Evidence map›Paper›PMID 28601938›Full record

ArticleJournal of cell communication and signaling2017

Enhanced gap junction intercellular communication inhibits catabolic and pro-inflammatory responses in tenocytes against heat stress.

Eijiro Maeda, Shunsuke Kimura, Masahiko Yamada, Masataka Tashiro, Toshiro Ohashi

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cell communication and signaling, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Frontiers in veterinary science · 2022
    Article
  8. Connexin 43 Is Necessary for Murine Tendon Enthesis Formation and Response to Loading.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2020
    Article
  9. Article
  10. Article
  11. Review
  12. Review
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.

Eijiro MaedaGraduate School of Engineering, Nagoya University, Nagoya, Aichi, Japan. e.maeda@nagoya-u.jp.
Shunsuke KimuraGraduate School of Medicine, Hokkaido University, Sapporo, Hokkaido, Japan.
Masahiko YamadaFaculty of Engineering, Hokkaido University, Sapporo, Hokkaido, Japan.
Masataka TashiroGraduate School of Engineering, Hokkaido University, Sapporo, Hokkaido, Japan.
Toshiro OhashiFaculty of Engineering, Hokkaido University, Sapporo, Hokkaido, Japan.
Hokkaido University · JP

Funding

Japan Society for the Promotion of Science 16K01346Japan Society for the Promotion of Science 25702022
6 · The paper itself

Abstract

Elevation of tendon core temperature during severe activity is well known. However, its effects on tenocyte function have not been studied in detail. The present study tested a hypothesis that heat stimulation upregulates tenocyte catabolism, which can be modulated by the inhibition or the enhancement of gap junction intercellular communication (GJIC). Tenocytes isolated from rabbit Achilles tendons were subjected to heat stimulation at 37 °C, 41 °C or 43 °C for 30 min, and changes in cell viability, gene expressions and GJIC were examined. It was found that GJIC exhibited no changes by the stimulation even at 43 °C, but cell viability was decreased and catabolic and proinflammatory gene expressions were upregulated. Inhibition of GJIC demonstrated further upregulated catabolic and proinflammatory gene expressions. In contrast, enhanced GJIC, resulting from forced upregulation of connexin 43 gene, counteracted the heat-induced upregulation of catabolic and proinflammatory genes. These findings suggest that the temperature rise in tendon core could upregulate catabolic and proinflammatory activities, potentially leading to the onset of tendinopathy, and such upregulations could be suppressed by the enhancement of GJIC. Therefore, to prevent tendon injury at an early stage from becoming chronic injury, tendon core temperature and GJIC could be targets for post-activity treatments.

Indexed as

FLIPGap junctionHeat stimulationIntercellular communicationTendinopathyTenocytes

Identifiers

PMID28601938
PMCPMC5704041
OpenAlexW2623179515

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.