Evidence map›Paper›PMID 32435966›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2020

The protective effects of phoenixin-14 against lipopolysaccharide-induced inflammation and inflammasome activation in astrocytes.

Jian Wang, Bo Zheng, Shu Yang, Xiaoying Tang, Jianhong Wang, Dong Wei

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In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.3field-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

31 citing papers in PubMed, 48 citations in OpenAlex.

  1. HMGB1 as a danger signal in vascular remodeling.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026
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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

6 authors at 1 institution in 1 country.

Jian WangDepartment of Neurology, Yaan People's Hospital, Yaan, 625000, Sichuan, China.
Bo ZhengDepartment of Neurology, Yaan People's Hospital, Yaan, 625000, Sichuan, China.
Shu YangDepartment of Neurology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Qingyang District, 32#W. Sec 2, 1st Ring Rd, Chengdu, 610000, Sichuan, China.
Xiaoying TangDepartment of Neurology, The People's Hospital of Lezhi, Ziyang, 641300, Sichuan, China.
Jianhong WangDepartment of Neurology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Qingyang District, 32#W. Sec 2, 1st Ring Rd, Chengdu, 610000, Sichuan, China. jianhw21@163.com.ORCID http://orcid.org/0000-0003-0806-233X
Dong WeiDepartment of Neurology, The People's Hospital of Lezhi, Ziyang, 641300, Sichuan, China.
University of Electronic Science and Technology of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionNeuroinflammation is a key aspect of various injuries and diseases of the central nervous system and brain, including stroke, Alzheimer's, Parkinson's, multiple sclerosis, etc. Phoenixin-14 is a naturally occurring pleiotropic peptide involved in reproduction, anxiety, pain, and other functions. MATERIALS AND

methodsPrimary astrocytes were isolated from new-born pups of c57bl/6 mice. The gene expression of GPR173, CHOP, and GADD34 was measured by real-time PCR. Protein expression was assessed by western blot analysis. Secretions of IL-1β and IL-18 were determined by ELISA.

resultsPhoenixin-14 (PNX-14) is a ligand for the G protein-coupled receptor GPR173, which we demonstrate to be expressed in astrocytes and suppressed by exposure to lipopolysaccharide (LPS). Endoplasmic reticulum (ER) stress resulting from injury or disease leads to the unfolded protein response, which is mediated by the activation of transcription factors including eIF-2α, ATF4, and CHOP, and regulated by GADD34. ER stress also leads to a robust neuroinflammatory response, which is mediated by HMGB1-induced activation of the NLRP3 inflammasome and subsequent production of IL-1β and IL-18. In the present study, we demonstrate that PNX-14 could attenuate LPS-induced ER stress response and NLRP3 inflammasome activation in mouse cerebral astrocytes. Our findings show that PNX-14 could suppress the production of ROS as well as the decrease in SOD induced by LPS. PNX-14 also inhibited HMGB1-mediated NLRP3 inflammasome activation and production of IL-1β and IL-18. Through a GPR173 siRNA knockdown experiment, we further demonstrate that GPR173 knockdown abolished the effects of PNX-14 on LPS-induced NLRP3 expression and IL-18 production.

conclusionThese findings suggest that PNX-14 may have potential in the treatment of neuroinflammation.

Indexed as

AstrocytesInflammasomesInflammationPeptidesAnimalsCells, CulturedEndoplasmic Reticulum StressLipopolysaccharidesMembrane ProteinsMiceMice, Inbred C57BLMitochondrial ProteinsNLR Family, Pyrin Domain-Containing 3 ProteinOxidative StressReceptors, G-Protein-CoupledGPR173 protein, mouseInflammasomesLipopolysaccharidesMembrane ProteinsMitochondrial ProteinsNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mousePeptidesReceptors, G-Protein-CoupledSmim20 protein, mouseAstrocytesATF6Caspase-1Caspase-11CHOP(eIF-2α)/ATF4GADD34LipopolysaccharideNeuroinflammationNLRP3 inflammasomePhoenixin-14

Identifiers

PMID32435966
OpenAlexW3026991975

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.