Evidence map›Paper›PMID 33886061›Full record

ArticleMolecular and cellular biochemistry2021

miR-145-5p targets paxillin to attenuate angiotensin II-induced pathological cardiac hypertrophy via downregulation of Rac 1, pJNK, p-c-Jun, NFATc3, ANP and by Sirt-1 upregulation.

Kuan-Ho Lin, V Bharath Kumar, Tamilselvi Shanmugam, Marthandam Asokan Shibu, Ray-Jade Chen, Chia-Hua Kuo, Tsung-Jung Ho, V Vijaya Padma, Yu-Lan Yeh, Chih-Yang Huang

Abstract read
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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
0.9field-weighted citation impact, top 32% 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, 15 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

10 authors at 8 institutions in 2 countries.

Kuan-Ho LinDepartment of Emergency Medicine, China Medical University Hospital, Taichung, Taiwan.
V Bharath KumarDepartment of Medical Laboratory Science and Biotechnology, Asia University, Taichung, Taiwan.
Tamilselvi ShanmugamCardiovascular and Mitochondrial Related Disease Research Center, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan.
Marthandam Asokan ShibuCardiovascular and Mitochondrial Related Disease Research Center, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan.
Ray-Jade ChenDepartment of Surgery, School of Medicine, College of Medicine, Taipei Medical University, Taipei, 11031, Taiwan.
Chia-Hua KuoLaboratory of Exercise Biochemistry, University of Taipei, Taipei, Taiwan.
Tsung-Jung HoChinese Medicine, Hualien Tzu Chi Hospital, Tzu Chi University, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan.
V Vijaya PadmaDepartment of Biotechnology, Bharathiar University, Coimbatore, 641046, India.
Yu-Lan Yeh *Department of Pathology, Changhua Christian Hospital, Changhua, Taiwan.
Chih-Yang HuangDepartment of Medical Laboratory Science and Biotechnology, Asia University, Taichung, Taiwan. cyhuang@mail.cmu.edu.tw.ORCID http://orcid.org/0000-0003-2347-0411
Asia University · TWTzu Chi Foundation · TWBharathiar University · INChina Medical University · TWKang-Ning Junior College of Medical Care and Management · TWTaipei Medical University · TWTzu Chi University · TWUniversity of Taipei · TW

Funding

China Medical University DMR-109-059Ministry of Health and Welfare MOHW107-TDU-B-212-123004
6 · The paper itself

Abstract

Pathological cardiac hypertrophy is associated with many diseases including hypertension. Recent studies have identified important roles for microRNAs (miRNAs) in many cardiac pathophysiological processes, including the regulation of cardiomyocyte hypertrophy. However, the role of miR-145-5p in the cardiac setting is still unclear. In this study, H9C2 cells were overexpressed with microRNA-145-5p, and then treated with Ang-II for 24 h, to study the effect of miR-145-5p on Ang-II-induced myocardial hypertrophy in vitro. Results showed that Ang-II treatment down-regulated miR-145-5p expression were revered after miR-145-5p overexpression. Based on results of bioinformatics algorithms, paxillin was predicted as a candidate target gene of miR-145-5p, luciferase activity assay revealed that the luciferase activity of cells was substantial downregulated the following co-transfection with wild paxillin 3'UTR and miR-145-5p compared to that in scramble control, while the inhibitory effect of miR-145-5p was abolished after transfection of mutant paxillin 3'UTR. Additionally, overexpression of miR-145-5p markedly inhibited activation of Rac-1/ JNK /c-jun/ NFATc3 and ANP expression and induced SIRT1 expression in Ang-II treated H9c2 cells. Jointly, our study suggested that miR-145-5p inhibited cardiac hypertrophy by targeting paxillin and through modulating Rac-1/ JNK /c-jun/ NFATc3/ ANP / Sirt1 signaling, therefore proving novel downstream molecular pathway of miR-145-5p in cardiac hypertrophy.

Indexed as

Angiotensin IIAnimalsAtrial Natriuretic FactorCardiomegalyCells, CulturedGene Expression RegulationMAP Kinase Kinase 4MicroRNAsMyoblasts, CardiacNFATC Transcription FactorsPaxillinProto-Oncogene Proteins c-junrac1 GTP-Binding ProteinRatsSirtuin 1Vasoconstrictor AgentsAngiotensin IIAtrial Natriuretic FactorMAP Kinase Kinase 4MicroRNAsMIRN145 microRNA, ratNFATC Transcription FactorsPaxillinProto-Oncogene Proteins c-junPxn protein, ratrac1 GTP-Binding ProteinRac1 protein, ratSirt1 protein, ratSirtuin 1Vasoconstrictor AgentsAng-IIANPHypertrophyJNKmiR-145-5pNFATc3PaxillinRac- 1

Identifiers

PMID33886061
OpenAlexW3155430750

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.