LAMB1 regulates COL3A1 and RAC1 expression during subchorionic hemorrhage progression

Subchorionic hemorrhage (SCH) is characterized by a fluid-filled hypoechoic area in early pregnancy. This study investigates how laminin subunit β1 (LAMB1) modulates type III collagen (COL3A1) and Rac family small GTPase 1 (RAC1) in SCH coagulation and immunity. We recruited ten early-pregnancy SCH patients and ten gestational age–matched women undergoing elective abortion as controls. Proteomic and transcriptomic analyses were performed on decidua and villous tissues to identify differentially expressed proteins (DEPs) and genes (DEGs). Key biomarkers were screened using bioinformatics and machine learning algorithms (LASSO, SVM-RFE). An in vivo SCH-like model was established via LPS induction in pregnant rats, and in vitro experiments were conducted using HTR-8/SVneo trophoblast cells. Proteomic analysis revealed enrichment in extracellular matrix and coagulation pathways, identifying LAMB1 as a central protein. Transcriptomic data confirmed upregulation of LAMB1 and COL3A1 and downregulation of RAC1 in SCH samples. Clinical blood analysis indicated coagulation abnormalities and Th1/Th2 imbalance in SCH patients. In vivo, LAMB1 knockdown alleviated inflammation, improved pregnancy outcomes, and restored Th2 cytokine expression. In vitro, LAMB1 silencing enhanced trophoblast proliferation, migration, and invasion while reducing pro-inflammatory cytokine levels. Mechanistically, LAMB1 modulated SCH progression via the COL3A1/RAC1 axis. LAMB1 promotes inflammation and coagulation dysfunction in SCH by regulating COL3A1 and RAC1 expression. Targeting LAMB1 may offer a novel strategy for early diagnosis and therapeutic intervention in SCH to improve pregnancy outcomes.