Evidence map›Paper›PMID 28780624›Full record

ArticleJournal of molecular neuroscience : MN2017

Carbon Monoxide-Releasing Molecule-2 Inhibits Connexin 43-Hemichannel Activity in Spinal Cord Astrocytes to Attenuate Neuropathic Pain.

Hui Wang, Xuejun Sun

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular neuroscience : MN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.0field-weighted citation impact, top 24% of its field
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

9 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. [Carbon Monoxide and Pain Regulation: A Review].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2021
    Review
  5. Intercellular communication and ion channels in neuropathic pain chronicization.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020
    Review
  6. Article
  7. Article
  8. Connexin Hemichannels in Astrocytes: Role in CNS Disorders.Frontiers in molecular neuroscience · 2019
    Review
  9. Review
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

2 authors at 2 institutions in 1 country.

Hui WangDepartment of Anesthesiology, The Third Affiliated Hospital of Xi'an Jiaotong University (Shaanxi Provincial People's Hospital), Xi'an, Shaanxi, 710068, People's Republic of China.
Xuejun SunDepartment of General Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, 277 West Yanta Road, Xi'an, Shaanxi, 710061, People's Republic of China. xawangemail@163.com.ORCID http://orcid.org/0000-0002-9555-6938
First Affiliated Hospital of Xi'an Jiaotong University · CNShaanxi Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Carbon monoxide-releasing molecule (CORM-2) acts as a carbon monoxide (CO) deliverer in a more controlled manner without altering carboxyhemoglobin level and exerts potential function in inhibiting inflammation and/or acute nociception. However, the regulatory mechanism of CORM-2 on spinal nerve ligation (SNL)-induced neuropathic pain is not currently clear. Our study aims to investigate the role of CORM-2 in neuropathic pain and the underlying mechanism. We found that spinal cord astrocytes were dramatically activated on day 7 after SNL. L-α-aminoadipate (L-α-AA), an astroglial toxin, reversed SNL-induced astrocyte activation at sub-toxic dose. Intrathecal administration of CO donor CORM-2 induced antiallodynic and antihyperalgesic effects in neuropathic animals induced by SNL and suppressed SNL-induced spontaneous excitatory postsynaptic current (EPSC) frequency in lamina II neurons of spinal cord slices. CORM-2 administration markedly inhibited SNL-induced connexin 43 (Cx43) expression, hemichannel function, and gap junction function on spinal astrocyte membranes. Moreover, exogenous CORM-2 could attenuate HO-1 expression, while overexpressed heme oxygenase-1 (HO-1) increased intracellular CO production, attenuated Cx43 expression, hemichannel function, and gap junction function on spinal astrocyte membranes. Additionally, Cx43 over-expression markedly reduced CORM-2-induced mechanical threshold and thermal hyperalgesia and elevated CORM-2-induced spontaneous EPSC frequency. In conclusion, CORM-2 attenuated SNL-induced neuropathic pain via suppressing Cx43-hemichannel function, which may contribute to understanding of the pathology of neuropathic pain.

Indexed as

AnalgesicsAnimalsAstrocytesCells, CulturedConnexin 43Excitatory Postsynaptic PotentialsHeme Oxygenase-1NeuralgiaNeuronsOrganometallic CompoundsRatsRats, Sprague-DawleySpinal CordAnalgesicsConnexin 43Gja1 protein, ratHeme Oxygenase-1Organometallic Compoundstricarbonyldichlororuthenium (II) dimerAstrocytesConnexin 43CORM-2Heme-oxygenase-1Neuropathic pain

Identifiers

PMID28780624
OpenAlexW2744602983

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.