Evidence map›Paper›PMID 26453297›Full record

ArticleThe Journal of biological chemistry2015

A Disintegrin and Metalloprotease 10 (ADAM10) Is Indispensable for Maintenance of the Muscle Satellite Cell Pool.

Sakiko Mizuno, Masaki Yoda, Masayuki Shimoda, Takahide Tohmonda, Yasunori Okada, Yoshiaki Toyama, Shin'ichi Takeda, Masaya Nakamura, Morio Matsumoto, Keisuke Horiuchi

Abstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. 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
–field-weighted citation impact
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.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Exercise/Resistance Training and Muscle Stem Cells.Endocrinology and metabolism (Seoul, Korea) · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. 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

10 authors.

Sakiko MizunoDepartments of Orthopedic Surgery, Keio University School of Medicine, Tokyo 160-8582, Japan.
Masaki YodaAnti-aging Orthopedic Research, Keio University School of Medicine, Tokyo 160-8582, Japan.
Masayuki ShimodaPathology, Keio University School of Medicine, Tokyo 160-8582, Japan.
Takahide TohmondaAnti-aging Orthopedic Research, Keio University School of Medicine, Tokyo 160-8582, Japan.
Yasunori OkadaPathology, Keio University School of Medicine, Tokyo 160-8582, Japan.
Yoshiaki ToyamaDepartments of Orthopedic Surgery, Keio University School of Medicine, Tokyo 160-8582, Japan.
Shin'ichi TakedaDepartment of Molecular Therapy, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo 187-8502, Japan.
Masaya NakamuraDepartments of Orthopedic Surgery, Keio University School of Medicine, Tokyo 160-8582, Japan.
Morio MatsumotoDepartments of Orthopedic Surgery, Keio University School of Medicine, Tokyo 160-8582, Japan.
Keisuke HoriuchiDepartments of Orthopedic Surgery, Keio University School of Medicine, Tokyo 160-8582, Japan; Anti-aging Orthopedic Research, Keio University School of Medicine, Tokyo 160-8582, Japan. Electronic address: horiuchi@z3.keio.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Satellite cells (SCs) are muscle-specific stem cells that are essential for the regeneration of damaged muscles. Although SCs have a robust capacity to regenerate myofibers, the number of SCs decreases with aging, leading to insufficient recovery after muscle injury. We herein show that ADAM10 (a disintegrin and metalloprotease 10), a membrane-bound proteolytic enzyme with a critical role in Notch processing (S2 cleavage), is essential for the maintenance of SC quiescence. We generated mutant mice in which ADAM10 in SCs can be conditionally abrogated by tamoxifen injection. Tamoxifen-treated mutant mice did not show any apparent defects and grew normally under unchallenged conditions. However, these mice showed a nearly complete loss of muscle regeneration after chemically induced muscle injury. In situ hybridization and flow cytometric analyses revealed that the mutant mice had significantly less SCs compared with wild type controls. Of note, we found that inactivation of ADAM10 in SCs severely compromised Notch signaling and led to dysregulated myogenic differentiation, ultimately resulting in deprivation of the SC pool in vivo. Taken together, the present findings underscore the role of ADAM10 as an indispensable component of Notch signaling in SCs and for maintaining the SC pool.

Indexed as

ADAM10 ProteinADAM ProteinsAmyloid Precursor Protein SecretasesAnimalsCell DifferentiationMembrane ProteinsMiceMice, TransgenicReceptors, NotchSatellite Cells, Skeletal MuscleSignal TransductionADAM10 ProteinAdam10 protein, mouseADAM ProteinsAmyloid Precursor Protein SecretasesMembrane ProteinsReceptors, NotchADAMmuscle regenerationmyogenesisNotch pathwaysatellite cellsskeletal muscle

Identifiers

PMID26453297
PMCPMC4653702

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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.