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Proteomic profiling of extracellular vesicles derived from TGF-β-treated mouse aortic endothelial cells

ABSTRACT: Endothelial cell dysfunction plays a critical role in the pathogenesis of chronic allograft dysfunction and tissue fibrosis. Autophagy deficiency in endothelial cells has been implicated in altered extracellular vesicle (EV) cargo composition, which may contribute to pericyte-to-myofibroblast transition. In this study, we performed quantitative proteomic analysis of EVs isolated from the culture supernatant of mouse aortic endothelial cells (MAECs) treated with or without TGF-β to identify differentially expressed proteins. EVs were isolated by ultracentrifugation and characterized according to MISEV2023 guidelines. LC-MS/MS-based proteomics was performed to compare the protein profiles between control (NC) and TGF-β-treated groups. This dataset provides insights into the molecular cargo alterations in endothelial cell-derived EVs under pro-fibrotic conditions.

ORGANISM(S): Mus Musculus

SUBMITTER: Ruoyun Tan

PROVIDER: PXD072389 | iProX | Wed Dec 24 00:00:00 GMT 2025

REPOSITORIES: iProX

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Project description:Tumor microenvironment contains various components including cancer cells, tumor vessels, and cancer associated fibroblasts (CAFs), comprising of tumor-promoting myofibroblasts and tumor-suppressing fibroblasts. Multiple lines of evidence indicated that transforming growth factor-β (TGF-β) induces the formation of myofibroblasts and other types of mesenchymal (non-myofibroblastic) cells from endothelial cells. Recent reports showed that fibroblast growth factor 2 (FGF2) modulates TGF-β-induced mesenchymal transition of endothelial cells, but the molecular mechanisms regarding the signals that control the transcriptional networks during the formation of different groups of fibroblasts remain largely unclear. Here, we studied the roles of FGF2 during the regulation of TGF-β-induced mesenchymal transition of tumor endothelial cells (TECs). We demonstrated that auto/paracrine FGF signals in TECs inhibit TGF-β-induced endothelial-to-myofibroblast transition (End-MyoT), leading to suppressed formation of contractile myofibroblast cells, but on the other hand can also collaborate with TGF-β in promoting the formation of active fibroblastic cells which have migratory and proliferative properties. FGF2 modulated TGF-β-induced formation of myofibroblastic and non-myofibroblastic cells from TECs via transcriptional regulation of the array of various mesenchymal markers and growth factors. Furthermore, we observed that TECs treated with TGF-β were more competent in promoting in vivo tumor growth than TECs treated with TGF-β and FGF2. Mechanistically, we showed that Elk1 mediated this FGF2-induced inhibition of End-MyoT via inhibition of TGF-β-induced transcriptional activation of α-SMA promoter by myocardin-related transcription factor (MRTF)-A. Our data suggest that TGF-β and FGF2 oppose and cooperate with each other during the formation of myofibroblastic and non-myofibroblastic cells from TECs to determine the characteristics of the mesenchymal cells in tumor microenvironment. Identification of marker genes for TGF-β-induced endothelial-to-myofibroblast transition

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Proteomic profiling of extracellular vesicles derived from TGF-β-treated mouse aortic endothelial cells

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