Evidence map›Paper›PMID 28947594›Full record

ArticlePhysiological reports2017

MiR-339 inhibits proliferation of pulmonary artery smooth muscle cell by targeting FGF signaling.

Jidong Chen, Xiaolei Cui, Li Li, Junle Qu, J Usha Raj, Deming Gou

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2017. 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
2.5field-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

12 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. MicroRNA miR-627-5p restrains pulmonary artery smooth muscle cell dysfunction by targeting MAP 2 K4 and PI3K/AKT signaling.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2022
    Article
  3. Review
  4. Review
  5. MiRNAs, lncRNAs, and circular RNAs as mediators in hypertension-related vascular smooth muscle cell dysfunction.Hypertension research : official journal of the Japanese Society of Hypertension · 2021
    Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  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

6 authors at 2 institutions in 2 countries.

Jidong ChenShenzhen Key Laboratory of Marine Bioresource and Eco-environmental Science, Shenzhen Key Laboratory of Microbial Genetic Engineering, College of Life Sciences, Shenzhen University, Shenzhen, Guangdong, China.
Xiaolei CuiShenzhen Key Laboratory of Marine Bioresource and Eco-environmental Science, Shenzhen Key Laboratory of Microbial Genetic Engineering, College of Life Sciences, Shenzhen University, Shenzhen, Guangdong, China.
Li LiShenzhen Key Laboratory of Marine Bioresource and Eco-environmental Science, Shenzhen Key Laboratory of Microbial Genetic Engineering, College of Life Sciences, Shenzhen University, Shenzhen, Guangdong, China.
Junle QuKey Laboratory of Optoelectronic Devices, Systems of Ministry of Education and Guangdong Province, College of Optoelectronic Engineering, Shenzhen University, Shenzhen, Guangdong, China.
J Usha RajDepartment of Pediatrics, University of Illinois at Chicago, Chicago, Illinois.
Deming GouShenzhen Key Laboratory of Marine Bioresource and Eco-environmental Science, Shenzhen Key Laboratory of Microbial Genetic Engineering, College of Life Sciences, Shenzhen University, Shenzhen, Guangdong, China dmgou@szu.edu.cn.
Shenzhen University · CNUniversity of Illinois Chicago · US

Funding

Role of microRNA-17-92 and PDLIM5 Signaling in Pulmonary Arterial HypertensionR01HL123804 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI RAJ, J. USHA, ZHOU, GUOFEI · 2015 to 2018
$1.6M
NHLBI NIH HHS R01 HL123804
6 · The paper itself

Abstract

Pulmonary artery hypertension (PAH) is a fatal disorder. Recent studies suggest that microRNA (miRNA) plays an important role in regulating proliferation of pulmonary artery smooth muscle cells (PASMC), which underlies the pathology of PAH However, the exact mechanism of action of miRNAs remains elusive. In this study, we found that miR-339 was highly expressed in the cardiovascular system and was downregulated by a group of cytokines and growth factors, especially PDGF-BB and FGF2. Functional analyses revealed that miR-339 can inhibit proliferation of PASMC Also, miR-339 inhibited FGF2-induced proliferation, but had no effect on proliferation induced by PDGF-BB The fibroblast growth factor receptor substrate 2 (FRS2) was identified as a potential direct target of miR-339. Consistent with the actions of miR-339, knockdown of FRS2 only inhibited FGF2- but not PDGF-BB-induced proliferation of PASMC In addition, our results showed that inhibition of ERK and PI3K abrogated the downregulation of miR-339 induced by PDGF-BB Finally, miR-339 expression was found to be decreased in the pulmonary arteries of rats with MCT-induced PAH Our study is the first report on the biological role of miR-339 in regulating proliferation of PASMC by targeting FGF signaling, providing new mechanistic insights into PASMC proliferation and pathogenesis of PAH.

Indexed as

Cell ProliferationSignal TransductionAdaptor Proteins, Signal TransducingAnimalsBecaplerminCells, CulturedFibroblast Growth FactorsHEK293 CellsHumansMicroRNAsMyocytes, Smooth MuscleProto-Oncogene Proteins c-sisPulmonary ArteryRatsAdaptor Proteins, Signal TransducingBecaplerminFibroblast Growth Factorsfibroblast receptor substrate 2, ratMicroRNAsMIRN-339 microRNA, ratProto-Oncogene Proteins c-sisFGF2FRS2miR‐339PASMCPDGF‐BBproliferation

Identifiers

PMID28947594
PMCPMC5617928
OpenAlexW2760477217

What OpenQuestion holds

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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.