Evidence map›Paper›PMID 30246229›Full record

ArticleCell stress & chaperones2019

CRYAB protects cardiomyocytes against heat stress by preventing caspase-mediated apoptosis and reducing F-actin aggregation.

Bin Yin, Shu Tang, Jiao Xu, Jiarui Sun, Xiaohui Zhang, Yubao Li, Endong Bao

Open access · bronzeAbstract read
In one paragraph

Article in Cell stress & chaperones, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

24 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  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

7 authors at 2 institutions in 1 country.

Bin Yin *College of Veterinary Medicine, Nanjing Agricultural University, Weigang 1, Nanjing, 210095, China.ORCID http://orcid.org/0000-0003-1011-7985
Shu Tang *College of Veterinary Medicine, Nanjing Agricultural University, Weigang 1, Nanjing, 210095, China.
Jiao XuCollege of Veterinary Medicine, Nanjing Agricultural University, Weigang 1, Nanjing, 210095, China.
Jiarui SunCollege of Veterinary Medicine, Nanjing Agricultural University, Weigang 1, Nanjing, 210095, China.
Xiaohui ZhangCollege of Veterinary Medicine, Nanjing Agricultural University, Weigang 1, Nanjing, 210095, China.
Yubao LiCollege of Agronomy, Liaocheng University, Hunan road 1, Liaocheng, 252000, China.
Endong BaoCollege of Veterinary Medicine, Nanjing Agricultural University, Weigang 1, Nanjing, 210095, China. b_endong@njau.edu.cn.
Nanjing Agricultural University · CNLiaocheng University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CRYAB is a small heat shock protein (sHSP) that has previously been shown to protect the heart against various cellular stresses; however, its precise function in myocardial cell injury caused by heat stress remains unclear. This study aimed to investigate the molecular mechanism by which CRYAB protects cardiomyocytes against heat stress. We constructed two H9C2 cell lines that stably express CRYAB protein to differing degrees: CRYAB-5 and CRYAB-7. Both CRYAB-5 and CRYAB-7 showed significantly reduced granular degeneration and vacuolar degeneration following heat stress compared to control cells. In addition, CRYAB overexpression in H9C2 cells relieved cell cycle proportion at the G0/G1 phase following heat stress compared to control cells. These protective effects were associated with the level of CRYAB protein expression. Our immunofluorescence analysis showed CRYAB could translocate from the cytoplasm to the nucleus under heat stress conditions, but that CRYAB co-localized with F-actin (which accumulates under stress conditions). Indeed, overexpression of CRYAB significantly reduced the aggregation of F-actin in H9C2 cells caused by heat stress. Furthermore, overexpressing CRYAB protein significantly reduced the apoptosis of cardiomyocytes induced by heat stress, likely by reducing the expression of cleaved-caspase 3. Collectively, our results show overexpression of CRYAB significantly increases the heat resistance of H9C2 cardiomyocytes, likely by reducing F-actin aggregation (thus stabilizing the cytoskeleton), regulating the cell cycle, and preventing caspase-mediated apoptosis.

Indexed as

ApoptosisHeat-Shock ResponseProtein AggregatesActinsAnimalsCaspasesCell CycleCell LineCrystallinsCytoprotectionMicrotubule-Associated ProteinsMyocytes, CardiacRatsRecombination, GeneticTranscription, GeneticActinsCaspasescryaB protein, ratCrystallinsMicrotubule-Associated ProteinsProtein AggregatesApoptosisCell cycleCRYABF-actinHeat stress

Identifiers

PMID30246229
PMCPMC6363628
OpenAlexW2892992546

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.