Evidence map›Paper›PMID 22815920›Full record

ArticlePloS one2012

Alterations in mouse hypothalamic adipokine gene expression and leptin signaling following chronic spinal cord injury and with advanced age.

Gregory E Bigford, Valerie C Bracchi-Ricard, Mark S Nash, John R Bethea

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 29% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
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  7. Article
  8. Article
  9. Effects of leptin on femoral fracture in rats.Journal of biomedical research · 2018
    Article
  10. Article
  11. Article
  12. Nutritional Health Considerations for Persons with Spinal Cord Injury.Topics in spinal cord injury rehabilitation · 2017
    Review
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  14. Article
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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

4 authors at 2 institutions in 1 country.

Gregory E BigfordThe Miami Project to Cure Paralysis, University of Miami Miller School of Medicine, Miami, Florida, United States of America. gbigford@med.miami.edu
Valerie C Bracchi-Ricard
Mark S Nash
John R Bethea
University of Miami · USNeurological Surgery · US

Funding

TNF in Injury and Repair Processes Following Traumatic SCIR01NS051709 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI John Roland Bethea · 2005 to 2026
$8.0M
NINDS NIH HHS R01 NS051709
6 · The paper itself

Abstract

Chronic spinal cord injury (SCI) results in an accelerated trajectory of several cardiovascular disease (CVD) risk factors and related aging characteristics, however the molecular mechanisms that are activated have not been explored. Adipokines and leptin signaling are known to play a critical role in neuro-endocrine regulation of energy metabolism, and are now implicated in central inflammatory processes associated with CVD. Here, we examine hypothalamic adipokine gene expression and leptin signaling in response to chronic spinal cord injury and with advanced age. We demonstrate significant changes in fasting-induced adipose factor (FIAF), resistin (Rstn), long-form leptin receptor (LepRb) and suppressor of cytokine-3 (SOCS3) gene expression following chronic SCI and with advanced age. LepRb and Jak2/stat3 signaling is significantly decreased and the leptin signaling inhibitor SOCS3 is significantly elevated with chronic SCI and advanced age. In addition, we investigate endoplasmic reticulum (ER) stress and activation of the uncoupled protein response (UPR) as a biological hallmark of leptin resistance. We observe the activation of the ER stress/UPR proteins IRE1, PERK, and eIF2alpha, demonstrating leptin resistance in chronic SCI and with advanced age. These findings provide evidence for adipokine-mediated inflammatory responses and leptin resistance as contributing to neuro-endocrine dysfunction and CVD risk following SCI and with advanced age. Understanding the underlying mechanisms contributing to SCI and age related CVD may provide insight that will help direct specific therapeutic interventions.

Indexed as

Gene Expression RegulationAdipokinesAgingAngiopoietin-Like Protein 4AngiopoietinsAnimalseIF-2 KinaseEukaryotic Initiation Factor-2FemaleHypothalamusInflammationLeptinMembrane ProteinsMiceMice, Inbred C57BLProtein Serine-Threonine KinasesAdipokinesAngiopoietin-Like Protein 4AngiopoietinsAngptl4 protein, mouseeIF-2 KinaseErn2 protein, mouseEukaryotic Initiation Factor-2LeptinMembrane ProteinsProtein Serine-Threonine KinasesReceptors, LeptinResistinSocs3 protein, mouseSuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling Proteins

Identifiers

PMID22815920
PMCPMC3397960
OpenAlexW2084281389

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.