RAB5C Increases Endothelial Release of VWF by Regulating Vesicle Trafficking.

ABSTRACT:

Background

Abnormal levels of VWF (von Willebrand Factor) are a risk factor for venous thromboembolism (VTE) and bleeding. Genome-wide association studies for VWF have identified novel candidate genes that may regulate VWF levels in humans, including RAB5C (RAS [rat sarcoma]-associated protein RAB5C). We hypothesized that RAB5C regulates VWF release from endothelial cells.

Methods

We studied the effect of RAB5C on vesicle trafficking in human endothelial cells. We performed CRISPR (clustered regularly interspaced short palindromic repeats) interference targeting 2 genetic variants linked to altered VWF levels and evaluated RAB5C expression by reverse transcription-quantitative polymerase chain reaction. We silenced RAB5C or overexpressed RAB5C wild-type, constitutive

SUBMITTER: Reventun P 

PROVIDER: S-EPMC12823045 | biostudies-literature | 2026 Mar

REPOSITORIES: biostudies-literature