Evidence map›Paper›PMID 35763934›Full record

ArticleRedox biology2022

Ablation of long noncoding RNA MALAT1 activates antioxidant pathway and alleviates sepsis in mice.

Jingshu Chen, Shu Tang, Sui Ke, James J Cai, Daniel Osorio, Andrei Golovko, Benjamin Morpurgo, Shaodong Guo, Yuxiang Sun, Melanie Winkle and 2 more

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.6field-weighted citation impact, top 5% 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

28 citing papers in PubMed, 39 citations in OpenAlex.

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  20. PXR Activation Relieves Deoxynivalenol-Induced Liver Oxidative Stress Via Malat1 LncRNA mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
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

12 authors at 2 institutions in 1 country.

Jingshu ChenDepartment of Veterinary Physiology and Pharmacology, Texas A&M University, College Station, Tx, 77843, USA.
Shu TangDepartment of Veterinary Physiology and Pharmacology, Texas A&M University, College Station, Tx, 77843, USA.
Sui KeDepartment of Veterinary Physiology and Pharmacology, Texas A&M University, College Station, Tx, 77843, USA.
James J CaiDepartment of Veterinary Integrative Biosciences, Texas A&M University, College Station, Tx, 77843, USA.
Daniel OsorioDepartment of Veterinary Integrative Biosciences, Texas A&M University, College Station, Tx, 77843, USA.
Andrei GolovkoTexas A&M Institute for Genomic Medicine (TIGM), College Station, TX, 77843, USA.
Benjamin MorpurgoTexas A&M Institute for Genomic Medicine (TIGM), College Station, TX, 77843, USA.
Shaodong GuoDepartment of Nutrition, Texas A&M University, College Station, Tx, 77843, USA.
Yuxiang SunDepartment of Nutrition, Texas A&M University, College Station, Tx, 77843, USA.
Melanie WinkleDepartment of Translational Molecular Pathology, University of Texas MD Anderson Cancer Center, Houston, Tx, 77230, USA.
George A CalinDepartment of Translational Molecular Pathology, University of Texas MD Anderson Cancer Center, Houston, Tx, 77230, USA.
Yanan TianDepartment of Veterinary Physiology and Pharmacology, Texas A&M University, College Station, Tx, 77843, USA. Electronic address: ytian@cvm.tamu.edu.
Texas A&M University · USThe University of Texas MD Anderson Cancer Center · US

Funding

Long noncoding RNA MALAT1 ablation reverses sepsis in mouse: epitranscriptomic mechanisms and therapeutic applicationR21AI152050 · NIAID · TEXAS A&M AGRILIFE RESEARCH · PI TIAN, YANAN · 2020 to 2021
$421k
NIAID NIH HHS R21 AI152050
6 · The paper itself

Abstract

The metastasis-associated lung adenocarcinoma transcript1 (MALAT1) is a long noncoding RNA (lncRNA) and is known for its role in cancer development and prognosis. In this study, we report that MALAT1 plays an important role in regulating acute inflammatory responses in sepsis. In patient samples, MALAT1 expression was positively correlated with severity of sepsis. In cultured macrophages, LPS treatment significantly induced MALAT1 expression, while genetic ablation of MALAT1 greatly reduced proinflammatory cytokine levels. Furthermore, MALAT1-ablated mice had significantly increased survival rates in cecal ligation and puncture (CLP)-induced sepsis and LPS-induced endotoxemia. One novel and salient feature of MALAT1-ablated mice is greatly reduced ROS level in macrophages and other cell types and increased glutathione/oxidized glutathione (GSH/GSSG) ratio in macrophages, suggesting an increased antioxidant capacity. We showed a mechanism for MALAT1 ablation leading to enhanced antioxidant capacity is through activation of methionine cycle by epitranscriptomical regulation of methionine adenosyltransferase 2A (MAT2A). MAT2A 3'UTR can be methylated by METTL16 which was known to directly bind to MALAT1. MALAT1 ablation was found to reduce methylation in MAT2A hairpin1 and increase MAT2A protein levels. Our results suggest a MALAT1-METTL16-MAT2A interactive axis which may be targeted for treatments of sepsis.

Indexed as

AdenocarcinomaMicroRNAsSepsisAnimalsAntioxidantsLipopolysaccharidesMiceRNA, Long NoncodingAntioxidantsLipopolysaccharidesMalat1 long non-coding RNA, mouseMicroRNAsRNA, Long Noncoding

Identifiers

PMID35763934
PMCPMC9241053
OpenAlexW4283066944

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.