• TBI exacerbates pulmonary aggregation of intravenously injected hUMSCs, correlating with increased BRG1 expression in lung tissue.
• Inflammatory stimuli (TNF-α, LPS) upregulate BRG1 in endothelial cells and hUMSCs in a dose- and time-dependent manner, promoting adhesion.
• Estrogen (E2) pretreatment suppresses BRG1 and adhesion protein expression, reducing pulmonary retention of MSCs without compromising therapeutic efficacy against TBI-induced inflammation.
• The study identifies BRG1 as a potential molecular target to improve MSC-based therapies for TBI by mitigating lung entrapment.