Evidence map›Paper›PMID 40916522›Full record

ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2025

[Exosome-derived miR-1275 mediates IL-38 upregulation in lymphocytes to suppress lipopolysaccharide-induced apoptosis of myocardial cells

Haimei Bo, Xinying Cao, Pingchuan Xing, Zhijun Wang

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Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Haimei BoSchool of Clinical Medicine, North China University of Science and Technology, Tangshan 063000, China.
Xinying CaoAffiliated Hospital of North China University of Science and Technology, Tangshan 063000, China.
Pingchuan XingSchool of Clinical Medicine, North China University of Science and Technology, Tangshan 063000, China.
Zhijun WangAffiliated Hospital of North China University of Science and Technology, Tangshan 063000, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTo investigate the effect of cardiomyocytes-derived exosomes on lipopolysaccharide (LPS)-induced cardiomyocyte injury and its mechanism.

methodsExosomes isolated from rat cardiomyocytes with or without LPS treatment were co-cultured with rat lymphocytes. The lymphocytes with or without exosome treatment were co-cultured with LPS-induced rat cardiomyocytes for 48 h. Cardiomyocyte apoptosis was detected using flow cytometry, and the expressions of apoptosis marker proteins and the PI3K/AKT pathway proteins were detected using Western blotting. The effects of human recombinant IL-38 protein on apoptosis and protein expressions in LPS-induced cardiomyocytes were examined.

resultsCompared with normal cardiomyocyte-derived exosomes, the exosomes from LPS-induced cardiomyocytes significantly enhanced proliferation and increased mRNA and protein expression levels of IL-38 in rat lymphocytes. Bioinformatics analysis suggested that miR-1275 in the exosome played a key role in LPS-induced cardiomyocyte injury, and in dual luciferase reporter gene assay, miR-1275 mimics significantly increased luciferase activity of WT-IL-38. Co-culture with lymphocytes treated with exosomes from LPS-induced cardiomyocytes significantly inhibited apoptosis of LPS-induced cardiomyocytes. Treatment with recombinant IL-38 also effectively lowered apoptosis rate of LPS-induced cardiomyocytes, reduced cellular expression of Bax protein, and increased the protein expression levels of Bcl-2, p-PI3K and p-AKT.

conclusionsmiR-1275 in exosomes derived from LPS-induced cardiomyocytes mediates IL-38 up-regulation expression in lymphocytes to activate the PI3K/AKT pathway and inhibit LPS-induced cardiomyocyte apoptosis.

Indexed as

ApoptosisExosomesInterleukinsLymphocytesMicroRNAsMyocytes, CardiacAnimalsCells, CulturedCoculture TechniquesHumansLipopolysaccharidesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleySignal TransductionInterleukinsLipopolysaccharidesMicroRNAsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktcardiomyocyteexosomesIL-38miR-1275sepsis

Identifiers

PMID40916522
PMCPMC12415573

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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.