Evidence map›Paper›PMID 24833710›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2014

Cannabinoid-induced autophagy regulates suppressor of cytokine signaling-3 in intestinal epithelium.

Luan C Koay, Rachael J Rigby, Karen L Wright

Registry-linked trialAbstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06842316 (In Vitro Effects of Phytocannabinoids on Immune Response and Autophagy During Chronic Immune-mediated Inflammatory Diseases), which is not on this map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.6field-weighted citation impact, top 12% 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.

NCT06842316 recruitingnot on this mapstarted 2025, after this paper: background citation

In Vitro Effects of Phytocannabinoids on Immune Response and Autophagy During Chronic Immune-mediated Inflammatory Diseases

TypeobservationalSponsorCentre Hospitalier Régional d'OrléansRan2025 to 2027Enrolled100ConditionsInflammatory Disorder of Immune System, Spondylitis, Ankylosing, Arthritis, Rheumatoid, Arthritis, PsoriaticArms1 blood sample, 40 mL (collection during a blood test, part of the standard of care for this disease)
3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 38 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

3 authors at 1 institution in 1 country.

Luan C KoayDivision of Biomedical and Life Sciences, Faculty of Health and Medicine, Lancaster University, Lancaster, United Kingdom.
Rachael J RigbyDivision of Biomedical and Life Sciences, Faculty of Health and Medicine, Lancaster University, Lancaster, United Kingdom.
Karen L WrightDivision of Biomedical and Life Sciences, Faculty of Health and Medicine, Lancaster University, Lancaster, United Kingdom karen.wright@lancaster.ac.uk.
Lancaster University · GB

Funding

Medical Research Council G1100211
6 · The paper itself

Abstract

Autophagy is a catabolic process involved in homeostatic and regulated cellular protein recycling and degradation via the lysosomal degradation pathway. Emerging data associate impaired autophagy, increased activity in the endocannabinoid system, and upregulation of suppressor of cytokine signaling-3 (SOCS3) protein expression during intestinal inflammation. We have investigated whether these three processes are linked. By assessing the impact of the phytocannabinoid cannabidiol (CBD), the synthetic cannabinoid arachidonyl-2'-chloroethylamide (ACEA), and the endocannabinoid N-arachidonoylethanolamine (AEA) on autophagosome formation, we explored whether these actions were responsible for cyclic SOCS3 protein levels. Our findings show that all three cannabinoids induce autophagy in a dose-dependent manner in fully differentiated Caco-2 cells, a model of mature intestinal epithelium. ACEA and AEA induced canonical autophagy, which was cannabinoid type 1 receptor-mediated. In contrast, CBD was able to bypass the cannabinoid type 1 receptor and the canonical pathway to induce autophagy, albeit to a lesser extent. Functionally, all three cannabinoids reduced SOCS3 protein expression, which was reversed by blocking early and late autophagy. In conclusion, the regulatory protein SOCS3 is regulated by autophagy, and cannabinoids play a role in this process, which could be important when therapeutic applications for the cannabinoids in inflammatory conditions are considered.

Indexed as

Arachidonic AcidsAutophagyBlotting, WesternCaco-2 CellsCannabidiolCannabinoid Receptor AgonistsCannabinoidsDose-Response Relationship, DrugDown-RegulationEndocannabinoidsHumansIntestinal MucosaMicroscopy, ConfocalPolyunsaturated AlkamidesReceptor, Cannabinoid, CB1RNA InterferenceanandamideArachidonic Acidsarachidonyl-2-chloroethylamideCannabidiolCannabinoid Receptor AgonistsCannabinoidsCNR1 protein, humanEndocannabinoidsPolyunsaturated AlkamidesReceptor, Cannabinoid, CB1SOCS3 protein, humanSuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling Proteinsautophagycannabinoidsuppressor of cytokine signaling-3

Identifiers

PMID24833710
PMCPMC4101681
OpenAlexW2064373390

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.