Evidence map›Paper›PMID 27121304›Full record

ArticleScientific reports2016

MicroRNA-223 Attenuates Hypoxia-induced Vascular Remodeling by Targeting RhoB/MLC2 in Pulmonary Arterial Smooth Muscle Cells.

Yan Zeng, Xiaoying Zhang, Kang Kang, Jidong Chen, Zhiqin Wu, Jinyong Huang, Wenju Lu, Yuqin Chen, Jie Zhang, Zhiwei Wang and 6 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

38 citing papers in PubMed, 69 citations in OpenAlex.

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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

16 authors at 5 institutions in 2 countries.

Yan ZengShenzhen Key Laboratory of Microbial Genetic Engineering, Shenzhen Key Laboratory of Marine Bioresource and Eco-environmental Science, College of Life Sciences, Shenzhen University, Shenzhen, Guangdong 518060, China.
Xiaoying ZhangShenzhen Key Laboratory of Microbial Genetic Engineering, Shenzhen Key Laboratory of Marine Bioresource and Eco-environmental Science, College of Life Sciences, Shenzhen University, Shenzhen, Guangdong 518060, China.
Kang KangDepartment of Physiology, Shenzhen University Health Science Center, Shenzhen, Guangdong 518060, China.
Jidong ChenShenzhen Key Laboratory of Microbial Genetic Engineering, Shenzhen Key Laboratory of Marine Bioresource and Eco-environmental Science, College of Life Sciences, Shenzhen University, Shenzhen, Guangdong 518060, China.
Zhiqin WuShenzhen Key Laboratory of Microbial Genetic Engineering, Shenzhen Key Laboratory of Marine Bioresource and Eco-environmental Science, College of Life Sciences, Shenzhen University, Shenzhen, Guangdong 518060, China.
Jinyong HuangShenzhen Key Laboratory of Microbial Genetic Engineering, Shenzhen Key Laboratory of Marine Bioresource and Eco-environmental Science, College of Life Sciences, Shenzhen University, Shenzhen, Guangdong 518060, China.
Wenju LuGuangzhou Institute of Respiratory Diseases, State Key Laboratory of Respiratory Diseases, The First Affiliated Hospital, Guangzhou Medical University, 151 Yanjiang Road, Guangzhou, Guangdong 510120, China.
Yuqin ChenGuangzhou Institute of Respiratory Diseases, State Key Laboratory of Respiratory Diseases, The First Affiliated Hospital, Guangzhou Medical University, 151 Yanjiang Road, Guangzhou, Guangdong 510120, China.
Jie ZhangGuangzhou Institute of Respiratory Diseases, State Key Laboratory of Respiratory Diseases, The First Affiliated Hospital, Guangzhou Medical University, 151 Yanjiang Road, Guangzhou, Guangdong 510120, China.
Zhiwei WangDepartment of Cardiovascular Surgery, Shenzhen Sun Yat-Sen Cardiovascular Hospital, Shenzhen, Guangdong 518060, China.
Yujia ZhaiDepartment of Cardiovascular Surgery, Shenzhen Sun Yat-Sen Cardiovascular Hospital, Shenzhen, Guangdong 518060, China.
Junle QuKey Laboratory of Optoelectronic Devices and Systems of Ministry of Education and Guangdong Province, College of Optoelectronic Engineering Shenzhen University, Shenzhen, Guangdong 518060, China.
Ramaswamy RamchandranDepartment of Pediatrics, University of Illinois at Chicago, Chicago, IL 60612, USA.
J Usha RajDepartment of Pediatrics, University of Illinois at Chicago, Chicago, IL 60612, USA.
Jian WangGuangzhou Institute of Respiratory Diseases, State Key Laboratory of Respiratory Diseases, The First Affiliated Hospital, Guangzhou Medical University, 151 Yanjiang Road, Guangzhou, Guangdong 510120, China.
Deming GouShenzhen Key Laboratory of Microbial Genetic Engineering, Shenzhen Key Laboratory of Marine Bioresource and Eco-environmental Science, College of Life Sciences, Shenzhen University, Shenzhen, Guangdong 518060, China.
Shenzhen University · CNGuangzhou Medical University · CNSun Yat-sen Memorial Hospital · CNUniversity of Illinois Chicago · USShenzhen University Health Science Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is growing evidence that microRNAs are implicated in pulmonary arterial hypertension (PAH), but underlying mechanisms remain elusive. Here, we identified that miR-223 was significantly downregulated in chronically hypoxic mouse and rat lungs, as well as in pulmonary artery and pulmonary artery smooth muscle cells (PASMC) exposed to hypoxia. Knockdown of miR-223 increased PASMC proliferation. In contrast, miR-223 overexpression abrogated cell proliferation, migration and stress fiber formation. Administering miR-223 agomir in vivo antagonized hypoxia-induced increase in pulmonary artery pressure and distal arteriole muscularization. RhoB, which was increased by hypoxia, was identified as one of the targets of miR-223. Overexpressed miR-223 suppressed RhoB and inhibited the consequent phosphorylation of myosin phosphatase target subunit (MYPT1) and the expression of myosin light chain of myosin II (MLC2), which was identified as another target of miR-223. Furthermore, serum miR-223 levels were decreased in female patients with PAH associated with congenital heart disease. Our study provides the first evidence that miR-223 can regulate PASMC proliferation, migration, and actomyosin reorganization through its novel targets, RhoB and MLC2, resulting in vascular remodeling and the development of PAH. It also highlights miR-223 as a potential circulating biomarker and a small molecule drug for diagnosis and treatment of PAH.

Indexed as

HypoxiaVascular RemodelingAnimalsCardiac MyosinsCells, CulturedHumansMiceMicroRNAsMyocytes, Smooth MuscleMyosin Light ChainsRatsrhoB GTP-Binding ProteinCardiac MyosinsMicroRNAsMIR223, humanmyosin light chain 2Myosin Light ChainsrhoB GTP-Binding Protein

Identifiers

PMID27121304
PMCPMC4848472
OpenAlexW2342530266

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.