ArticleInternational journal of molecular sciences2025
Beta Interferon 1a and Laquinimod Differentially Affect Coagulation-Related Gene Expression in Multiple Sclerosis Patients: Implications for Clinical Efficacy and Side Effects.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Laquinimod (LAQ) and interferon-β1a (IFN-β1a, Rebif) are immunomodulatory therapies for relapsing-remitting multiple sclerosis (RRMS) that may also influence vascular and hemostatic pathways. This study investigated transcriptional regulation of coagulation- and fibrinolysis-related genes in peripheral blood mononuclear cells (PBMCs) from LAQ- and IFN-β1a-treated RRMS patients. In the LAQ cohort, within-subject paired analysis revealed significant downregulation of procoagulant and antifibrinolytic transcripts, including F2, F10, SERPINE1 (PAI-1), and TFPI, after six months of treatment (FDR < 0.01, |fold change| ≥ 1.5). These findings suggest that LAQ exerts an anticoagulant and antifibrinolytic transcriptional effect, potentially mediated through aryl hydrocarbon receptor (AhR) signaling. Western blot analysis confirmed decreased PAI-1 protein expression. In contrast, IFN-β1a treatment induced a distinct transcriptional pattern. Genes associated with fibrinolysis and endothelial stabilization (THBD, ANXA2, SERPINA1) were upregulated, while procoagulant mediators (F2R, F13A1, PROS1) were downregulated. Correlation analysis demonstrated significant relationships between interferon-inducible genes and coagulation-related transcripts, suggesting coordinated regulation between type I interferon signaling and vascular pathways. Collectively, these results indicate that LAQ and IFN-β1a exert opposing yet convergent influences on coagulation and fibrinolytic networks in immune cells. Both therapies modulate transcriptional regulators of vascular homeostasis, revealing a potential molecular interface between immune modulation and hemostatic balance in RRMS. These findings are exploratory and hypothesis-generating, warranting further functional and clinical validation.
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