Evidence map›Paper›PMID 25717188›Full record

ArticleMolecular biology of the cell2015

Musashi-1 maintains blood-testis barrier structure during spermatogenesis and regulates stress granule formation upon heat stress.

Sun ErLin, Wei WenJie, Wang LiNing, Lu BingXin, Lei MingDe, Sun Yan, Han RuiFa

RetractedAbstract readRetracted Publication
In one paragraph

Article in Molecular biology of the cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
3.0field-weighted citation impact, top 10% 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, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Magnolol pretreatment attenuates heat stress-induced IEC-6 cell injury.Journal of Zhejiang University. Science. B · 2016
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Sun ErLinDepartment of Urology, Tianjin Institute of Urology, Second Hospital of Tianjin Medical University, Tianjin 300211, People's Republic of China sunerlintj@163.com hanruifatj@163.com.
Wei WenJieDepartment of Anatomy and Cell Biology, University of Pennsylvania, Philadelphia, PA 19104 Department of Urology, Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325027, People's Republic of China.
Wang LiNingDepartment of Urology, Tianjin Institute of Urology, Second Hospital of Tianjin Medical University, Tianjin 300211, People's Republic of China.
Lu BingXinDepartment of Urology, Tianjin Institute of Urology, Second Hospital of Tianjin Medical University, Tianjin 300211, People's Republic of China.
Lei MingDeDepartment of Urology, Tianjin Institute of Urology, Second Hospital of Tianjin Medical University, Tianjin 300211, People's Republic of China.
Sun YanDepartment of Urology, Tianjin Institute of Urology, Second Hospital of Tianjin Medical University, Tianjin 300211, People's Republic of China.
Han RuiFaDepartment of Urology, Tianjin Institute of Urology, Second Hospital of Tianjin Medical University, Tianjin 300211, People's Republic of China sunerlintj@163.com hanruifatj@163.com.
Second Hospital of Tianjin Medical University · CNWenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In mouse testes, Musashi-1 (Msi-1) was predominantly expressed in the cytoplasm and nuclei of Sertoli cells. Here we demonstrate that knockdown of Msi-1 in Sertoli cells altered the levels and distribution of blood-testis barrier (BTB)-associated proteins. Moreover, Msi-1 knockdown in vivo disrupted BTB functional structure and spermatogenesis. In addition, we report a novel role of Msi-1 in regulating Sertoli cells survival following heat-induced injury. Endogenous Msi-1 protein in heat-treated Sertoli cells was recruited to stress granules. The formation of stress granules was considerably disrupted, and apoptosis was significantly up-regulated in Msi-1-knockdown Sertoli cells after heat treatment. p-ERK1/2 acted downstream of stress granule formation, and inhibition of p-ERK1/2 signaling triggered Sertoli cell apoptosis upon heat stress. In conclusion, we demonstrate that Msi-1 is critical for constructing a functional BTB structure and maintaining spermatogenesis. We also note a role for Msi-1 in regulating Sertoli cell fate following heat-induced injury, likely through the induction of stress granule formation and subsequent activation of p-ERK1/2 signaling.

Indexed as

Heat-Shock ResponseAnimalsBlood-Testis BarrierCytoplasmic GranulesGene Knockdown TechniquesMaleMAP Kinase Signaling SystemMiceNerve Tissue ProteinsRNA-Binding ProteinsSertoli CellsSpermatogenesisMsi1h protein, mouseNerve Tissue ProteinsRNA-Binding Proteins

Identifiers

PMID25717188
PMCPMC4436837
OpenAlexW2123561106

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.