Evidence map›Paper›PMID 30459569›Full record

ArticleFrontiers in integrative neuroscience2018

NF-KappaB Pathway Is Involved in Bone Marrow Stromal Cell-Produced Pain Relief.

Wei Guo, Satoshi Imai, Jia-Le Yang, Shiping Zou, Huijuan Li, Huakun Xu, Kamal D Moudgil, Ronald Dubner, Feng Wei, Ke Ren

Open access · goldAbstract read
In one paragraph

Article in Frontiers in integrative neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

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  12. Dihydroartemisinin: A Potential Natural Anticancer Drug.International journal of biological sciences · 2021
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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

10 authors at 2 institutions in 3 countries.

Wei GuoDepartment of Neural and Pain Sciences, School of Dentistry & Program in Neuroscience, University of Maryland, Baltimore, MD, United States.
Satoshi ImaiDepartment of Neural and Pain Sciences, School of Dentistry & Program in Neuroscience, University of Maryland, Baltimore, MD, United States.
Jia-Le YangDepartment of Neural and Pain Sciences, School of Dentistry & Program in Neuroscience, University of Maryland, Baltimore, MD, United States.
Shiping ZouDepartment of Neural and Pain Sciences, School of Dentistry & Program in Neuroscience, University of Maryland, Baltimore, MD, United States.
Huijuan LiDepartment of Neural and Pain Sciences, School of Dentistry & Program in Neuroscience, University of Maryland, Baltimore, MD, United States.
Huakun XuDepartment of Advanced Oral Sciences and Therapeutics, University of Maryland School of Dentistry, Baltimore, MD, United States.
Kamal D MoudgilDepartment of Microbiology & Immunology, University of Maryland, Baltimore, MD, United States.
Ronald DubnerDepartment of Neural and Pain Sciences, School of Dentistry & Program in Neuroscience, University of Maryland, Baltimore, MD, United States.
Feng WeiDepartment of Neural and Pain Sciences, School of Dentistry & Program in Neuroscience, University of Maryland, Baltimore, MD, United States.
Ke RenDepartment of Neural and Pain Sciences, School of Dentistry & Program in Neuroscience, University of Maryland, Baltimore, MD, United States.
University of Maryland, Baltimore · USSun Yat-sen University · CN

Funding

Central mechanisms of maintenance of orofacial pain after injuryR01DE021804 · NIDCR · UNIVERSITY OF MARYLAND BALTIMORE · PI DUBNER, RONALD, KELLER, ASAF · 2011 to 2015
$3.2M
Immune activation of the endogenous control of persistent painR01DE025137 · NIDCR · UNIVERSITY OF MARYLAND BALTIMORE · PI REN, KE · 2016 to 2020
$2.2M
Supraspinal mechanism of 5-HT-dependent descending facilitation in chronic painR01NS091296 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI WEI, FENG · 2015 to 2019
$1.7M
NIDCR NIH HHS R01 DE021804NIDCR NIH HHS R01 DE025137NINDS NIH HHS R01 NS091296
6 · The paper itself

Abstract

Bone marrow stromal cells (BMSCs) produce long-lasting attenuation of pain hypersensitivity. This effect involves BMSC's ability to interact with the immune system and activation of the endogenous opioid receptors in the pain modulatory circuitry. The nuclear factor kappa B (NF-κB) protein complex is a key transcription factor that regulates gene expression involved in immunity. We tested the hypothesis that the NF-κB signaling plays a role in BMSC-induced pain relief. We focused on the rostral ventromedial medulla (RVM), a key structure in the descending pain modulatory pathway, that has been shown to play an important role in BMSC-produced antihyperalgesia. In Sprague-Dawley rats with a ligation injury of the masseter muscle tendon (TL), BMSCs (1.5 M/rat) from donor rats were infused i.v. at 1 week post-TL. P65 exhibited predominant neuronal localization in the RVM with scattered distribution in glial cells. At 1 week, but not 8 weeks after BMSC infusion, western blot and immunostaining showed that p65 of NF-κB was significantly increased in the RVM. Given that chemokine signaling is critical to BMSCs' pain-relieving effect, we further evaluated a role of chemokine signaling in p65 upregulation. Prior to infusion of BMSCs, we transduced BMSCs with

Indexed as

BAY 11-7082chemokinemesenchymal stromal cellsorofacial painrostral ventromedial medullatendon ligation

Identifiers

PMID30459569
PMCPMC6232783
OpenAlexW2897167764

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.