Evidence map›Paper›PMID 29737477›Full record

ArticleInflammation2018

Cyclic Tensile Strain Upregulates Pro-Inflammatory Cytokine Expression Via FAK-MAPK Signaling in Chondrocytes.

Makoto Yanoshita, Naoto Hirose, Yuki Okamoto, Chikako Sumi, Mami Takano, Sayuri Nishiyama, Yuki Asakawa-Tanne, Kayo Horie, Azusa Onishi, Yuka Yamauchi and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-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

21 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. [Effect of mechanical stimuli on physicochemical properties of joint fluid in osteoarthritis].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2025
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Mechanical Loading Disrupts Focal Adhesion Kinase Activation in Mandibular Fibrochondrocytes During Murine Temporomandibular Joint Osteoarthritis.Journal of oral and maxillofacial surgery : official journal of the American Association of Oral and Maxillofacial Surgeons · 2021
    Article
  17. Review
  18. [Research progress of different mechanical stimulation regulating chondrocytes metabolism].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2020
    Review
  19. Article
  20. 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

13 authors at 2 institutions in 1 country.

Makoto YanoshitaDepartment of Orthodontics and Craniofacial Developmental Biology, Hiroshima University Graduate School of Biomedical and Health Sciences, Kasumi 1-2-3 Minami-ku, Hiroshima-shi, Hiroshima prefecture, Japan.
Naoto HiroseDepartment of Orthodontics and Craniofacial Developmental Biology, Hiroshima University Graduate School of Biomedical and Health Sciences, Kasumi 1-2-3 Minami-ku, Hiroshima-shi, Hiroshima prefecture, Japan. hirose@hiroshima-u.ac.jp.
Yuki OkamotoDepartment of Orthodontics, Division of Oral Health and Development, Hiroshima University Hospital, Hiroshima, Japan.
Chikako SumiDepartment of Orthodontics and Craniofacial Developmental Biology, Hiroshima University Graduate School of Biomedical and Health Sciences, Kasumi 1-2-3 Minami-ku, Hiroshima-shi, Hiroshima prefecture, Japan.
Mami TakanoDepartment of Orthodontics and Craniofacial Developmental Biology, Hiroshima University Graduate School of Biomedical and Health Sciences, Kasumi 1-2-3 Minami-ku, Hiroshima-shi, Hiroshima prefecture, Japan.
Sayuri NishiyamaDepartment of Orthodontics and Craniofacial Developmental Biology, Hiroshima University Graduate School of Biomedical and Health Sciences, Kasumi 1-2-3 Minami-ku, Hiroshima-shi, Hiroshima prefecture, Japan.
Yuki Asakawa-TanneDepartment of Orthodontics and Craniofacial Developmental Biology, Hiroshima University Graduate School of Biomedical and Health Sciences, Kasumi 1-2-3 Minami-ku, Hiroshima-shi, Hiroshima prefecture, Japan.
Kayo HorieDepartment of Orthodontics and Craniofacial Developmental Biology, Hiroshima University Graduate School of Biomedical and Health Sciences, Kasumi 1-2-3 Minami-ku, Hiroshima-shi, Hiroshima prefecture, Japan.
Azusa OnishiDepartment of Orthodontics and Craniofacial Developmental Biology, Hiroshima University Graduate School of Biomedical and Health Sciences, Kasumi 1-2-3 Minami-ku, Hiroshima-shi, Hiroshima prefecture, Japan.
Yuka YamauchiDepartment of Orthodontics and Craniofacial Developmental Biology, Hiroshima University Graduate School of Biomedical and Health Sciences, Kasumi 1-2-3 Minami-ku, Hiroshima-shi, Hiroshima prefecture, Japan.
Tomomi MitsuyoshiDepartment of Orthodontics, Division of Oral Health and Development, Hiroshima University Hospital, Hiroshima, Japan.
Ryo KunimatsuDepartment of Orthodontics, Division of Oral Health and Development, Hiroshima University Hospital, Hiroshima, Japan.
Kotaro TanimotoDepartment of Orthodontics and Craniofacial Developmental Biology, Hiroshima University Graduate School of Biomedical and Health Sciences, Kasumi 1-2-3 Minami-ku, Hiroshima-shi, Hiroshima prefecture, Japan.
Hiroshima University · JPHiroshima University Hospital · JP

Funding

Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology, Japan. 26861788
6 · The paper itself

Abstract

Excessive mechanical stimulation is considered an important factor in the destruction of chondrocytes. Focal adhesion kinase (FAK) is non-receptor tyrosine kinase related to a number of different signaling proteins. Little is known about the function of FAK in chondrocytes under mechanical stimulation. In the present study, we investigated the function of FAK in mechanical signal transduction and the mechanism through which cyclic tensile strain (CTS) induces expression of inflammation-related factors. Mouse ATDC5 chondrogenic cells were subjected to CTS of 0.5 Hz to 10% cell elongation with an FAK inhibitor. The expression of genes encoding COX-2, IL-1β, and TNF-α was examined using real-time RT-PCR after CTS application with FAK inhibitor. Phosphorylation of p-38, ERK, and JNK was analyzed by Western blotting. Differences in COX-2 expression following pretreatment with FAK, p-38, ERK, and JNK inhibitors were compared by Western blotting. We found that CTS increased the expression of genes encoding COX-2, IL-1β, and TNF-α and activated the phosphorylation of FAK, p-38, ERK, and JNK. Pretreatment with an FAK inhibitor for 2 h reduced the expression of genes encoding COX-2, IL-1β, and TNF-α induced by CTS-associated inflammation and decreased phosphorylation of FAK, p-38, ERK, and JNK. Pretreatment with FAK, p-38, ERK, and JNK inhibitors markedly suppressed COX-2 and IL-1β protein expression. In conclusion, FAK appears to regulate inflammation in chondrocytes under CTS via MAPK pathways.

Indexed as

MAP Kinase Signaling SystemTensile StrengthAnimalsCell LineChondrocytesCytokinesFocal Adhesion Protein-Tyrosine KinasesGene ExpressionInflammationMicePhosphorylationUp-RegulationCytokinesFocal Adhesion Protein-Tyrosine Kinaseschondrocytefocal adhesion kinasemechanical stimulationmitogen-activated protein kinases

Identifiers

PMID29737477
OpenAlexW2802690975

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.