Person:
Juarranz Moratilla, Yasmina

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First Name
Yasmina
Last Name
Juarranz Moratilla
Affiliation
Universidad Complutense de Madrid
Faculty / Institute
Ciencias Biológicas
Department
Biología Celular
Area
Biología Celular
Identifiers
UCM identifierORCIDScopus Author IDWeb of Science ResearcherIDDialnet IDGoogle Scholar ID

Search Results

Now showing 1 - 4 of 4
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    Profile of Matrix-Remodeling Proteinases in Osteoarthritis: Impact of Fibronectin
    (Cells, 2019) Pérez García, Selene; Carrión Caballo, Mar; Gutiérrez Cañas, Irene; Villanueva Romero, Raúl; Castro Vázquez, David; Martínez Mora, María Del Carmen; González-Álvaro, Isidoro; Blanco, Francisco J.; Juarranz Moratilla, Yasmina; Pérez Gomáriz, Rosa María
    The extracellular matrix (ECM) is a complex and specialized three-dimensional macromolecular network, present in nearly all tissues, that also interacts with cell surface receptors on joint resident cells. Changes in the composition and physical properties of the ECM lead to the development of many diseases, including osteoarthritis (OA). OA is a chronic degenerative rheumatic disease characterized by a progressive loss of synovial joint function as a consequence of the degradation of articular cartilage, also associated with alterations in the synovial membrane and subchondral bone. During OA, ECM-degrading enzymes, including urokinase-type plasminogen activator (uPA), matrix metalloproteinases (MMPs), and a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTSs), cleave ECM components, such as fibronectin (Fn), generating fibronectin fragments (Fn-fs) with catabolic properties. In turn, Fn-fs promote activation of these proteinases, establishing a degradative and inflammatory feedback loop. Thus, the aim of this review is to update the contribution of ECM-degrading proteinases to the physiopathology of OA as well as their modulation by Fn-fs.
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    The Neuropeptide VIP Limits Human Osteoclastogenesis: Clinical Associations with Bone Metabolism Markers in Patients with Early Arthritis
    (Biomedicines, 2021) Castro Vázquez, David; Lamana Rodríguez, Amalia; Arribas Castaño, Paula; Gutiérrez Cañas, Irene; Villanueva Romero, Raúl; Pérez García, Selene; Martínez Mora, María Del Carmen; Juarranz Moratilla, Yasmina; Fernández de Córdoba, Sara; González Álvaro, Isidoro; Gomáriz, Rosa P.; Carrión Caballo, Mar
    We aimed to evaluate the direct action of VIP on crucial molecules involved in human osteoclast differentiation and function. We also investigated the relationship between VIP serum levels and bone remodeling mediators in early arthritis patients. The expression of VIP receptors and osteoclast gene markers in monocytes and in vitro differentiated osteoclasts was studied by real-time PCR. NFATc1 activity was measured using a TransAM® kit. Osteoclastogenesis was confirmed by quantification of tartrate-resistant acid phosphatase positive multinucleated cells. OsteoAssay® Surface Multiple Well Plate was used to evaluate bone-resorbing activity. The ring-shaped actin cytoskeleton and the VPAC1 and VPAC2 expression were analyzed by immunofluorescence. We described the presence of VIP receptors in monocytes and mature osteoclasts. Osteoclasts that formed in the presence of VIP showed a decreased expression of osteoclast differentiation gene markers and proteolytic enzymes involved in bone resorption. VIP reduced the resorption activity and decreased both β3 integrin expression and actin ring formation. Elevated serum VIP levels in early arthritis patients were associated with lower BMD loss and higher serum OPG concentration. These results demonstrate that VIP exerts an anti-osteoclastogenic action impairing both differentiation and resorption activity mainly through the negative regulation of NFATc1, evidencing its bone-protective effects in humans.
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    Vasoactive intestinal peptide exerts an osteoinductive effect in human mesenchymal stem cells
    (BioFactors, 2024) Castro Vázquez, David; Arribas Castaño, Paula; García López, Iván; Gutiérrez Cañas, Irene; Pérez García, Selene; Lamana Domínguez, Amalia; Villanueva Romero, Raúl; Cabrera Martín, Alicia; Tecza , Karolina; Martínez Mora, María Del Carmen; Juarranz Moratilla, Yasmina; Pérez Gomáriz, Rosa María; Carrión Caballo, Mar
    Several neuropeptides present in bone tissues, produced by nerve fibers and bone cells, have been reported to play a role in regulating the fine-tuning of osteoblast and osteoclast functions to maintain bone homeostasis. This study aims to characterize the influence of the neuropeptide vasoactive intestinal peptide (VIP) on the differentiation process of human mesenchymal stem cells (MSCs) into osteoblasts and on their anabolic function. We describe the mRNA and protein expression profile of VIP and its receptors in MSCs as they differentiate into osteoblasts, suggesting the presence of an autocrine signaling pathway in these cells. Our findings reveal that VIP enhances the expression of early osteoblast markers in MSCs under osteogenic differentiation and favors both bone matrix formation and proper cytoskeletal reorganization. Finally, our data suggest that VIP could be exerting a direct modulatory role on the osteoblast to osteoclast signaling by downregulating the receptor activator of nuclear factor-κB ligand/osteoprotegerin ratio. These results highlight the potential of VIP as an osteoinductive differentiation factor, emerging as a key molecule in the maintenance of human bone homeostasis.
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    Proteomic analysis of synovial fibroblasts and articular chondrocytes co-cultures reveals valuable VIP-modulated inflammatory and degradative proteins in osteoarthritis
    (International Journal of Molecular Sciences, 2021) Pérez García, Selene; Calamia, Valentina; Hermida-Gómez, Tamara; Gutiérrez Cañas, Irene; Carrión Caballo, Mar; Villanueva Romero, Raúl; Castro Vázquez, David; Martínez Mora, María Del Carmen; Juarranz Moratilla, Yasmina; Blanco, Francisco J.; Pérez Gomáriz, Rosa María
    Osteoarthritis (OA) is the most common musculoskeletal disorder causing a great disability and a reduction in the quality of life. In OA, articular chondrocytes (AC) and synovial fibroblasts (SF) release innate-derived immune mediators that initiate and perpetuate inflammation, inducing cartilage extracellular matrix (ECM) degradation. Given the lack of therapies for the treatment of OA, in this study, we explore biomarkers that enable the development of new therapeutical approaches. We analyze the set of secreted proteins in AC and SF co-cultures by stable isotope labeling with amino acids (SILAC). We describe, for the first time, 115 proteins detected in SF-AC co-cultures stimulated by fibronectin fragments (Fn-fs). We also study the role of the vasoactive intestinal peptide (VIP) in this secretome, providing new proteins involved in the main events of OA, confirmed by ELISA and multiplex analyses. VIP decreases proteins involved in the inflammatory process (CHI3L1, PTX3), complement activation (C1r, C3), and cartilage ECM degradation (DCN, CTSB and MMP2), key events in the initiation and progression of OA. Our results support the anti-inflammatory and anti-catabolic properties of VIP in rheumatic diseases and provide potential new targets for OA treatment.