Evidence map›Paper›PMID 26481700›Full record

ArticleSpinal cord2016

Focal adhesion kinase signaling is decreased 56 days following spinal cord injury in rat gastrocnemius.

Z A Graham, W Qin, L C Harlow, N H Ross, W A Bauman, P M Gallagher, C P Cardozo

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Spinal cord, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

8 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Identification of serum exosomal microRNAs in acute spinal cord injured rats.Experimental biology and medicine (Maywood, N.J.) · 2019
    Article
  7. Mitochondrial health and muscle plasticity after spinal cord injury.European journal of applied physiology · 2019
    Review
  8. 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

7 authors at 3 institutions in 1 country.

Z A GrahamJames J. Peters Veterans Affairs Medical Center, National Center of Excellence for the Medical Consequences of Spinal Cord Injury, Bronx, NY, USA.
W QinJames J. Peters Veterans Affairs Medical Center, National Center of Excellence for the Medical Consequences of Spinal Cord Injury, Bronx, NY, USA.
L C HarlowJames J. Peters Veterans Affairs Medical Center, National Center of Excellence for the Medical Consequences of Spinal Cord Injury, Bronx, NY, USA.
N H RossJames J. Peters Veterans Affairs Medical Center, National Center of Excellence for the Medical Consequences of Spinal Cord Injury, Bronx, NY, USA.
W A BaumanJames J. Peters Veterans Affairs Medical Center, National Center of Excellence for the Medical Consequences of Spinal Cord Injury, Bronx, NY, USA.
P M GallagherApplied Physiology Laboratory, University of Kansas, Lawrence, KS, USA.
C P CardozoJames J. Peters Veterans Affairs Medical Center, National Center of Excellence for the Medical Consequences of Spinal Cord Injury, Bronx, NY, USA.
Icahn School of Medicine at Mount Sinai · USJames J. Peters VA Medical Center · USUniversity of Kansas · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

STUDY

designDescriptive study.

objectivesThe goal of this study was to determine the effects of spinal cord injury (SCI) on aspects of the focal adhesion kinase (FAK) signaling pathway 56 days post injury in rat gastrocnemius.

settingThis study was conducted in Bronx, NY, USA.

methodsThree-month-old male Wistar rats were exposed to either a sham surgery (n=10) or complete T4 spinal cord transection (n=10). Rats were killed 56 days following surgery and the muscle was collected. Following homogenization, proteins of the FAK pathway were analyzed by western immunoblotting or reverse transcription-qPCR. In addition, cellular markers for proteins that target the degradation of FAK were investigated.

resultsSCI resulted in significantly lower levels of total and phosphorylated FAK, cSrc and p70S6k, and a trend for increased FRNK protein expression. SCI did not change levels of the α7 or β1 integrin subunits, total or phosphorylated ERK1/2, phosphorylated Akt and TSC2 or total p70S6k. SCI resulted in a greater expression of total Akt. mRNA expression of FAK and the α7 or β1 integrins remained unchanged between sham and SCI groups. Caspase-3/7 activity and Trim72 mRNA and protein expression remained unchanged following SCI.

conclusionSCI results in diminished FAK signaling and is independent of ERK1/2 and Akt. SCI has no effect on mRNA levels for genes encoding components of the focal adhesion 56 days after injury.

Indexed as

AnimalsCaspasesDisease Models, AnimalFocal Adhesion Kinase 1Gene Expression RegulationMaleMAP Kinase Signaling SystemMuscle, SkeletalOncogene Protein v-aktPhosphorylationRatsRats, WistarRibosomal Protein S6 Kinases, 70-kDaRNA, MessengerSignal TransductionSpinal Cord InjuriesCaspasesFocal Adhesion Kinase 1Oncogene Protein v-aktPtk2 protein, ratRibosomal Protein S6 Kinases, 70-kDaRNA, Messenger

Identifiers

PMID26481700
OpenAlexW1766753582

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.