Evidence map›Paper›PMID 39145838›Full record

ArticleCurrent medical science2024

LncRNA NPTN-IT1-201 Ameliorates Depressive-like Behavior by Targeting miR-142-5p and Regulating Inflammation and Apoptosis via BDNF.

Jun He, Peng Xie, Xiao-Qiong An, Dong-Fen Guo, Bin Bi, Gang Wu, Wen-Feng Yu, Zhen-Kui Ren, Li Zuo

Abstract read
PubMed Publisher
In one paragraph

Article in Current medical science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. 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

9 authors.

Jun HeDepartment of Immunology, School of Basic Medical Science, Guizhou Medical University, Guiyang, 550004, China.
Peng XieKey Laboratory of Endemic and Ethnic Diseases, Ministry of Education, School of Basic Medical Science, Guizhou Medical University, Guiyang, 550004, China.
Xiao-Qiong AnKey Laboratory of Endemic and Ethnic Diseases, Ministry of Education, School of Basic Medical Science, Guizhou Medical University, Guiyang, 550004, China.
Dong-Fen GuoKey Laboratory of Endemic and Ethnic Diseases, Ministry of Education, School of Basic Medical Science, Guizhou Medical University, Guiyang, 550004, China.
Bin BiPsychosomatic Department, The Second People's Hospital of Guizhou Province, Guiyang, 550004, China.
Gang WuPsychosomatic Department, The Second People's Hospital of Guizhou Province, Guiyang, 550004, China.
Wen-Feng YuKey Laboratory of Endemic and Ethnic Diseases, Ministry of Education, School of Basic Medical Science, Guizhou Medical University, Guiyang, 550004, China. wenfengyu2013@126.com.
Zhen-Kui RenDepartment of Laboratory Medicine, The Second People's Hospital of Guizhou Province, Guiyang, 550004, China. 2639092792@qq.com.
Li ZuoDepartment of Immunology, School of Basic Medical Science, Guizhou Medical University, Guiyang, 550004, China. zuoligymc@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveLong noncoding RNAs (lncRNAs) and microRNAs (miRNAs) are widely expressed in the brain and are associated with the development of neurological and neurodegenerative diseases. However, their roles and molecular mechanisms in major depressive disorder (MDD) remain largely unknown. This study aimed to identify lncRNAs and miRNAs involved in the development of MDD and elucidate their molecular mechanisms.

methodsTranscriptome and bioinformatic analyses were performed to identify miRNAs and lncRNAs related to MDD. C57 mice were subjected to chronic unpredictable mild stress (CUMS) to establish a depression model. Lentiviruses containing either lncRNA NPTN-IT1-201 or miR-142-5p were microinjected into the hippocampal region of these mice. Behavioral tests including the sucrose preference test (SPT), tail suspension test (TST), and forced swim test (FST) were conducted to evaluate depressive-like behaviors.

resultsThe results revealed that overexpression of lncRNA NPTN-IT1-201 or inhibition of miR-142-5p significantly ameliorated depressive-like behaviors in CUMS-treated mice. Dual-luciferase reporter assays confirmed interactions between miR-142-5p with both brain-derived neurotrophic factor (BDNF) and NPTN-IT1-201. ELISA analysis revealed significant alterations in relevant biomarkers in the blood samples of MDD patients compared to healthy controls. Histological analyses, including HE and Nissl staining, showed marked structural changes in brain tissues following CUMS treatment, which were partially reversed by lncRNA NPTN-IT1-201 overexpression or miR-142-5p inhibition. Immunofluorescence imaging demonstrated significant differences in the levels of BAX, Bcl2, p65, Iba1 among different treatment groups. TUNEL assays confirmed reduced apoptosis in brain tissues following these interventions. Western blotting showed the significant differences in BDNF, BAX, and Bcl2 protein levels among different treatment groups.

conclusionNPTN-IT1-201 regulates inflammation and apoptosis in MDD by targeting BDNF via miR-142-5p, making it a potential therapeutic target for MDD.

Indexed as

ApoptosisBrain-Derived Neurotrophic FactorInflammationMicroRNAsRNA, Long NoncodingAdultAnimalsBehavior, AnimalDepressionDisease Models, AnimalFemaleGene Expression RegulationHippocampusHumansMajor Depressive DisorderMaleBDNF protein, humanBdnf protein, mouseBrain-Derived Neurotrophic FactorMicroRNAsMIRN142 microRNA, humanMirn142 microRNA, mouseRNA, Long Noncodingbrain-derived neurotrophic factorchronic unpredictable mild stressdepressive-like behaviorlong noncoding RNAmicroRNA

Identifiers

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.