Oncostatin M-driven leak in human endothelial cells with preserved tight junctions

Oncostatin M drives a previously unrecognized vascular leak in endothelial cells recovered from critically ill children by forming narrow nanoscale channels around intact tight junctions.

• Why it matters: Acute critical illness involves barrier failure and organ dysfunction, yet therapies based on cultured-cell junction disruption have largely failed because in vivo endothelial responses remain unclear.
• What they did: Endothelial cells from critically ill children were profiled, and oncostatin M–induced permeability was mapped to nanoscale channel formation requiring JAK1 signaling through ERK1 and AKT1 converging on c-Fos.
• The result: Inhibiting JAK1, blocking either ERK1 or AKT1, or depleting c-Fos prevented oncostatin M–induced loss of barrier function, suggesting regulated nanoscale remodeling as an intervention target.