Evidence map›Paper›PMID 29287085›Full record

ArticlePloS one2017

Loss of TLR4 in mouse Müller cells inhibits both MyD88-dependent and -independent signaling.

Li Liu, Jena J Steinle

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 25% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
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  7. IL-4-secreting CD40LInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
  8. Chondrosarcoma of the spine-a case report.Wiener medizinische Wochenschrift (1946) · 2023
    Article
  9. Article
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  11. The innate immune system in diabetic retinopathy.Progress in retinal and eye research · 2021
    Review
  12. Article
  13. Review
  14. Article
  15. Conditional deletion of Des1 in the mouse retina does not impair the visual cycle in cones.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  16. Article
  17. Article
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

2 authors at 1 institution in 1 country.

Li LiuDepartment of Anatomy and Cell Biology, Wayne State University School of Medicine, Detroit, MI, United States of America.
Jena J SteinleDepartment of Anatomy and Cell Biology, Wayne State University School of Medicine, Detroit, MI, United States of America.ORCID 0000-0002-7539-2892
Wayne State University · US

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
VISION RESEARCH--COREP30EY004068 · NEI · WAYNE STATE UNIVERSITY · PI LINDA D HAZLETT · 1985 to 2026
$13.2M
Mechanisms of TNFalpha-Induced Insulin Resistance in Retinal CellsR01EY022330 · NEI · WAYNE STATE UNIVERSITY · PI STEINLE, JENA J · 2013 to 2017
$1.5M
NEI NIH HHS P30 EY004068NEI NIH HHS R01 EY022330NIDDK NIH HHS P30 DK020572NIH HHS P30EY04068NIH HHS R01EY022330
6 · The paper itself

Abstract

Müller cells are key to metabolic and ionic regulation in the retina. They also produce a number of inflammatory mediators and are significantly affected in diabetic retinopathy. To investigate the role of toll-like receptor 4 (TLR4) in retinal Müller cells, we crossed TLR4 floxed with PDGFRα-Cre mice to eliminate TLR4 in retinal Müller cells. We performed Western blotting and ELISA analyses to determine whether loss of TLR4 affected myeloid differentiation primary response protein (MyD88)-dependent or -independent signaling, leading to reduced levels of tumor necrosis factor alpha (TNFα) and interleukin 1 beta (IL1β) in whole retinal lysates from the TLR4 floxed and TLR4-PDGFRα-Cre mice. Data show that TLR4-PDGFRα-Cre mice have reduced levels of both the MyD88-dependent and -independent signaling pathways. These studies confirm successful development of a Müller cell-specific TLR4 knockout mouse colony. These mice have reduced MyD88-dependent and -independent signaling pathway proteins, as well as reduced TNFα and IL1β levels. These mice can be used to dissect TLR4 signaling in disorders affecting retinal Müller cells.

Indexed as

Signal TransductionAnimalsBlotting, WesternEnzyme-Linked Immunosorbent AssayEpendymoglial CellsInterleukin-1betaMiceMice, TransgenicMyeloid Differentiation Factor 88Toll-Like Receptor 4Tumor Necrosis Factor-alphaInterleukin-1betaMyd88 protein, mouseMyeloid Differentiation Factor 88Tlr4 protein, mouseToll-Like Receptor 4Tumor Necrosis Factor-alpha

Identifiers

PMID29287085
PMCPMC5747480
OpenAlexW2779577500

What OpenQuestion holds

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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.