A disintegrin and metalloproteinase with thrombospondin motifs 18 (ADAMTS18) cleaves fibronectin and negatively regulates its fibrillogenesis.

ABSTRACT: Remodeling of the extracellular matrix (ECM) plays a crucial role in the development, maintenance, and repair of all tissues. Therefore, identifying the regulators of this process is essential. Among these, A disintegrin and metalloproteinase with thrombospondin motifs 18 (ADAMTS18) has been implicated in fibronectin (FN) matrix regulation. Knockout of ADAMTS18, either in mouse models or in vitro, was shown to lead to FN accumulation, mutation in epithelial branching, and reduction in endothelial sprouting. However, the mechanisms by which ADAMTS18 influences endothelial-specific functions and the ECM, particularly in the regulation of FN fibrils, remain unclear. In this study, using both siRNA-mediated knockdown and overexpression of ADAMTS18 in primary endothelial cells (ECs), we delinea

SUBMITTER: Barbiera M 

PROVIDER: S-EPMC12666562 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature