Evidence map›Paper›PMID 34678261›Full record

ArticleLife sciences2021

Enhanced pro-BDNF-p75NTR pathway activity in denervated skeletal muscle.

Katherine Aby, Ryan Antony, Mary Eichholz, Rekha Srinivasan, Yifan Li

Open access · greenAbstract read
In one paragraph

Article in Life sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

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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

5 authors at 1 institution in 1 country.

Katherine AbyDivision of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, Vermillion, SD 57069, USA.
Ryan AntonyDivision of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, Vermillion, SD 57069, USA.
Mary EichholzDivision of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, Vermillion, SD 57069, USA.
Rekha SrinivasanDivision of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, Vermillion, SD 57069, USA.
Yifan LiDivision of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, Vermillion, SD 57069, USA. Electronic address: yifan.li@usd.edu.
University of South Dakota · US

Funding

The role of pro-BDNF/mature-BDNF balance in skeletal muscle inactivity-induced capillary regressionR01HL147105 · NHLBI · UNIVERSITY OF SOUTH DAKOTA · PI LI, YIFAN · 2019 to 2022
$1.5M
NHLBI NIH HHS R01 HL147105
6 · The paper itself

Abstract

aimsBrain derived neurotrophic factor (BDNF) and the related receptors TrkB and p75NTR are expressed in skeletal muscle, yet their functions remain to be fully understood. Skeletal muscle denervation, which occurs in spinal injury, peripheral neuropathies, and aging, negatively affects muscle mass and function. In this study, we wanted to understand the role of BDNF, TrkB, and p75NTR in denervation-induced adverse effects on skeletal muscle. MAIN

methodsMice with unilateral sciatic denervation were used. Protein levels of pro- and mature BDNF, TrkB, p75NTR, activations of their downstream signaling pathways, and inflammation in the control and denervated muscle were measured with Western blot and tissue staining. Treatment with a p75NTR inhibitor and BDNF skeletal muscle specific knockout in mice were used to examine the role of p75NTR and pro-BDNF. KEY

findingsIn denervated muscle, pro-BDNF and p75NTR were significantly upregulated, and JNK and NF-kB, two major downstream signaling pathways of p75NTR, were activated, along with muscle atrophy and inflammation. Inhibition of p75NTR using LM11A-31 significantly reduced JNK activation and inflammatory cytokines in the denervated muscle. Moreover, skeletal muscle specific knockout of BDNF reduced pro-BDNF level, JNK activation and inflammation in the denervated muscle. SIGNIFICANCE: These results reveal for the first time that the upregulation of pro-BDNF and activation of p75NTR pathway are involved in denervation-induced inflammation in skeletal muscle. The results suggest that inhibition of pro-BDNF-p75NTR pathway can be a new target to treat skeletal muscle inflammation.

Indexed as

AnimalsBrain-Derived Neurotrophic FactorFemaleIsoleucineMaleMembrane GlycoproteinsMiceMice, Inbred C57BLMorpholinesMuscle DenervationMuscle, SkeletalMuscular AtrophyPeripheral Nervous System DiseasesProtein PrecursorsProtein-Tyrosine KinasesReceptors, Nerve Growth FactorBrain-Derived Neurotrophic Factorbrain-derived neurotrophic factor precursorIsoleucineLM11A-31Membrane GlycoproteinsMorpholinesNgfr protein, mouseNtrk2 protein, mouseProtein PrecursorsProtein-Tyrosine KinasesReceptors, Nerve Growth FactorReceptor, trkBBDNFDenervationInflammationMyokinep75NTR

Identifiers

PMID34678261
PMCPMC8595791
OpenAlexW3205291713

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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.