Evidence map›Paper›PMID 35589941›Full record

ArticleCommunications biology2022

IL-33 enhances Jagged1 mediated NOTCH1 intracellular domain (NICD) deubiquitination and pathological angiogenesis in proliferative retinopathy.

Deepti Sharma, Shivantika Bisen, Geetika Kaur, Eric C Van Buren, Gadiparthi N Rao, Nikhlesh K Singh

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

19 citing papers in PubMed, 16 citations in OpenAlex.

  1. The Role of the Notch1 Signaling Pathway in the Pathogenesis and Treatment of Diabetic Foot: A Review.Diabetes therapy : research, treatment and education of diabetes and related disorders · 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 2 institutions in 1 country.

Deepti SharmaIntegrative Biosciences Center, Wayne State University, Detroit, MI, 48202, USA.
Shivantika BisenIntegrative Biosciences Center, Wayne State University, Detroit, MI, 48202, USA.
Geetika KaurIntegrative Biosciences Center, Wayne State University, Detroit, MI, 48202, USA.
Eric C Van BurenDepartment of Oncology, Wayne State University School of Medicine, Detroit, MI, 48201, USA.
Gadiparthi N RaoDepartment of Physiology, University of Tennessee Health Science Center, Memphis, TN, 38163, USA.
Nikhlesh K SinghIntegrative Biosciences Center, Wayne State University, Detroit, MI, 48202, USA. nsingh2@wayne.edu.ORCID 0000-0002-3665-6023
Wayne State University · USUniversity of Tennessee Health Science Center · US

Funding

Tumor Biology and Microenvironment (Program 1)P30CA022453 · NCI · WAYNE STATE UNIVERSITY · PI Julie Lynn Boerner · 1985 to 2026
$68.4M
VISION RESEARCH--COREP30EY004068 · NEI · WAYNE STATE UNIVERSITY · PI LINDA D HAZLETT · 1985 to 2026
$13.2M
Phospholipases and retinal angiogenesisR01EY014856 · NEI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI RAO, GADIPARTHI N · 2006 to 2021
$5.0M
CELLULAR MECHANISMS OF PATHOLOGICAL RETINAL NEOVASCULARIZATIONR01EY029709 · NEI · WAYNE STATE UNIVERSITY · PI SINGH, NIKHLESH KUMAR · 2019 to 2023
$1.9M
A stable path for a core based scientist to advance imaging and cytometry in basic and preclinical research at the Karmanos Cancer InstituteR50CA251068 · NCI · WAYNE STATE UNIVERSITY · PI MOIN, KAMIAR · 2020 to 2024
$1.4M
NCI NIH HHS P30 CA022453NCI NIH HHS R50 CA251068NEI NIH HHS P30 EY004068NEI NIH HHS R01 EY014856NEI NIH HHS R01 EY029709
6 · The paper itself

Abstract

Pathological retinal neovascularization (NV) is a clinical manifestation of various proliferative retinopathies, and treatment of NV using anti-VEGF therapies is not selective, as it also impairs normal retinal vascular growth and function. Here, we show that genetic deletion or siRNA-mediated downregulation of IL-33 reduces pathological NV in a murine model of oxygen-induced retinopathy (OIR) with no effect on the normal retinal repair. Furthermore, our fluorescent activated cell sorting (FACS) data reveals that the increase in IL-33 expression is in endothelial cells (ECs) of the hypoxic retina and conditional genetic deletion of IL-33 in retinal ECs reduces pathological NV. In vitro studies using human retinal microvascular endothelial cells (HRMVECs) show that IL-33 induces sprouting angiogenesis and requires NFkappaB-mediated Jagged1 expression and Notch1 activation. Our data also suggest that IL-33 enhances de-ubiquitination and stabilization of Notch1 intracellular domain via its interaction with BRCA1-associated protein 1 (BAP1) and Numb in HRMVECs and a murine model of OIR.

Indexed as

Retinal DiseasesVitreoretinopathy, ProliferativeAnimalsDisease Models, AnimalEndothelial CellsHumansInterleukin-33MiceNeovascularization, PathologicOxygenReceptor, Notch1Interleukin-33NOTCH1 protein, humanOxygenReceptor, Notch1

Identifiers

PMID35589941
PMCPMC9120174
OpenAlexW4280524550

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.