Evidence map›Paper›PMID 35171433›Full record

ArticleNeurochemical research2022

ER Stress is Involved in Mast Cells Degranulation via IRE1α/miR-125/Lyn Pathway in an Experimental Intracerebral Hemorrhage Mouse Model.

Zhengyu Yang, Juan Huang, Yuhui Liao, Shengwei Gan, Shujuan Zhu, Shiye Xu, Yue Shu, Weitian Lu

Abstract read
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In one paragraph

Article in Neurochemical research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 18% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.

  1. Pooled it
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  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
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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

8 authors at 1 institution in 1 country.

Zhengyu Yang *Department of Anatomy & Institute of Neuroscience, Basic Medical College, Chongqing Medical University, Chongqing, 400016, China.
Juan Huang *Department of Anatomy & Institute of Neuroscience, Basic Medical College, Chongqing Medical University, Chongqing, 400016, China.
Yuhui LiaoDepartment of Anatomy & Institute of Neuroscience, Basic Medical College, Chongqing Medical University, Chongqing, 400016, China.
Shengwei GanDepartment of Anatomy & Institute of Neuroscience, Basic Medical College, Chongqing Medical University, Chongqing, 400016, China.
Shujuan ZhuDepartment of Anatomy & Institute of Neuroscience, Basic Medical College, Chongqing Medical University, Chongqing, 400016, China.
Shiye XuDepartment of Anatomy & Institute of Neuroscience, Basic Medical College, Chongqing Medical University, Chongqing, 400016, China.
Yue ShuDepartment of Anatomy & Institute of Neuroscience, Basic Medical College, Chongqing Medical University, Chongqing, 400016, China.
Weitian LuDepartment of Anatomy & Institute of Neuroscience, Basic Medical College, Chongqing Medical University, Chongqing, 400016, China. weitianlu@cqmu.edu.cn.ORCID http://orcid.org/0000-0001-8242-2327
Chongqing Medical University · CN

Funding

National Natural Science Foundation of China NSFC 81601051National Natural Science Foundation of China NSFC 82171457
6 · The paper itself

Abstract

The degranulation of mast cells accounts for the development of neuroinflammation following intracerebral hemorrhage (ICH). Inhibition of IRE1α, a sensor signaling protein related to endoplasmic reticulum stress, has been shown to exert anti-inflammatory effects in several neurological diseases. The objective of this study was to investigate the effects of IRE1α inhibition on mast cells degranulation in an ICH mouse model and to explore the contribution of miR-125/Lyn pathway in IRE1α-mediated mast cells degranulation. Male mice were subjected to ICH by intraparenchymal injection of autologous blood. STF083010, an inhibitor of IRE1α, was administered intranasally at 1 h after ICH induction. AntimiR-125 was delivered by intracerebroventricular (i.c.v.) injection prior to ICH induction to elucidate the possible mechanisms. Western blot analysis, immunofluorescence staining, neurological test, hematoma volume, brain water content, toluidine blue staining and reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR) were performed. Endogenous phosphorylated IRE1α (p-IRE1α), tryptase, interleukin-17A (IL-17A), tumor necrosis factor α (TNF-α) and tryptase mRNA were increased in time dependent manner while miR-125b-2-3p was decreased after ICH. Inhibition of IRE1α, with STF083010, remarkably reduced brain water content, improved neurological function, decreased hematoma volume, upregulated the expression of miR-125b-2-3p, decreased the number of mast cells, and downregulated the protein expression of Lyn kinase, XBP1s (spliced X-box binding protein-1), tryptase, IL-17A and TNF-α. The downregulation of Lyn kinase, tryptase, IL-17A, TNF-α, and decreased mast cells number were reversed by antimiR-125. The present findings demonstrate that IRE1α inhibition attenuates mast cells degranulation and neuroinflammation, at least partially, through IRE1α/miR-125/Lyn signaling pathway after ICH.

Indexed as

EndoribonucleasesMicroRNAsAnimalsCerebral HemorrhageDisease Models, AnimalEndoplasmic Reticulum StressHematomaInterleukin-17MaleMast CellsMiceProtein Serine-Threonine Kinasessrc-Family KinasesTryptasesTumor Necrosis Factor-alphaWaterEndoribonucleasesInterleukin-17lyn protein-tyrosine kinaseMicroRNAsProtein Serine-Threonine Kinasessrc-Family KinasesTryptasesTumor Necrosis Factor-alphaWaterIntracerebral hemorrhageIRE1αLynMast cellmiR-125Neuroinflammation

Identifiers

PMID35171433
OpenAlexW4212871563

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.