RAB3B facilitates the repair of membrane rupture by enhancing cell tight junctions and material transport

Sequencing of differential genes in patients with normal and premature rupture of membranes revealed the downregulation of RAB3B. Experiments demonstrated that the downregulation of RAB3B led to the loosening of fetal membrane tissues, weakened intercellular connections, increased permeability, and reduced exosome production. Conversely, the upregulation of RAB3B resulted in increased proliferation, migration, and invasion of trophoblast cells, as well as enhanced secretion of vesicles by these cells.