Evidence map›Paper›PMID 30770735›Full record

ArticleBMC genomics2019

Alterations in tissue microRNA after heat stress in the conscious rat: potential biomarkers of organ-specific injury.

Matthew G Permenter, Bonna C McDyre, Danielle L Ippolito, Jonathan D Stallings

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2019. 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
1.0field-weighted citation impact, top 25% 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, 23 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. The Ambivalent Role of miRNA-21 in Trauma and Acute Organ Injury.International journal of molecular sciences · 2024
    Review
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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.

Matthew G PermenterExcet, Inc., Fort Detrick, MD, 21702-5010, USA.ORCID http://orcid.org/0000-0002-8010-076X
Bonna C McDyreOak Ridge Institute for Science and Education, Fort Detrick, MD, 21702-5010, USA.
Danielle L IppolitoU.S. Army Center for Environmental Health Research, Fort Detrick, Maryland, MD, 21702-5010, USA.
Jonathan D StallingsU.S. Army Center for Environmental Health Research, Fort Detrick, Maryland, MD, 21702-5010, USA. jonathan.d.stallings.mil@mail.mil.
Center for Environmental Health · USMiles College · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHeat illness remains a significant cause of morbidity in susceptible populations. Recent research elucidating the cellular mechanism of heat stress leading to heat illness may provide information to develop better therapeutic interventions, risk assessment strategies, and early biomarkers of organ damage. microRNA (miRNA) are promising candidates for therapeutic targets and biomarkers for a variety of clinical conditions since there is the potential for high specificity for individual tissues and unique cellular functions. The objective of this study was to identify differentially expressed microRNAs and their putative mRNA targets in the heart, liver, kidney, and lung in rats at three time points: during heat stress (i.e., when core temperature reached 41.8 °C), or following a 24 or 48 h recovery period.

resultsRats did not show histological evidence of tissue pathology until 48 h after heat stress, with 3 out of 6 rats showing cardiac inflammation and renal proteinosis at 48 h. The three rats with cardiac and renal pathology had 86, 7, 159, and 37 differentially expressed miRNA in the heart, liver, kidney, or lung, respectively compared to non-heat stressed control animals. During heat stress one differentially expressed miRNA was found in the liver and five in the lung, with no other modulated miRNA after 24 h or 48 h in animals with no evidence of organ injury. Pathway enrichment analysis revealed enrichment in functional pathways associated with heat stress, with the greatest effects observed in animals with histological evidence of cardiac and renal damage at 48 h. Inhibiting miR-21 in cultured cardiomyocytes increased the percent apoptotic cells five hours after heat stress from 70.9 ± 0.8 to 84.8 ± 2.2%.

conclusionsGlobal microRNA and transcriptomics analysis suggested that perturbed miRNA due to heat stress are involved in biological pathways related to organ injury, energy metabolism, the unfolded protein response, and cellular signaling. These miRNA may serve as biomarkers of organ injury and potential pharmacological targets for preventing heat illness or organ injury.

Indexed as

AnimalsApoptosisBiomarkersCell LineEnergy MetabolismGene ExpressionHeartHeat-Shock ResponseHeat Stress DisordersKidneyMicroRNAsMolecular Targeted TherapyMyocytes, CardiacRatsRats, Inbred F344Signal TransductionBiomarkersMicroRNAsmirn21 microRNA, ratBiomarkerHeat shockHeat stressmiRNATranscriptomics

Identifiers

PMID30770735
PMCPMC6377737
OpenAlexW2912727201

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LicenceCC BY
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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.