Evidence map›Paper›PMID 33336085›Full record

ArticleBiochemistry and biophysics reports2020

Phospholipase C epsilon mediates cytokine cascade induced by acute disruption of epidermal permeability barrier in mice.

Jing Zhang, Jiangmei Wu, Mengke Sun, Shuchang Zhang, Junkai Huang, Maoqiang Man, Lizhi Hu

Open access · goldAbstract read
In one paragraph

Article in Biochemistry and biophysics reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 35% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Phospholipases: Where Do We Stand?Methods in molecular biology (Clifton, N.J.) · 2027
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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 2 institutions in 2 countries.

Jing ZhangImmunology Department, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Medical University, Tianjin, 300070, China.
Jiangmei WuDepartment of Pathogen Biology and Immunology, Basic Medical College, Tianjin Medical University, Tianjin, 300070, China.
Mengke SunDepartment of Pathogen Biology and Immunology, Basic Medical College, Tianjin Medical University, Tianjin, 300070, China.
Shuchang ZhangDepartment of Pathogen Biology and Immunology, Basic Medical College, Tianjin Medical University, Tianjin, 300070, China.
Junkai HuangDepartment of Pathogen Biology and Immunology, Basic Medical College, Tianjin Medical University, Tianjin, 300070, China.
Maoqiang ManDermatology Services, University of California San Francisco, San Francisco, CA, 94121, USA.
Lizhi HuImmunology Department, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Medical University, Tianjin, 300070, China.
Tianjin Medical University · CNUniversity of California, San Francisco · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Disruption of epidermal barrier is an important trigger in abnormal cutaneous inflammation. Phospholipase C epsilon (PLCε), a Ras/Rap1 effector, is essential for regulating cytokines production in different types of skin inflammation. Our previous studies have demonstrated that elevated expression of PLCε participates in the psoriasis-like inflammation in PLCε overexpressing transgenic mice model, while the reduction in PLCε expression attenuates inflammatory responses in either TPA- or DNFB-induced cutaneous inflammation. Here, we determined the role of PLCε in cutaneous inflammation induced by acute abrogation of epidermal permeability barrier. In comparison to wild type controls, PLCε KO mice exhibited reduced ear swelling and infiltration of granulocytes after tape-stripping. Moreover, expression levels of pro-inflammatory cytokines (IL-1α, IL-1β), chemokines (CXCL-1, CXCL-2, CCL20), and antimicrobial peptides (S100 proteins, MBD3) were lower in PLCε-deficient versus wild type mice. Likewise, expression levels of cytokines and chemokines were also lower in PLCε deficient keratinocytes and fibroblasts following IL-22 stimulation

Indexed as

Barrier functionBMP4, bone morphogenetic protein 4CCL20, chemokine (C–C motif) ligand 20CXCL, chemokine (C-X-C motif) ligandFLG, filaggrinHEK, human epidermal keratinocytesIL-22IVL, involucrinK15, keratin 15K1, keratin 1LHX2, LIM homeobox 2LOR, loricrinMBD, murine beta defensinPLCεPLCε, phospholipase C epsilonPMA, Phorbol-12-myristate-13-acetatePsoriasisSHH, sonic hedgehogSkin inflammationSOX9, SRY-box 9SPT1, serine palmitoyltransferase 1STAT3, transducer and activator of transcription 3TGF, transforming growth factorTLR2, toll like receptor 2TNF, tumor necrosis factor

Identifiers

PMID33336085
PMCPMC7733008
OpenAlexW3110906631

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.