ArticleBlood advances2026
Endothelial activation and damage associated with steroid-refractory aGVHD are counteracted by ruxolitinib.
Article in Blood advances, 2026. 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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15 authors.
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Abstract
abstractSteroid-refractory acute GVHD (SR-aGVHD) is a severe complication of allogeneic hematopoietic cell transplantation. While endothelial dysfunction is implicated in aGVHD pathophysiology, the status of the endothelium in patients with SR-aGVHD and the effect of the JAK1/2 inhibitor ruxolitinib remain incompletely understood. This study aimed to characterize the endothelial damage phenotype induced by SR-aGVHD serum and to evaluate the potential modulatory effects of ruxolitinib. Human microvascular endothelial cells (HMEC-1) were exposed to serum from SR-aGVHD patients (n = 21) or healthy donors (C), with or without ruxolitinib (0.4 µM). Markers of endothelial activation (VCAM-1, ICAM-1), junctional integrity (VE-cadherin), prothrombotic state (VWF), apoptosis (cleaved caspase 3), and intracellular signalling (JAK-STAT and MAPK pathways) were analyzed by immunofluorescence and immunoblotting. Compared with C, SR-aGVHD serum caused increased VCAM-1 and ICAM-1 expression (P< .05 for both), reduced VE-cadherin (P< .01), elevated VWF production, and cleaved caspase 3 presence (P< .05 for both). These changes were associated with phosphorylation of STAT3 (P< .05), STAT1 (P< .05), and MAPK proteins (Erk1/2, p38, SAP/JNK, and cJun) (P< .05, all). Ruxolitinib treatment mitigated these responses, reducing adhesion molecule expression, restoring VE-cadherin localization, normalizing VWF production, and suppressing apoptosis. These protective effects were associated with inhibition of the activated JAK-STAT and MAPK signalling pathways. SR-aGVHD serum directly induces endothelial activation in vitro, promoting an inflammatory and prothrombotic phenotype. Ruxolitinib counteracts these effects, providing mechanistic insight into its therapeutic efficacy in SR-aGVHD.
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