Evidence map›Paper›PMID 33859296›Full record

ArticleScientific reports2021

Ceramide kinase regulates TNF-α-induced immune responses in human monocytic cells.

Fatema Al-Rashed, Zunair Ahmad, Ashley J Snider, Reeby Thomas, Shihab Kochumon, Motasem Melhem, Sardar Sindhu, Lina M Obeid, Fahd Al-Mulla, Yusuf A Hannun and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

32 citing papers in PubMed, 42 citations in OpenAlex.

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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

11 authors at 3 institutions in 3 countries.

Fatema Al-RashedImmunology & Microbiology Department, Dasman Diabetes Institute, Al-Soor Street, Dasman, P.O. Box 1180, 15462, Kuwait, Kuwait.
Zunair AhmadRoyal College of Surgeons in Ireland, Busaiteen, Bahrain.
Ashley J SniderStony Brook Cancer Center and Department of Medicine, Stony Brook University, Stony Brook, NY, 11794, USA.
Reeby ThomasImmunology & Microbiology Department, Dasman Diabetes Institute, Al-Soor Street, Dasman, P.O. Box 1180, 15462, Kuwait, Kuwait.
Shihab KochumonImmunology & Microbiology Department, Dasman Diabetes Institute, Al-Soor Street, Dasman, P.O. Box 1180, 15462, Kuwait, Kuwait.
Motasem MelhemGenetics and Bioinformatics Department, Dasman Diabetes Institute, Kuwait, Kuwait.
Sardar SindhuAnimal and Imaging Core Facility, Dasman Diabetes Institute, Kuwait, Kuwait.
Lina M ObeidStony Brook Cancer Center and Department of Medicine, Stony Brook University, Stony Brook, NY, 11794, USA.
Fahd Al-MullaGenetics and Bioinformatics Department, Dasman Diabetes Institute, Kuwait, Kuwait.
Yusuf A HannunStony Brook Cancer Center and Department of Medicine, Stony Brook University, Stony Brook, NY, 11794, USA.
Rasheed AhmadImmunology & Microbiology Department, Dasman Diabetes Institute, Al-Soor Street, Dasman, P.O. Box 1180, 15462, Kuwait, Kuwait. rasheed.ahmad@dasmaninstitute.org.
Dasman Diabetes Institute · KWStony Brook University · USRoyal College of Surgeons in Ireland - Bahrain · BH

Funding

Sphingolipids in Cancer Therapy and AngiogenesisP01CA097132 · NCI · STATE UNIVERSITY NEW YORK STONY BROOK · PI YUSUF AWNI HANNUN · 2003 to 2026
$30.8M
NCI NIH HHS P01 CA097132
6 · The paper itself

Abstract

Ceramide kinase (CERK) phosphorylates ceramide to produce ceramide-1-phosphate (C1P), which is involved in the development of metabolic inflammation. TNF-α modulates inflammatory responses in monocytes associated with various inflammatory disorders; however, the underlying mechanisms remain not fully understood. Here, we investigated the role of CERK in TNF-α-induced inflammatory responses in monocytes. Our results show that disruption of CERK activity in monocytes, either by chemical inhibitor NVP-231 or by small interfering RNA (siRNA), results in the defective expression of inflammatory markers including CD11c, CD11b and HLA-DR in response to TNF-α. Our data show that TNF-α upregulates ceramide phosphorylation. Inhibition of CERK in monocytes significantly reduced the secretion of IL-1β and MCP-1. Similar results were observed in CERK-downregulated cells. TNF-α-induced phosphorylation of JNK, p38 and NF-κB was reduced by inhibition of CERK. Additionally, NF-κB/AP-1 activity was suppressed by the inhibition of CERK. Clinically, obese individuals had higher levels of CERK expression in PBMCs compared to lean individuals, which correlated with their TNF-α levels. Taken together, these results suggest that CERK plays a key role in regulating inflammatory responses in human monocytes during TNF-α stimulation. CERK may be a relevant target for developing novel therapies for chronic inflammatory diseases.

Indexed as

CeramidesHumansInflammationMolecular Targeted TherapyMonocytesPhosphorylationPhosphotransferases (Alcohol Group Acceptor)THP-1 CellsTumor Necrosis Factor-alphaceramide kinaseCeramidesPhosphotransferases (Alcohol Group Acceptor)Tumor Necrosis Factor-alpha

Identifiers

PMID33859296
PMCPMC8050074
OpenAlexW3126595801

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.