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PXD067178

PXD067178 is an original dataset announced via ProteomeXchange.

Dataset Summary
TitleEndothelial cell-derived apoptotic bodies modulate innate and adaptive immune responses during inflammation
DescriptionEndothelial cells (ECs) act as gatekeepers and signalling hubs that coordinate communication between blood vessels and surrounding tissues by regulating vascular tone, immune responses and numerous other physiological processes. During vascular inflammation commonly associated with aging, atherosclerosis, diabetes and autoimmunity, a range of biological, environmental and physical stressors can induce activation and apoptosis of ECs. Apoptotic bodies (ApoBDs) are large (~1–5 μm), membrane‑bound extracellular vesicles generated solely through apoptotic cell disassembly, that are increasingly recognised as mediators of intercellular communication via the transfer of bioactive molecules to target cells. Although EC apoptosis is a central feature of vascular inflammatory disorders, the formation of EC‑derived ApoBDs and their immunomodulatory roles when formed in an inflammatory environment, remains poorly defined. This study aimed to characterise the functional properties of EC‑derived ApoBDs generated under inflammatory conditions in vitro. A proteomics analysis of EC‑derived ApoBDs revealed that EC‑ApoBDs generated during inflammation (‘iApoBDs’) were enriched in inflammatory cytokines/chemokines, adhesion molecules and antigen presentation machinery compared with non inflammatory (‘ApoBD’) controls. Functionally, iApoBDs promoted monocyte chemotaxis via the release of MCP-1, while altered expression of the adhesion molecule ICAM 1 enhanced efferocytosis by macrophages in vitro and in vivo. Furthermore, iApoBDs generated from antigen pulsed HUVECs promoted IFN‑𝛾 expression by peptide specific CD8+ T cells in an in vitro model of antigen presentation. These findings demonstrate that within an inflammatory setting, apoptotic ECs can participate in continued communication with their environment via the generation of ApoBDs, thereby modulating innate and adaptive immune processes. The formation of ApoBDs by ECs may serve as a target for therapeutic interventions in inflammatory vascular diseases.
HostingRepositoryPRIDE
AnnounceDate2025-10-20
AnnouncementXMLSubmission_2025-10-19_16:39:18.048.xml
DigitalObjectIdentifier
ReviewLevelPeer-reviewed dataset
DatasetOriginOriginal dataset
RepositorySupportUnsupported dataset by repository
PrimarySubmitterCaitlin Vella
SpeciesList scientific name: Homo sapiens (Human); NCBI TaxID: NEWT:9606;
ModificationListacetylated residue; monohydroxylated residue; deamidated residue; iodoacetamide derivatized residue
InstrumentOrbitrap Eclipse
Dataset History
RevisionDatetimeStatusChangeLog Entry
02025-08-10 22:39:44ID requested
12025-10-19 16:39:19announced
Publication List
Vella CL, Fonseka P, Grant EJ, Rutter SF, Abeid DY, Ozkocak DC, Nguyen TK, Vinh A, Paone S, Drummond GR, Sobey CG, Gras S, Hulett MD, Mathivanan S, Poon IKH, Baxter AA, Endothelial cell-derived apoptotic bodies modulate innate and adaptive immune responses during inflammation. Cell Commun Signal, 23(1):418(2025) [pubmed]
10.1186/s12964-025-02382-x;
Keyword List
submitter keyword: Human, LC-MSMS, Endothelial, Inflammation Apoptosis
Contact List
Amy Baxter
contact affiliationDepartment of Biochemistry and Chemistry, Centre for Cardiovascular Biology and Disease Research, La Trobe Institute for Molecular Science, School of Agriculture, Biomedicine and Environment, La Trobe University, Bundoora, Victoria 3086, Australia
contact emaila.baxter@latrobe.edu.au
lab head
Caitlin Vella
contact affiliationLa Trobe Institute for Molecular Sciences
contact emailc.vella@latrobe.edu.au
dataset submitter
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