Evidence map›Paper›PMID 34872453›Full record

ArticleBioengineered2021

Long non-coding RNA OIP5-AS1 regulates smoke-related chronic obstructive pulmonary disease via targeting micro RNA -410-3p/IL-13.

Wenbo Hao, Fei Lin, Hanbing Shi, Zhanjiang Guan, Yunfei Jiang

Abstract read
In one paragraph

Article in Bioengineered, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Revealing lncRNA Biomarkers Related to Chronic Obstructive Pulmonary Disease Based on Bioinformatics.International journal of chronic obstructive pulmonary disease · 2022
    Article
  9. Review
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.

Wenbo HaoCardiothoracic Surgery, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, Heilongjiang, China.
Fei LinEndocrinology Department, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, Heilongjiang, China.
Hanbing ShiDepartment of Respiratory and Critical Care Medicine, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, Heilongjiang, China.
Zhanjiang GuanDepartment of Critical Care Medicine, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, Heilongjiang, China.
Yunfei JiangDepartment of Respiratory and Critical Care Medicine, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, Heilongjiang, China.ORCID 0000-0002-4663-4549

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This investigation aimed to assess the levels of serum OIP5-AS1 and micro RNA-410-3p (miR-410-3p) in patients with chronic obstructive pulmonary disease (COPD) and their potential molecular mechanism. The levels of OIP5-AS1 and miR-410-3p as well as mRNA levels of IL-13 were measured. Pearson variable linear test was applied to analyze the correlations between forced expiratory volume in 1 second (FEV1) and OIP5-AS1. The receiver operating characteristic curve was used to predict the predictive possibility of OIP5-AS1. The viable cells were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and flow cytometry was used to detect the cell apoptosis. An enzyme-linked immunosorbent assay was performed to indicate the inflammatory situation of 16HBE cells. Luciferase activity assay was conducted to examine the relationships between OIP5-AS1 and miR-410-3p together with miR-410-3p and IL-13. Augmented levels of OIP5-AS1, declined levels of miR-410-3p, and enhanced expression of IL-13 were unveiled. The expression of OIP5-AS1 and miR-410-3p was related to the ratio of FEV1 respectively. OIP5-AS1 might serve as a diagnostic biomarker. Interference of OIP5-AS1 restored the abnormal cell viability, apoptosis, and inflammation in cigarette smoke extract (CSE)-stimulated 16HBE cells by regulating miR-410-3p and IL-13. OIP5-AS1 appeared to be a biomarker for distinguishing COPD patients from smokers. OIP5-AS1/miR-410-3p/IL-13 exerted function on the cell viability, apoptosis, and inflammation in CSE-steered cell models.

Indexed as

Base SequenceCell LineGene Expression RegulationHumansInterleukin-13MicroRNAsMiddle AgedPulmonary Disease, Chronic ObstructiveRNA, Long NoncodingRNA, MessengerSmokingInterleukin-13MicroRNAsMIRN410 microRNA, humanRNA, Long NoncodingRNA, MessengerbiomarkerIL-13inflammationmiR-410-3pOIP5-AS1

Identifiers

PMID34872453
PMCPMC8810017

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Registered trials

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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.