Evidence map›Paper›PMID 39244479›Full record

ArticleBritish journal of anaesthesia2024

RNA-binding protein SYNCRIP contributes to neuropathic pain through stabilising CCR2 expression in primary sensory neurones.

Yang Zhang, Bing Wang, Xiaozhou Feng, Huixing Wang, Ju Gao, Xu Li, Xiaodong Huo, Bushra Yasin, Alex Bekker, Huijuan Hu and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in British journal of anaesthesia, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. Article
  2. Article
  3. RNA-binding protein MBNL2 mitigates neuropathic pain after chemotherapy through destabilizing CCR2 expression in primary sensory neurons.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  4. Article
  5. Review
  6. Lysophosphatidic acid receptor 5 in insular cortex as a potential analgesic target in neuropathic pain.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Yang ZhangDepartment of Anesthesiology, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, NJ, USA.
Bing WangDepartment of Anesthesiology, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, NJ, USA.
Xiaozhou FengDepartment of Anesthesiology, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, NJ, USA.
Huixing WangDepartment of Anesthesiology, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, NJ, USA.
Ju GaoDepartment of Anesthesiology, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, NJ, USA.
Xu LiDepartment of Anesthesiology, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, NJ, USA.
Xiaodong HuoDepartment of Anesthesiology, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, NJ, USA.
Bushra YasinDepartment of Anesthesiology, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, NJ, USA.
Alex BekkerDepartment of Anesthesiology, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, NJ, USA.
Huijuan HuDepartment of Anesthesiology, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, NJ, USA; Department of Physiology, Pharmacology & Neuroscience, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, NJ, USA.
Yuan-Xiang TaoDepartment of Anesthesiology, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, NJ, USA; Department of Physiology, Pharmacology & Neuroscience, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, NJ, USA; Department of Cell Biology & Molecular Medicine, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, NJ, USA. Electronic address: yuanxiang.tao@njms.rutgers.edu.

Funding

Discovery and validation of a new long noncoding RNA as a novel target for neuropathic painRF1NS113881 · NINDS · RBHS-NEW JERSEY MEDICAL SCHOOL · PI DAVIDSON, STEVE, TAO, YUAN-XIANG · 2019 to 2019
$3.5M
Role of dorsal root ganglion FTO, a RNA demethylase, in neuropathic painR01NS111553 · NINDS · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI TAO, YUAN-XIANG · 2019 to 2023
$2.5M
Identification of a Novel DRG-Specific Long Noncoding RNA and its Role in Neuropathic PainR01NS117484 · NINDS · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI HU, HUIJUAN, TAO, YUAN-XIANG · 2021 to 2025
$2.4M
NINDS NIH HHS R01 NS111553NINDS NIH HHS R01 NS117484NINDS NIH HHS RF1 NS113881
6 · The paper itself

Abstract

backgroundNerve injury-induced changes in gene expression in the dorsal root ganglion (DRG) contribute to the genesis of neuropathic pain. SYNCRIP, an RNA-binding protein, is critical for the stabilisation of gene expression. Whether SYNCRIP participates in nerve injury-induced alterations in DRG gene expression and nociceptive hypersensitivity is unknown.

methodsThe expression and distribution of SYNCRIP in mouse DRG after chronic constriction injury (CCI) of the unilateral sciatic nerve were assessed. Effect of microinjection of Syncrip small interfering RNA into the ipsilateral L3 and L4 DRGs on the CCI-induced upregulation of chemokine (C-C motif) receptor 2 (CCR2) and nociceptive hypersensitivity were examined. Additionally, effects of microinjection of adeno-associated virus 5 expressing full length Syncrip mRNA (AAV5-Syncrip) on basal DRG CCR2 expression and nociceptive thresholds were observed.

resultsSYNCRIP is expressed predominantly in DRG neurones, where it co-exists with CCR2. Levels of Syncrip mRNA and SYNCRIP protein in injured DRG increased time-dependently on days 3-14 after CCI. Blocking this increase through microinjection of Syncrip small interfering RNA into injured DRG attenuated CCI-induced upregulation of DRG CCR2 and development and maintenance of nociceptive hypersensitivities. Mimicking this increase through DRG microinjection of AAV5-Syncrip elevated CCR2 expression in microinjected DRGs, enhanced the responses to mechanical, heat, and cold stimuli, and induced ongoing pain in naive mice. Mechanistically, SYNCRIP bound to 3-UTR of Ccr2 mRNA and stabilised its expression in DRG neurones.

conclusionsSYNCRIP contributes to the induction and maintenance of neuropathic pain likely through stabilising expression of CCR2 in injured DRG. SYNCRIP may be a potential target for treating this disorder.

Indexed as

Ganglia, SpinalNeuralgiaReceptors, CCR2AnimalsDisease Models, AnimalMaleMiceMice, Inbred C57BLRNA-Binding ProteinsRNA, Small InterferingSensory Receptor CellsCcr2 protein, mouseReceptors, CCR2RNA-Binding ProteinsRNA, Small Interferingchemokine (C-C motif) receptor 2dorsal root ganglionneuropathic painperipheral nerve injurySYNCRIP

Identifiers

PMID39244479
PMCPMC11488160

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.