Evidence map›Paper›PMID 34403009›Full record

ArticleJournal of molecular histology2021

LINC01123 promotes cell proliferation and migration via regulating miR-1277-5p/KLF5 axis in ox-LDL-induced vascular smooth muscle cells.

Guohu Weng, Minhua Gu, Yifan Zhang, Guangfeng Zhao, Yong Gu

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular histology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
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  6. Long Non-Coding RNAs in Venous Thromboembolism: Where Do We Stand?International journal of molecular sciences · 2023
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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

5 authors at 1 institution in 1 country.

Guohu Weng *Department of Encephalopathy, Hainan Provincial Hospital of Chinese Medicine, 47# Heping North Road, Haikou, 570203, Hainan, People's Republic of China.
Minhua Gu *Department of Cardiology, Hainan Provincial Hospital of Chinese Medicine, Haikou, 570203, Hainan, People's Republic of China.
Yifan ZhangDepartment of Encephalopathy, Hainan Provincial Hospital of Chinese Medicine, 47# Heping North Road, Haikou, 570203, Hainan, People's Republic of China.
Guangfeng ZhaoDepartment of Encephalopathy, Hainan Provincial Hospital of Chinese Medicine, 47# Heping North Road, Haikou, 570203, Hainan, People's Republic of China.
Yong GuDepartment of Encephalopathy, Hainan Provincial Hospital of Chinese Medicine, 47# Heping North Road, Haikou, 570203, Hainan, People's Republic of China. guyongweb@126.com.ORCID http://orcid.org/0000-0002-4444-9382
Hainan Provincial Hospital of Traditional Chinese Medicine · CN

Funding

Natural Science Foundation of Guangdong Province (2017A030313622) and Guangzhou Provincial Program of Science and Technology 201804010446
6 · The paper itself

Abstract

The pathophysiological mechanism of carotid atherosclerosis (CAS) involves endothelial cell dysfunction, vascular smooth muscle cells (VSMCs), and macrophage activation, which ultimately leads to fibrosis of the vessel wall. lncRNA works weightily in the formation of CAS, but the function and mechanism of lncRNA LINC01123 in stable plaque formation are still equivocal. We collected blood samples from 35 CAS patients as well as 33 healthy volunteers. VSMCs treated with oxidized low-density lipoprotein (ox-LDL) were utilized as the CAS cell models. We applied qRT-PCR for detecting LINC01123, miR-1277-5p and KLF5 mRNA expression, CCK-8 method and BrdU test for determining cell proliferation, Transwell test for measuring cell migration, as well as Western blot for assaying KLF5 protein expression. Dual-luciferase reporter experiment was adopted for assessing the interaction between LINC01123 and miR-1277-5p, as well as KLF5 and miR-1277-5p. LINC01123 and KLF5 expression were dramatically up-regulated, while miR-1277-5p expression was down-regulated in CAS patients and ox-LDL-induced CAS cell models. Overexpressed LINC01123 notedly promoted VSMCs migration and proliferation. LINC01123 knockdown repressed cell proliferation and migration. Also, LINC01123 targeted miR-1277-5p and down-regulated its expression, while miR-1277-5p could negatively regulate KLF5 expression. LINC01123 is highly expressed in CAS patients, and promotes cell proliferation and migration via regulating miR-1277-5p/KLF5 axis in ox-LDL-induced VSMCs. It might be involved in the fibrous plaque formation.

Indexed as

Signal TransductionBase SequenceCarotid Artery DiseasesCell MovementCell ProliferationFemaleHumansKruppel-Like Transcription FactorsLipoproteins, LDLMaleMicroRNAsMiddle AgedMuscle, Smooth, VascularMyocytes, Smooth MuscleRNA, Long NoncodingUp-RegulationKLF5 protein, humanKruppel-Like Transcription FactorsLipoproteins, LDLMicroRNAsMIRN1277 microRNA, humanoxidized low density lipoproteinRNA, Long NoncodingKLF5LINC01123MigrationmiR-1277-5pProliferationVSMCs

Identifiers

PMID34403009
OpenAlexW3195434531

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.