Evidence map›Paper›PMID 34092081›Full record

ArticleInnate immunity2021

miR-150 and SRPK1 regulate AKT3 expression to participate in LPS-induced inflammatory response.

Yanfen Yao, Hong Wang, Xueqin Xi, Wei Sun, Junke Ge, Pibao Li

Open access · goldAbstract read
In one paragraph

Article in Innate immunity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 37% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. 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

6 authors at 2 institutions in 1 country.

Yanfen YaoDepartment of Intensive Care Unit, Shandong Provincial Third Hospital, Cheeloo College of Medicine, Shandong University, China.
Hong WangDepartment of General Surgery, Shandong Provincial Third Hospital, Cheeloo College of Medicine, Shandong University, China.
Xueqin XiDepartment of Pediatrics, Maternal and Child Health Hospital of Shandong Province, China.
Wei SunDepartment of Intensive Care Unit, Shandong Provincial Third Hospital, Cheeloo College of Medicine, Shandong University, China.ORCID 0000-0002-8970-9037
Junke GeDepartment of Intensive Care Unit, Shandong Provincial Third Hospital, Cheeloo College of Medicine, Shandong University, China.
Pibao LiDepartment of Intensive Care Unit, Shandong Provincial Third Hospital, Cheeloo College of Medicine, Shandong University, China.ORCID 0000-0003-3830-626X
Shandong University · CNShandong Maternal and Child Health Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

miR-150 was found to target the 3'-untranslated regions of AKT3, and the AKT pathway was affected by SR protein kinase 1 (SRPK1). However, the expression and significance of miR-150, AKT3 and SRPK1 in acute lung injury (ALI) were not clear. Here, we found that the expression of miR-150 was significantly reduced, while the expression of AKT3 and SRPK1 were markedly increased in LPS-treated A549, THP-1 and RAW 264.7 cells. miR-150 significantly decreased levels of pro-inflammatory cytokines IL-1β, IL-6 and TNF-α, reduced the expression of AKT3, but had no impact on SRPK1 expression compared with the control group in LPS-treated A549, THP-1 and RAW 264.7 cells. AKT3 silencing only reduced the production of pro-inflammatory cytokines and showed no effect on miR-150 and SRPK1 expression. Finally, we observed that miR-150 mimics and/or silencing of SRPK1 decreased the expression of AKT3 mRNA. Besides, over-expression of miR-150 or silencing of SRPK1 also reduced the expression of AKT3 protein, which exhibited the lowest level in the miR-150 mimics plus si-SRPK1 group. However, si-SRPK1 had no effect on miR-150 level. In conclusion, miR-150 and SRPK1 separately and cooperatively participate into inflammatory responses in ALI through regulating AKT3 pathway. Increased miR-150 and silenced SRPK1 may be a novel potential factor for preventing and treating more inflammatory lung diseases.

Indexed as

3' Untranslated RegionsA549 CellsAcute Kidney InjuryAnimalsCytokinesGene Expression RegulationHumansInflammationLipopolysaccharidesMiceMicroRNAsProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktRAW 264.7 Cells3' Untranslated RegionsAKT3 protein, humanAkt3 protein, mouseCytokinesLipopolysaccharidesMicroRNAsMIR150, humanMirn150 microRNA, mouseProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktSRPK1 protein, humanSrpk1 protein, mouseAKT3ALIinflammationmiR-150SRPK1

Identifiers

PMID34092081
PMCPMC8186154
OpenAlexW3172429018

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.