Evidence map›Paper›PMID 30684253›Full record

ArticleInflammation2019

PP2ACα of Alveolar Macrophages Is a Novel Protective Factor for LPS-Induced Acute Respiratory Distress Syndrome.

Zhixing He, Lijun Du, Yuehai Ke, Chengping Wen, Yun Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Saturated fatty acids stimulate cytokine production in tanycytes via the PP2Ac-dependent signaling pathway.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
    Article
  3. Article
  4. Review
  5. Protein phosphatases in TLR signaling.Cell communication and signaling : CCS · 2021
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. 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 at 2 institutions in 1 country.

Zhixing HeInstitute of Basic Research in Clinical Medicine, College of Basic Medical Science, Zhejiang Chinese Medical University, 548 Binwen Rd, Hangzhou, 310053, China.
Lijun DuInstitute of Basic Research in Clinical Medicine, College of Basic Medical Science, Zhejiang Chinese Medical University, 548 Binwen Rd, Hangzhou, 310053, China.
Yuehai KeDepartment of Pathology and Pathophysiology, Zhejiang University School of Medicine, Hangzhou, 310058, China.
Chengping WenInstitute of Basic Research in Clinical Medicine, College of Basic Medical Science, Zhejiang Chinese Medical University, 548 Binwen Rd, Hangzhou, 310053, China. wengcp@yeah.net.
Yun ZhangInstitute of Basic Research in Clinical Medicine, College of Basic Medical Science, Zhejiang Chinese Medical University, 548 Binwen Rd, Hangzhou, 310053, China. zhangyun@zcmu.edu.cn.ORCID http://orcid.org/0000-0002-4832-8916
Zhejiang Chinese Medical University · CNZhejiang University · CN

Funding

Department of Science and Technology for Social Development 2018YFC1705500National Natural Science Foundation of China 81700022
6 · The paper itself

Abstract

Protein phosphatase 2A (PP2A) is one main serine/threonine phosphatase in eukaryotes, and its activation changes have been linked to modulation of numerous pathological processes, such as cancer, inflammation, fibrosis, and neurodegenerative diseases. Acute respiratory distress syndrome (ARDS), the major cause of respiratory failure, remains with limited therapies available up to now. Alveolar macrophages (AMs) are essential to innate immunity and host defense, participating in the pathogenesis of ARDS. As a result, AMs are considered as a potential therapeutic target for ARDS. In our study, we firstly found that PP2A activity was significantly decreased in the lipopolysaccharide (LPS)-stimulated AMs. Furthermore, adoptive transfer of AMs with enhanced PP2A enzyme activity that was improved by C2-ceramide prior to LPS exposure alleviated acute lung inflammation. Conversely, AM-specific ablation of PP2ACα exacerbated inflammatory responses to LPS. Mechanistically, PP2ACα negatively regulates LPS-induced cytokine secretion of AMs by NF-κB and MAPK pathways. Together, these findings provide the evidence to guide the development of novel therapeutic options targeting PP2ACα for ARDS/acute lung injury.

Indexed as

AnimalsCytokinesHumansLipopolysaccharidesMacrophages, AlveolarMAP Kinase Signaling SystemNF-kappa BProtective FactorsProtein Phosphatase 2CRespiratory Distress SyndromeCytokinesLipopolysaccharidesNF-kappa BPPM1A protein, humanProtein Phosphatase 2CAcute respiratory distress syndromeAlveolar macrophagesC2-ceramidePP2ACα

Identifiers

PMID30684253
OpenAlexW2914934161

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.