Surgery for chronic arthropathy in people with haemophilia.

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Abstract

[Indexed for MEDLINE] Conflict of interest statement: Brian Chin: none known Ian Wee: none known Nicholas Syn: none known Gavin O'Neill: none known Eng Soo Yap: none known Pei Lin Koh: none known 15. Blood. 2026 Jan 15;147(3):299-311. doi: 10.1182/blood.2024027143. Factor VIIa-released extracellular vesicles attenuate joint bleed-induced hemophilic arthropathy. Kavadipula P(1), Keshava S(1), Das K(1)(2), Magisetty J(1)(3), DeJong C(1), Penchalaneni J(4), Pendurthi UR(1), Rao LVM(1). Author information: (1)Department of Cellular and Molecular Biology, The University of Texas Health Science Center at Tyler, Tyler, TX. (2)Biotechnology Research and Innovation Council-National Institute of Biomedical Genomics, Kalyani, India. (3)Department of Zoology, Central University of Punjab, Bathinda, India. (4)Department of Biotechnology, Sri Padmavati Mahila Visvavidyalayam, Tirupati, India. Comment in Blood. 2026 Jan 15;147(3):226-227. doi: 10.1182/blood.2025030987. Repeated bleeding into joints in hemophilia leads to chronic inflammation that plays a central role in the pathogenesis of hemophilic arthropathy (HA). Our recent studies revealed that factor VIIa (FVIIa) treatment releases extracellular vesicles from endothelial cells (eEVs) and FVIIa-released eEVs exhibit anti-inflammatory and barrier-protective functions. The present study was undertaken to investigate the effect of FVIIa-released eEVs on HA and the mechanism of their protective effect. Joint bleeding in hemophilia (F8-/-) mice was induced by a needle puncture injury. Injured mice were treated with saline, control eEVs, or FVIIa-released eEVs, and the changes in the knee joints were analyzed by gross examination of knees as well as histological and immunohistochemical analysis. Joint tissues were examined for evidence of synovial hyperplasia, macrophage infiltration, neoangiogenesis, cartilage degeneration, and chondrocyte apoptosis. The data showed that treatment of mice with control eEVs had no significant effect on the development of HA, whereas treatment with FVIIa-released eEVs markedly reduced all pathological features of joint bleed-induced HA. Incorporation of microRNA10a (miR10a) inhibitor into FVIIa-released eEVs abrogated the protective effect of FVIIa-released eEVs on HA. More importantly, loading miR10a mimic into control eEVs conferred a protective effect. Administration of miR10a-containing FVIIa-released eEVs or control eEVs loaded with miR10a mimic was found to abrogate joint bleed-induced interleukin-6 production in the synovium. miR10a in eEVs had no effect on hemostasis. Cumulatively, our data indicate that EVs containing miR10a that effectively suppress synovial inflammation would have immense therapeutic value in treating HA. © 2026 American Society of Hematology. Published by Elsevier Inc. All rights are reserved, including those for text and data mining, AI training, and similar technologies. DOI: 10.1182/blood.2024027143 PMCID: PMC13122308