Evidence map›Paper›PMID 34613548›Full record

ArticleInflammation2022

PDCD4 Simultaneously Promotes Microglia Activation via PDCD4-MAPK-NF-κB Positive Loop and Facilitates Neuron Apoptosis During Neuroinflammation.

Quan Chen, Hongjian Lu, Chengwei Duan, Xiangyang Zhu, Yi Zhang, Mengmeng Li, Dongmei Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

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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

7 authors at 1 institution in 1 country.

Quan Chen *Medical Research Center, Affiliated Hospital 2 of Nantong University, Nantong, 226001, People's Republic of China.
Hongjian Lu *Medical Research Center, Affiliated Hospital 2 of Nantong University, Nantong, 226001, People's Republic of China.
Chengwei DuanMedical Research Center, Affiliated Hospital 2 of Nantong University, Nantong, 226001, People's Republic of China.
Xiangyang ZhuNeurology Department, Affiliated Hospital 2 of Nantong University, 226001, Nantong, People's Republic of China.
Yi ZhangNeurosurgery Department, Affiliated Hospital 2 of Nantong University, 226001, Nantong, People's Republic of China.
Mengmeng LiMedical Research Center, Affiliated Hospital 2 of Nantong University, Nantong, 226001, People's Republic of China.
Dongmei ZhangMedical Research Center, Affiliated Hospital 2 of Nantong University, Nantong, 226001, People's Republic of China. zdm_ntyy@163.com.ORCID http://orcid.org/0000-0002-4132-7363
Nantong University · CN

Funding

Nantong Science and Technology Project JC2019031 and JCZ20078Nantong University School-level Fund Project 2019JZ005Scientific Research Project of 333 Project in Jiangsu Province BRA2018224Scientific Research Project of Health Commission of Jiangsu Province H2018035Scientific Research Project of Health Commission of Jiangsu Province LGY2017042the Top Six Types of Financial Assistance of Jiangsu Province 2019-WSW-199
6 · The paper itself

Abstract

Neuroinflammation and neuron injury are common features of the central nervous system (CNS) diseases. It is of great significance to identify their shared key regulatory molecules and thus explore the potential therapeutic targets. Programmed cell death factor 4 (PDCD4), an apoptosis-related molecule, extensively participates in tumorigenesis and inflammatory diseases, but its expression and biological function during CNS neuroinflammation remain unclear. In the present study, utilizing the lipopolysaccharide (LPS)-induced neuroinflammation model in mice, we reported an elevated expression of PDCD4 both in injured neurons and activated microglia of the inflamed brain. A similar change in PDCD4 expression was observed in vitro in the microglial activation model. Silencing PDCD4 by shRNA significantly inhibited the phosphorylation of MAPKs (p38, ERK, and JNK), prevented the phosphorylation and nuclear translocation of NF-κB p65, and thus attenuated the LPS-induced microglial inflammatory activation. Interestingly, LPS also required the MAPK/NF-κB signaling activation to boost PDCD4 expression in microglia, indicating the presence of a positive loop. Moreover, a persistent elevation of PDCD4 expression was detected in the H

Indexed as

AnimalsApoptosisApoptosis Regulatory ProteinsBiomarkersLipopolysaccharidesMaleMiceMice, Inbred C57BLMicrogliaMitogen-Activated Protein Kinase KinasesNeuroinflammatory DiseasesNeuronsNF-kappa BRandom AllocationRNA-Binding ProteinsApoptosis Regulatory ProteinsBiomarkersLipopolysaccharidesMitogen-Activated Protein Kinase KinasesNF-kappa BPdcd4 protein, mouseRNA-Binding Proteinsmicrogliamitogen-activated protein kinases (MAPKs)neuroinflammationneuron apoptosisnuclear factor-κB (NF-κB)programmed cell death factor 4 (PDCD4)

Identifiers

PMID34613548
OpenAlexW3204205200

What Socratic 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 Socratic graph.