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Proinflammatory stress activates neutral sphingomyelinase 2-based generation of a ceramide-enriched ß-cell ev subpopulation
Journal article   Open access   Peer reviewed

Proinflammatory stress activates neutral sphingomyelinase 2-based generation of a ceramide-enriched ß-cell ev subpopulation

Jerry Xu, Irene Amalaraj, Andre De Oliveira, Arianna Harris-Kawano, Jacob R. Enriquez, Raghavendra G. Mirmira, Josie G. Eder, Meagan C. Burnet, Ivo Díaz Ludovico, Javier E. Flores, …
Diabetes (New York, N.Y.), Vol.74(11), pp.1964-1975
11/01/2025
DOI: 10.2337/db24-0341
PMCID: PMC12585158
PMID: 40896819
url
https://scholarworks.indianapolis.iu.edu/bitstreams/3d197a70-509c-45a8-abae-be6548cf5fa9/downloadView
Open Access

Abstract

β-Cell extracellular vesicles (EVs) play a role as paracrine effectors in islet health, yet mechanisms connecting β-cell stress to changes in EV cargo and potential impacts on diabetes remain poorly defined. We hypothesized that β-cell inflammatory stress engages neutral sphingomyelinase 2 (nSMase2)-dependent EV formation pathways, generating ceramide-enriched small EVs that could impact surrounding β-cells. Consistent with this, proinflammatory cytokine treatment of INS-1 β-cells and human islets concurrently increased β-cell nSMase2 and ceramide abundance, as well as small EV ceramide species. Direct chemical activation or genetic knockdown of nSMase2, chemical treatment to inhibit cell death pathways, or treatment with a glucagon-like peptide-1 (GLP-1) receptor agonist also modulated β-cell EV ceramide. RNA sequencing of ceramide-enriched EVs identified a distinct set of miRNAs linked to β-cell function and identity. EV treatment from cytokine-exposed parent cells inhibited peak glucose-stimulated insulin secretion in wild-type recipient cells; this effect was abrogated when using EVs from nSMase2 knockdown parent cells. Finally, plasma EVs in children with recent-onset type 1 diabetes showed increases in multiple ceramide species. These findings highlight nSMase2 as a regulator of β-cell EV cargo and identify ceramide-enriched EV populations as a contributor to EV-related paracrine signaling under conditions of β-cell inflammatory stress and death.

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