile rodents: the role of SIRT1-mediated ClC-3 trafficking in sensory neurons.
Pain.
3.
Vriens, J.
, Owsianik, G.
, Hofmann, T.
, Philipp, SE, Stab, J.
, Chen , X.
, Benoit, M.
, Xue, F.
, Janssens, A.
, Kerselaers, S.
, et al.
(2011).
TRPM3 is a nociceptor channel involved in the detection of noxious heat.
Neuron 70, 482-494.
4 .
Vandewauw, I.
, De Clercq,K.
, Mulier, M.
, Held, K.
, Pinto, S.
, Van Ranst, N.
, Segal, A.
, Voet, T.
, Vennekens, R.
, Zimmermann, K.
, et al.
(2018) .
A TRP channel trio mediates acute noxious heat sensing.
Nature 555, 662-666.
5.
Chen, A.
, Muzzio, IA, Malleret, G.
, Bartsch, D.
, Verbitsky, M.
, Pavlidis, P.
, Yonan, AL , Vronskaya, S.
, Grody, MB, Cepeda, I.
, et al.
(2003).
Inducible enhancement of memory storage and synaptic plasticity in transgenic mice expressing an inhibitor of ATF4 (CREB-2) and C/EBP proteins.
Neuron 39, 655-669.
6.
Costa-Mattioli, M.
, Gobert, D.
, Stern, E.
, Gamache, K.
, Colina, R.
, Cuello, C.
, Sossin, W.
, Kaufman, R.
, Pelletier, J.
, Rosenblum, K.
, et al.
(2007).
eIF2alpha phosphorylation bidirectionally regulates the switch from short- to long-term synaptic plasticity and memory.
Cell 129, 195-206.
Reprinting instructions [Non-original articles] The copyright of this article belongs to the author of the article.
Personal forwarding and sharing are welcome.
Reprinting is prohibited without permission.
The author has all legal rights and offenders must be investigated.
Certain noxious stimuli, such as thermal, mechanical or chemical stimuli, can cause pain and escape reactions in the body, thereby protecting the body from harm.
It is generally believed that different types of stimuli activate different ion channels on the cell membranes of sensory neurons, thereby converting stimulus signals into electrical signals and transmitting these signals to the brain to make the body perceive different sensations.
The team of Associate Researcher Zhang Xiaolong of the Medical Research Center of Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences) has been committed to the study of the mechanism of the relationship between abnormal ion channel membrane translocation and chronic pain.
The previous study revealed the Nav1.
6 and ClC-3 channel membrane translocation The underlying mechanism of abnormal induction of chronic pain [1,2].
Recent studies have shown that TRPM3 channel is a non-selective cation channel, which is highly expressed in the cell membrane of sensory neurons [3], and mainly senses heat noxious stimuli [4].
How the TRPM3 channel translocates from the cytoplasm of neurons to the cell membrane is still unclear.
Recently, Associate Professor Zhang Xiaolong of the Medical Research Center of Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences) and Professor Liu Xianguo of the Pain Research Center of Sun Yat-sen University jointly published a research paper entitled ATF4 selectively regulates heat nociception and contributes to kinesin-mediated TRPM3 trafficking in Nature Communications It was found that ATF4 binds to ion channel TRPM3 and kinesin KIF17, and the three form a complex.
Through the transport of kinesin KIF17, it promotes the translocation of sensory neuron TRPM3 membrane, thereby mediating heat conduction and nociceptive stimulation.Activating Transcription Factor 4 (Activating Transcription Factor 4) is highly expressed in the nervous system, and its deletion can impair the synaptic plasticity and memory formation of hippocampal neurons [5, 6].
The role of ATF4 in pain is still unclear.
The study found that knocking down and knocking out ATF4 significantly reduced the sensitivity of mice to heat noxious stimuli, but did not affect the sensitivity of mice to mechanical and cold stimuli.
In addition, in mouse sensory neurons ATF4 binds to the heat-sensitive ion channel TRPM3, and it is interesting that knocking out ATF4 significantly reduces the expression of TRPM3 on the neuronal cell membrane and increases the expression of TRPM3 in the cytoplasm without affecting the total TRPM3 Expression, suggesting that ATF4 can mediate TRPM3 membrane translocation.
It is further found that ATF4 binds to kinesin KIF17, knocking down KIF17 inhibits TRPM3 membrane translocation, and ATF4, TRPM3, and KIF17 are co-localized in sensory neurons.
In summary, ATF4 binds to TRPM3 and KIF17, and the three form a complex.
Under the transport of kinesin KIF17, it promotes the translocation of the sensory neuron TRPM3 membrane, thereby mediating the thermal pain response.
Xie Manxiu, Zeng Wei'an and Lai Renchun, Department of Anesthesiology, Sun Yat-sen University Cancer Center, and Cao Xianying, School of Food Science and Technology, Hainan University, are the co-first authors, and Zhang Xiaolong and Liu Xianguo are the co-corresponding authors.
Original link: Platemaker: 11 References 1.
Zhang, XL, Ding, HH, Xu, T.
, Liu, M.
, Ma , C.
, Wu, SL, Wei, JY, Liu, CC, Zhang, SB, and Xin, WJ (2018).
Palmitoylation of delta-catenin promotes kinesin-mediated membrane trafficking of Nav1.
6 in sensory neurons to promote neuropathic pain .
Science signaling 11.
2.
Zhang, XL, Zhang, JJ, Chen, ZH, Yang, KB, Zhang, X.
, Xiao, YB, Lei, Y.
, Cao, XY, and Xie, MX (2021).
Difference of pain vulnerability in adult and juvenile rodents: the role of SIRT1-mediated ClC-3 trafficking in sensory neurons.
Pain.
3.
Vriens, J.
, Owsianik, G.
, Hofmann, T.
, Philipp, SE, Stab, J.
, Chen , X.
, Benoit, M.
, Xue, F.
, Janssens, A.
, Kerselaers, S.
, et al.
(2011).
TRPM3 is a nociceptor channel involved in the detection of noxious heat.
Neuron 70, 482-494.
4 .
Vandewauw, I.
, De Clercq,K.
, Mulier, M.
, Held, K.
, Pinto, S.
, Van Ranst, N.
, Segal, A.
, Voet, T.
, Vennekens, R.
, Zimmermann, K.
, et al.
(2018) .
A TRP channel trio mediates acute noxious heat sensing.
Nature 555, 662-666.
5.
Chen, A.
, Muzzio, IA, Malleret, G.
, Bartsch, D.
, Verbitsky, M.
, Pavlidis, P.
, Yonan, AL , Vronskaya, S.
, Grody, MB, Cepeda, I.
, et al.
(2003).
Inducible enhancement of memory storage and synaptic plasticity in transgenic mice expressing an inhibitor of ATF4 (CREB-2) and C/EBP proteins.
Neuron 39, 655-669.
6.
Costa-Mattioli, M.
, Gobert, D.
, Stern, E.
, Gamache, K.
, Colina, R.
, Cuello, C.
, Sossin, W.
, Kaufman, R.
, Pelletier, J.
, Rosenblum, K.
, et al.
(2007).
eIF2alpha phosphorylation bidirectionally regulates the switch from short- to long-term synaptic plasticity and memory.
Cell 129, 195-206.
Reprinting instructions [Non-original articles] The copyright of this article belongs to the author of the article.
Personal forwarding and sharing are welcome.
Reprinting is prohibited without permission.
The author has all legal rights and offenders must be investigated.
