Evidence map›Paper›PMID 30362186›Full record

ArticleCell proliferation2019

LncRNA XIST mediates bovine mammary epithelial cell inflammatory response via NF-κB/NLRP3 inflammasome pathway.

Mengru Ma, Yifei Pei, Xixi Wang, Jiaxin Feng, Yong Zhang, Ming-Qing Gao

Open access · hybridAbstract read
In one paragraph

Article in Cell proliferation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 4% 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

86 citing papers in PubMed, 1 synthesis or guideline pooled it, 134 citations in OpenAlex.

  1. Pooled it
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  13. NArchives of microbiology · 2024
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  20. Unveiling the Hidden Regulators: The Impact of lncRNAs on Zoonoses.International journal of molecular sciences · 2024
    Review

26 more citing papers are in PubMed but not listed here.

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

6 authors at 1 institution in 1 country.

Mengru MaCollege of Veterinary Medicine, Northwest A&F University, Yangling, China.
Yifei PeiCollege of Animal Science and Technology, Northwest A&F University, Yangling, China.
Xixi WangCollege of Veterinary Medicine, Northwest A&F University, Yangling, China.
Jiaxin FengCollege of Veterinary Medicine, Northwest A&F University, Yangling, China.
Yong ZhangCollege of Veterinary Medicine, Northwest A&F University, Yangling, China.
Ming-Qing GaoCollege of Veterinary Medicine, Northwest A&F University, Yangling, China.ORCID http://orcid.org/0000-0002-8904-7758
Northwest A&F University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesThe correlations between long non-coding RNAs (lncRNAs) and diverse mammal diseases have been clarified by many researches, but the cognition about bovine mastitis-related lncRNAs remains limited. This study aimed to investigate the potential role of lncRNA X-inactive specific transcript (XIST) in the inflammatory response of bovine mammary epithelial cells. MATERIALS AND

methodsTwo inflammatory bovine mammary alveolar cell-T (MAC-T) models were established by infecting the cells with Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus). The expressions of pro-inflammatory cytokines were measured, and the proliferation, viability and apoptosis of the inflammatory cells were evaluated after XIST was knocked down by an siRNA. The relationship among XIST, NF-κB pathway and NOD-like receptor protein 3 (NLRP3) inflammasome was investigated using an inhibitor of NF-κB signal pathway.

resultsThe expression of XIST was abnormally increased in bovine mastitic tissues and inflammatory MAC-T cells. Silencing of XIST significantly increased the expression of E. coli or S. aureus-induced pro-inflammatory cytokines. Additionally, knockdown of XIST could inhibit cell proliferation, suppress cell viability and promote cell apoptosis under inflammatory conditions. Furthermore, XIST inhibited E. coli or S. aureus-induced NF-κB phosphorylation and the production of NLRP3 inflammasome.

conclusionsThe expression of XIST was promoted by activated NF-κB pathway and, in turn, XIST generated a negative feedback loop to regulate NF-κB/NLRP3 inflammasome pathway for mediating the process of inflammation.

Indexed as

AnimalsApoptosisCattleCell ProliferationCell SurvivalEpithelial CellsEscherichia coliEscherichia coli InfectionsFemaleInflammationMammary Glands, AnimalMastitis, BovineNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinRNA InterferenceRNA, Long NoncodingNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinRNA, Long NoncodingRNA, Small InterferingXIST non-coding RNAbovinelncRNA XISTmastitisNF-κB pathwayNLRP3 inflammasome

Identifiers

PMID30362186
PMCPMC6430464
OpenAlexW2898341891

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.