Evidence map›Paper›PMID 28739278›Full record

ArticleAntiviral research2017

p38MAPK plays a critical role in induction of a pro-inflammatory phenotype of retinal Müller cells following Zika virus infection.

Shuang Zhu, Huanle Luo, Hua Liu, Yonju Ha, Elizabeth R Mays, Ryan E Lawrence, Evandro Winkelmann, Alan D Barrett, Sylvia B Smith, Min Wang and 2 more

Open access · greenAbstract read
In one paragraph

Article in Antiviral research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. The regulatory roles of STAT3 protein in the pathogenesis of viral infections.Frontiers in cellular and infection microbiology · 2025
    Review
  5. Article
  6. Zika Virus Neuropathogenesis-Research and Understanding.Pathogens (Basel, Switzerland) · 2024
    Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Potential for Protein Kinase Pharmacological Regulation inInternational journal of molecular sciences · 2020
    Review
  18. Article
  19. Review
  20. 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

12 authors at 2 institutions in 1 country.

Shuang ZhuDepartment of Ophthalmology and Visual Sciences, University of Texas Medical Branch, Galveston, TX, 77555, USA.
Huanle LuoDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX, 77555, USA.
Hua LiuDepartment of Ophthalmology and Visual Sciences, University of Texas Medical Branch, Galveston, TX, 77555, USA; Center for Biomedical Engineering, University of Texas Medical Branch, Galveston, TX, 77555, USA.
Yonju HaDepartment of Ophthalmology and Visual Sciences, University of Texas Medical Branch, Galveston, TX, 77555, USA.
Elizabeth R MaysDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX, 77555, USA.
Ryan E LawrenceDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX, 77555, USA.
Evandro WinkelmannDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX, 77555, USA.
Alan D BarrettDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX, 77555, USA; Department of Pathology, University of Texas Medical Branch, Galveston, TX, 77555, USA.
Sylvia B SmithCellular Biology and Anatomy, Augusta University, Augusta, GA, 30912, USA.
Min WangFutraTech Inc., San Diego, CA, 92121, USA.
Tian WangDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX, 77555, USA; Institute for Human Infections and Immunity, University of Texas Medical Branch, Galveston, TX, 77555, USA. Electronic address: ti1wang@utmb.edu.
Wenbo ZhangDepartment of Ophthalmology and Visual Sciences, University of Texas Medical Branch, Galveston, TX, 77555, USA; Institute for Human Infections and Immunity, University of Texas Medical Branch, Galveston, TX, 77555, USA; Neuroscience and Cell Biology, University of Texas Medical Branch, Galveston, TX, 77555, USA. Electronic address: we2zhang@utmb.edu.
The University of Texas Medical Branch at Galveston · USAugusta University · US

Funding

Mechanisms of Retinal Neuronal InjuryR01EY022694 · NEI · UNIVERSITY OF TEXAS MED BR GALVESTON · PI ZHANG, WENBO · 2012 to 2021
$3.8M
Diabetic retinopathy: sigma receptor 1 (??R1) as a novel therapeutic target.R01EY014560 · NEI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI SMITH, SYLVIA B. · 2004 to 2013
$2.7M
Pathogenic Role of EPAC1 Signaling in Retinopathy of PrematurityR01EY026629 · NEI · UNIVERSITY OF TEXAS MED BR GALVESTON · PI ZHANG, WENBO · 2017 to 2021
$2.6M
Rational Development of Candidate Attenuated Flavivirus VaccinesR01AI099123 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI WANG, TIAN · 2013 to 2016
$1.8M
Infectious Diseases and Inflammatory Disorders Training ProgramT35AI078878 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI WANG, TIAN · 2008 to 2025
$701k
NEI NIH HHS R01 EY014560NEI NIH HHS R01 EY022694NEI NIH HHS R01 EY026629NIAID NIH HHS R01 AI099123NIAID NIH HHS T35 AI078878
6 · The paper itself

Abstract

Zika virus (ZIKV) infection has been associated with ocular abnormalities such as chorioretinal atrophy, optic nerve abnormalities, posterior uveitis and idiopathic maculopathy. Yet our knowledge about ZIKV infection in retinal cells and its potential contribution to retinal pathology is still very limited. Here we found that primary Müller cells, the principal glial cells in the retina, expressed a high level of ZIKV entry cofactor AXL gene and were highly permissive to ZIKV infection. In addition, ZIKV-infected Müller cells exhibited a pro-inflammatory phenotype and produced many inflammatory and growth factors. While a number of inflammatory signaling pathways such as ERK, p38MAPK, NF-κB, JAK/STAT3 and endoplasmic reticulum stress were activated after ZIKV infection, inhibition of p38MAPK after ZIKV infection most effectively blocked ZIKV-induced inflammatory and growth molecules. In comparison to ZIKV, Dengue virus (DENV), another Flavivirus infected Müller cells more efficiently but induced much lower pro-inflammatory responses. These data suggest that Müller cells play an important role in ZIKV-induced ocular pathology by induction of inflammatory and growth factors in which the p38MAPK pathway has a central role. Blocking p38MAPK may provide a novel approach to control ZIKV-induced ocular inflammation.

Indexed as

AnimalsCells, CulturedDengue VirusEndoplasmic Reticulum StressEpendymoglial CellsInflammationMicep38 Mitogen-Activated Protein KinasesPhenotypeReceptor Protein-Tyrosine KinasesVirus InternalizationZika Virusp38 Mitogen-Activated Protein KinasesReceptor Protein-Tyrosine KinasesInflammationMüller cellsOcular abnormalitiesp38MAPKZika virus

Identifiers

PMID28739278
PMCPMC5576517
OpenAlexW2737013320

What OpenQuestion holds

Textmetadata
LicenceTDM
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.