Evidence map›Paper›PMID 33961664›Full record

ArticlePloS one2021

Effects of fluid flow shear stress to mouse muscle cells on the bone actions of muscle cell-derived extracellular vesicless.

Yoshimasa Takafuji, Kohei Tatsumi, Naoyuki Kawao, Kiyotaka Okada, Masafumi Muratani, Hiroshi Kaji

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Roles of skeletal muscle-derived exosomes in osteoporosis.Journal of translational medicine · 2025
    Review
  5. Review
  6. Bone-muscle interactions.Osteoporosis and sarcopenia · 2025
    Review
  7. Article
  8. Review
  9. Crosstalk between muscle and bone.Journal of bone and mineral metabolism · 2024
    Review
  10. Article
  11. Review
  12. Article
  13. 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

6 authors at 2 institutions in 1 country.

Yoshimasa TakafujiDepartment of Physiology and Regenerative Medicine, Kindai University Faculty of Medicine, Osaka, Japan.
Kohei TatsumiDepartment of Physiology and Regenerative Medicine, Kindai University Faculty of Medicine, Osaka, Japan.
Naoyuki KawaoDepartment of Physiology and Regenerative Medicine, Kindai University Faculty of Medicine, Osaka, Japan.
Kiyotaka OkadaDepartment of Physiology and Regenerative Medicine, Kindai University Faculty of Medicine, Osaka, Japan.
Masafumi MurataniFaculty of Medicine, Department of Genome Biology, University of Tsukuba, Tsukuba, Japan.
Hiroshi KajiDepartment of Physiology and Regenerative Medicine, Kindai University Faculty of Medicine, Osaka, Japan.ORCID 0000-0001-7433-5135
Kindai University · JPUniversity of Tsukuba · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The interactions between skeletal muscle and bone have been recently noted, and muscle-derived humoral factors related to bone metabolism play crucial roles in the muscle/bone relationships. We previously reported that extracellular vesicles from mouse muscle C2C12 cells (Myo-EVs) suppress osteoclast formation in mice. Although mechanical stress is included in extrinsic factors which are important for both muscle and bone, the detailed roles of mechanical stress in the muscle/bone interactions have still remained unknown. In present study, we examined the effects of fluid flow shear stress (FFSS) to C2C12 cells on the physiological actions of muscle cell-derived EV. Applying FFSS to C2C12 cells significantly enhanced muscle cell-derived EV-suppressed osteoclast formation and several osteoclast-related gene levels in mouse bone marrow cells in the presence of receptor activator nuclear factor κB ligand (RANKL). Moreover, FFSS to C2C12 cells significantly enhanced muscle cell-derived EV-suppressed mitochondria biogenesis genes during osteoclast formation with RANKL treatment. In addition, FFSS to C2C12 cells significantly enhanced muscle cell-derived EV-suppressed osteoclast formation and several osteoclast-related gene levels in Raw264.7 cells in the presence of RANKL. Small RNA-seq-analysis showed that FFSS elevated the expression of miR196a-5p and miR155-5p with the suppressive actions of osteoclast formation and low expression in mouse bone cells. On the other hand, muscle cell-derived EVs with or without FFSS to C2C12 cells did not affect the expression of osteogenic genes, alkaline phosphatase activity and mineralization in mouse osteoblasts. In conclusion, we first showed that FFSS to C2C12 cells enhances the suppressive effects of muscle cell-derived EVs on osteoclast formation in mouse cells. Muscle cell-derived EVs might be partly involved in the effects of mechanical stress on the muscle/bone relationships.

Indexed as

Extracellular VesiclesOsteoclastsStress, MechanicalAnimalsBone and BonesCell LineMiceMicroRNAsMuscle CellsMuscle, SkeletalOsteogenesisRANK LigandRAW 264.7 CellsMicroRNAsRANK Ligand

Identifiers

PMID33961664
PMCPMC8104413
OpenAlexW3159202308

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.