SEARCH · Search PubMed

Results for “EVP”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

4 recordsLinked to original sources

PubMed2026

Protocol for the isolation and characterization of extracellular vesicles and particles from human and murine cell lines.

Cells produce a heterogeneous population of extracellular vesicles and particles (EVPs). Small extracellular vesicles (sEVs or exosomes) are lipid membrane-enclosed vesicles with sizes ranging from 30 to 150 nm. Here, we present a protocol to isolate and characterize EVPs from the conditioned medium of cell lines. We describe steps for cell culture, conditioned media collection, differential ultracentrifugation, and EVP characterization. We then detail procedures for proteomic and biodistribution analyses. For complete details on the use and execution of this protocol, please refer to Yeung et al.1.

Animals↗

PubMed2026

Host metadherin coordinates hepatic lipid metabolism and CD8+ T cell immunity to promote tumor progression.

Cancer progression is systemically influenced by distant organ dysfunction induced by primary tumors, yet how long-distance tumor-organ crosstalk regulates antitumor immunity remains unclear. Here, we identify host metadherin (MTDH) as a critical regulator of tumor-induced immunosuppression and metabolic reprogramming via tumor-liver interactions. Using Mtdh knockout mouse models, we show that concurrent MTDH loss in hepatocytes and CD8+ T cells enhances effector T cell function and suppresses tumor growth and metastasis. Mechanistically, tumor-derived extracellular vesicles and particles (EVPs) activate Kupffer cells to secrete tumor necrosis factor α (TNF-α) and TGF-β, which suppress hepatic PPARα-mediated lipid oxidation via nuclear factor κB (NF-κB) signaling. MTDH loss restores hepatic lipid catabolism, reduces systemic lipid levels, and promotes mitochondrial metabolic reprogramming in CD8+ T cells under lipid-reduced conditions, thereby boosting antitumor immunity. Genetic or pharmacological targeting of MTDH synergizes with anti-PD-1 therapy. These findings establish host MTDH as a key mediator of tumor-liver crosstalk through metabolic and immune interactions, driving systemic cancer progression.

CD8(+) T cells↗

PubMed1979

Determination of pseudofacility in man.

Based on a new method of measuring episcleral venous pressure (EVP), i.e., using the 'air-jet principle' of Krakau et al. (1973), pseudofacility was determined in 20 human eyes. According to Bárány's formula, a mean value of 23.3% of the total facility was found, and a mean value of 16.9% according to Goldmann's formula.

Adult↗

PubMed2025

Identification of molecular markers and exploration of the oncogenic role of exomeres in hepatocellular carcinoma.

Extracellular vesicles and particles (EVPs) serve as functional mediators delivering their cargoes to specific destinations. Exomeres (EMs) represent a newly discovered subset of nanoparticles, with limited understanding of their biophysical characteristics and functionalities. Here, we isolated and studied EMs from different normal and cancer cell lines. Proteomic analysis reveals distinctive features of EMs compared to small extracellular vesicles (sEVs) and identifies galactosamine (N-acetyl)-6-sulfatase (GALNS) and mannosidase alpha class 2B member 1 (MAN2B1) to be expressed in EMs, indicating their potential as specific EM molecular markers. Subsequent investigations into tumor-derived EMs demonstrate their oncogenic properties to support cancer growth and metastasis. Furthermore, analysis of murine hepatocellular carcinoma-derived EM reveals their ability to induce cell cycle progression and metabolic alterations. Collectively, our data highlight the distinct nature of EMs as a nanoparticle subpopulation different from sEVs, with cancer-derived EMs significantly contributing to tumor growth and dissemination.

Carcinoma, Hepatocellular↗