2026-08-21T00:04:16Zhttps://docta.ucm.es/rest/oai/request

oai:docta.ucm.es:20.500.14352/46882025-02-13T17:14:20Zcom_20.500.14352_14col_20.500.14352_15

00925njm 22002777a 4500 dc Serrano, Luis author De la Torre, Paz author Liras, Antonio author Flores, Ana author 2021 Deficiency of factor V is a congenital autosomal recessive coagulopathy associated with mutations in the F5 gene that results in mild-to-severe bleeding episodes. Factor V is a component of the prothrombinase complex responsible for accelerating conversion of prothrombin to thrombin. At the present time there are no therapeutic factor V concentrates available. This study was designed to lay the preliminary foundations for future cell-based therapy for patients with severe factor V deficiency. The study showed that hepatospheres, which produce coagulation factors VIII, IX, and V, synthetize and store intracellular glycogen and express albumin levels up to 8 times higher than those of undifferentiated cells. Factor IX and factor V gene expression increased significantly in hepatospheres as compared to undifferentiated cells, whereas factor VIII gene expression remained constant. The factor V protein was detected in the hepatospheres´ secretome. Considering the enormous potential of mesenchymal stem cells as therapeutic agents, this study proposes a highly reproducible method to induce differentiation of mesenchymal stem cells from human placenta to factor V-producing hepatospheres. This strategy constitutes a preliminary step towards a curative treatment of factor V deficiency through advanced therapies such as cell therapy. 0753-3322 10.1016/j.biopha.2021.112059 https://hdl.handle.net/20.500.14352/4688 https://doi.org/10.1016/j.biopha.2021.112059 Cell therapy for factor V deficiency: an approach based on human decidua mesenchymal stem cells