Evidence map›Paper›PMID 33095380›Full record

ArticleMolecular and cellular biochemistry2021

Rab27a deletion impairs the therapeutic potential of endothelial progenitor cells for myocardial infarction.

Wenyi Zhou, Xuefei Zheng, Chuanfang Cheng, Guixian Guo, Yun Zhong, Weihua Liu, Kefeng Liu, Yanfang Chen, Shiming Liu, Shaojun Liu

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular and cellular biochemistry, 2021. 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
0.8field-weighted citation impact, top 30% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Black Chokeberry (Life (Basel, Switzerland) · 2024
    Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. CD34 positive cells as endothelial progenitor cells in biology and medicine.Frontiers in cell and developmental biology · 2023
    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

10 authors at 4 institutions in 2 countries.

Wenyi ZhouGuangzhou Institute of Cardiovascular Disease, Guangdong Key Laboratory of Vascular Diseases, State Key Laboratory of Respiratory Disease, the Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 510260, People's Republic of China.
Xuefei ZhengGuangzhou Institute of Cardiovascular Disease, Guangdong Key Laboratory of Vascular Diseases, State Key Laboratory of Respiratory Disease, the Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 510260, People's Republic of China.
Chuanfang ChengGuangzhou Institute of Cardiovascular Disease, Guangdong Key Laboratory of Vascular Diseases, State Key Laboratory of Respiratory Disease, the Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 510260, People's Republic of China.
Guixian GuoGuangzhou Institute of Cardiovascular Disease, Guangdong Key Laboratory of Vascular Diseases, State Key Laboratory of Respiratory Disease, the Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 510260, People's Republic of China.
Yun ZhongGuangzhou Institute of Cardiovascular Disease, Guangdong Key Laboratory of Vascular Diseases, State Key Laboratory of Respiratory Disease, the Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 510260, People's Republic of China.
Weihua LiuGuangzhou Institute of Cardiovascular Disease, Guangdong Key Laboratory of Vascular Diseases, State Key Laboratory of Respiratory Disease, the Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 510260, People's Republic of China.
Kefeng LiuDepartment of Histology and Embryology, School of Basic Medical Sciences, Xiangnan University, Chenzhou, Hunan, 423000, People's Republic of China.
Yanfang ChenDepartment of Pharmacology and Toxicology, Boonshoft School of Medicine, Wright State University, Dayton, OH, 45435, USA.
Shiming LiuGuangzhou Institute of Cardiovascular Disease, Guangdong Key Laboratory of Vascular Diseases, State Key Laboratory of Respiratory Disease, the Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 510260, People's Republic of China. liushiming@gzhmu.edu.cn.
Shaojun LiuGuangzhou Institute of Cardiovascular Disease, Guangdong Key Laboratory of Vascular Diseases, State Key Laboratory of Respiratory Disease, the Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 510260, People's Republic of China. shaojunliu@gzhmu.edu.cn.ORCID http://orcid.org/0000-0001-7895-5577
State Key Laboratory of Respiratory Disease · CNSecond Affiliated Hospital of Guangzhou Medical University · CNWright State University · USXiangnan University · CN

Funding

National Natural Science Foundation of China 81570259, 81873474, 81600350
6 · The paper itself

Abstract

Endothelial progenitor cell (EPC) transplantation has shown advantages in the treatment of myocardial infarction (MI) in animal models and clinical trials through mechanisms of direct intercellular contacts, autocrine, and paracrine. However, the effects of EPC transplantation for MI treatment remain controversial and the underlying mechanisms have not been fully elucidated. Here, we explored the role of Rab27a in the therapeutic potential of EPC transplantation in MI. We found that Rab27a knockout impaired the viability, and reduced the proliferation and tube formation function of ECPs. The recovery of cardiac function and improvement of ventricular remodeling from EPCs transplantation were significantly damaged by Rab27a deletion in vivo. Rab27a deletion inhibited the protein expression of phosphoinositide 3-kinase (PI3K) and cyclin D1 and the phosphorylation levels of Akt and FoxO3a. Therefore, Rab27a knockout suppressed the PI3K-Akt-FoxO3a/cyclin D1 signaling pathway. Furthermore, Rab27a ablation dramatically reduced exosome release in EPCs. These results demonstrated that Rab27a plays an essential role in EPC functions. The elucidation of this mechanism provides novel insights into EPC transplantation as a promising treatment for post-MI injuries.

Indexed as

Gene DeletionAnimalsBone Marrow CellsCells, CulturedDisease Models, AnimalEndothelial Progenitor CellsExosomesMaleMiceMice, Inbred C57BLMice, KnockoutMyocardial InfarctionPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktrab27 GTP-Binding ProteinsSignal TransductionPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRab27a protein, mouserab27 GTP-Binding ProteinsCell therapyEndothelial progenitor cellsExosomesMyocardial infarctionRab27a

Identifiers

PMID33095380
OpenAlexW3093689554

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.