Person:
Carrión Caballo, Mar

First Name

Mar

Last Name

Carrión Caballo

Affiliation

Universidad Complutense de Madrid

Faculty / Institute

Ciencias Biológicas

Department

Biología Celular

Area

Biología Celular

Identifiers

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Now showing 1 - 10 of 19

Aplicación de la clase invertida en la asignatura Biología Celular e Histología
(2020-07-01) Gutiérrez Cañas, Irene; Carrión Caballo, Mar; Juarranz Moratilla, Yasmina; Lamana Domínguez, Amalia; López Redondo, Jesús María; Morona Arribas, Ruth; Muñoz Céspedes, Alberto; Ortega Moreno, Álvaro Dario; Pérez García, Selene; Pérez Gomariz, Rosa María
La clase invertida o clase al revés, también conocida por el anglicismo flipped classroom, es una metodología docente en la que, como su nombre indica, se invierten los procesos que clásicamente tienen lugar dentro y fuera del aula. De manera que se pasa de una clase centrada en el profesor, como transmisor de la información y con un alumno receptor pasivo de la información cuyo trabajo fuera del aula consiste en la realización de tareas, a un modelo en el que el alumno, debe recibir y asimilar la información que le es facilitada previamente a la clase. En el aula, los alumnos resuelven dudas y realizan tareas, en muchos casos en equipo, de manera que el trabajo en el aula pasa a estar centrado en el alumno, que debe ser responsable de su propio aprendizaje. Los profesores que ya aplican esta metodología en distintos niveles educativos, se muestran muy satisfechos con el aumento del rendimiento de los estudiantes, la gran aceptación que tiene esta metodología, el aumento del aprendizaje significativo, es decir, la capacidad de relacionar los conocimientos previos con los nuevos y ser capaces de aplicar lo aprendido para la resolución de problemas. La asignatura “Biología Celular e Histología” del Grado en Biología se imparte con carácter anual durante el primer curso del grado, con una carga docente de 12 ECTS. Cada año se matriculan en la asignatura más de 400 alumnos, 300 en primera matrícula. Los contenidos teóricos que deben adquirir los alumnos son extensos y complejos, lo que supone una notable carga de trabajo para los alumnos que, si se limitan a una mera asistencia pasiva a clase, no son capaces de obtener un aprovechamiento óptimo de los contenidos y por tanto obtener buenos resultados. Además de esos contenidos teóricos, los alumnos deben adquirir unos contenidos prácticos mediante 5 sesiones de laboratorio de Biología Celular y 9 sesiones de laboratorio de Histología. Existen varios profesores implicados en la docencia teórica de esta asignatura, ya que los alumnos matriculados se dividen en 6 grupos y en algunos casos, la docencia se divide entre dos profesores, uno encargado de la parte de Biología Celular y otro de la parte de Histología. Cada profesor tiene su propio perfil docente, pero todos basamos nuestras clases en una metodología tradicional de clase magistral, es decir, una docencia centrada en el profesor, como foco transmisor de información que el alumno debe asimilar. Todos utilizamos el Campus Virtual donde colocamos las presentaciones que utilizamos en clase y donde organizamos las sesiones de seminarios. En general, año tras año, los profesores de esta asignatura observamos una falta de implicación de los alumnos en su propio aprendizaje, de manera que reciben la información de manera pasiva, escuchando al profesor, en muchos casos sin ni siquiera tomar apuntes. Esta pasividad y escasa implicación del alumnado conlleva unos resultados reflejados en las calificaciones globales generalmente decepcionantes, y que a nuestro juicio son susceptibles de mejora aumentando la motivación del alumnado mediante nuevas metodologías docentes. Con este proyecto de innovación docente, hemos elaborado el material necesario para aplicar el método “flipped learning” o clase invertida en un bloque de temas de Biología Celular y en otro bloque de temas de Histología. Este tipo de metodología centrada en el alumno, permite que el estudiante procese y maneje la información suministrada de forma autónoma, antes de acudir a clase, a su ritmo, de manera que el tiempo de clase puede usarse de otras maneras, por ejemplo, para solucionar dudas, discutir a fondo los aspectos más complicados del tema, o para realizar tareas de aplicación de los conocimientos previamente aprendidos en casa. De esta manera se puede lograr un aprendizaje significativo alejado de la mera memorización de los contenidos expuestos, y en donde el alumno se sienta protagonista de su propio avance y capacitación teórica de la asignatura.
Wnt and RUNX2 mediate cartilage breakdown by osteoarthritis synovial fibroblast‐derived ADAMTS‐7 and ‐12
(Wiley Open Acces, 2019) Pérez García, Selene; Carrión Caballo, Mar; Villanueva Romero, Raúl; Hermida Gómez, Tamara; Fernández Moreno, Mercedes; Mellado, Mario; Blanco, Francisco J.; Juarranz Moratilla, Yasmina; Gomáriz, Rosa P.
Failure of therapeutic approaches for the treatment of osteoarthritis (OA) based on the inhibition of metalloproteinases, might be because of their constitutive expres‐ sion in homeostasis, together with their network complexity. The knowledge of this network would contribute to selective target pathological conditions. In this sense, blockade of mediators produced by neighbouring joint cells, such as synovial fibro‐ blasts (SF), would prevent cartilage damage. Thus, we studied the contribution of ADAMTS‐7 and ‐12 from SF to cartilage oligomeric matrix protein (COMP) degrada‐ tion, and the signalling pathways involved in their expression. We report for the first time in SF, the involvement of ERK‐Runx2 axis and Wnt/β‐catenin signalling in ADAMTS‐12 and ADAMTS‐7 expressions, respectively, with the subsequent conse‐ quences in COMP degradation from cartilage extracellular matrix. After stimulation with IL‐1β or fibronectin fragments, we showed that ERK inhibition decreased Runx2 activation and ADAMTS‐12 expression in OA‐SF, also reducing Fn‐fs‐induced COMP degradation. Blockage of Wnt signalling by DKK1 reduced ADAMTS‐7 and COMP degradation in OA‐SF as well. In addition, Wnt7B expression was induced by IL‐1β and by itself, also increasing ADAMTS‐7. Our results could contribute to the develop‐ ment of disease‐modifying OA drugs targeting ADAMTS‐7 and ‐12 for the prevention of extracellular matrix components degradation like COMP.
Digitalización de la histoteca de las prácticas de Organografía Microscópica
(2018-05-31) Morona Arribas, Ruth; González Gallegos, Agustín; Gutiérrez Cañas, Irene; García-Ceca Hernández, José Javier; López Redondo, Jesús María; Alfaro Sánchez, David; Muñiz Hernando, Enriqueta; Carrión Caballo, Mar; Moreno García, Nerea; Pérez García, Selene; Pérez Gomáriz, Rosa María
Histoteca digital para que los alumnos puedan consultar un material gráfico actualizado y concreto, similar a lo que observan en el microscopio cuando realizan sus prácticas de Organografía de la asignatura de “Organografía microscópica” del Grado en Biología.
Profile of Matrix-Remodeling Proteinases in Osteoarthritis: Impact of Fibronectin
(MDPI, 2019-12-22) Pérez García, Selene; Carrión Caballo, Mar; Gutiérrez-Cañas, Irene; Villanueva-Romero, Raúl; Castro Moreno, David; Martínez, Carmen; González-Álvaro, Isidoro; Blanco, Francisco J.; Juarranz Moratilla, Yasmina; Gomáriz, Rosa P.
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.
The Neuropeptide VIP Limits Human Osteoclastogenesis: Clinical Associations with Bone Metabolism Markers in Patients with Early Arthritis
(MDPI, 2021-12-10) Castro Vázquez, David; Lamana, Amalia; Arribas Castaño, Paula; Gutiérrez Cañas, Irene; Villanueva Romero, Raúl; Pérez García, Selene; Martínez Mora, 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.
Vasoactive Intestinal Peptide maintains the non-pathogenic profile of human Th17-polarized cells
(Springer, 2014-11) Jimeno Lumeras, Rebeca Gema; Leceta Martínez, Javier; Martínez, Carmen; Gutiérrez-Cañas, Irene; Carrión Caballo, Mar; Pérez García, Selene; Garín, Marina I.; Mellado, Mario; Pérez Gomáriz, Rosa María; Juarranz Moratilla, Yasmina
The cytokine microenvironment modulates CD4 T cell differentiation causing the shift of naïve CD4 T cells into different cell subsets. This process is also regulated by modulators such as VIP, a neuropeptide with known immunomodulatory properties on CD4 T cells that exert this action through specific receptors, VPAC1 and VPAC2. Our results show that the pattern of VIP receptors expression ratio is modified during Th17 differentiation. In this report, we evaluate the capacity of VIP to modulate naïve human cells into Th17 cells in vitro by analyzing their functional phenotype. The presence of VIP maintains the non-pathogenic profile of Th17-polarized cells, increases the proliferation rate and decreases their Th1 potential. VIP induces the up-regulation of the STAT3 gene interaction with the VPAC1 receptor during the onset of Th17 differentiation. Moreover, RORC, RORA and IL-17A genes are up-regulated in the presence of VIP through interaction with VPAC1 and VPAC2 receptors. Interestingly, VIP induces the expression of the IL-23R gene through interaction with the VPAC2 receptor during the expansion phase. This is the first report that describes the differentiation of naïve human T cells to Th17-polarized cells in the presence of VIP and demonstrates how this differentiation regulates the expression of the VIP receptors.
A Clinical Approach for the Use of VIP Axis in Inflammatory and Autoimmune Diseases
(MDPI, 2019-12-20) Martínez, Carmen; Juarranz Moratilla, Yasmina; Gutiérrez Cañas, Irene; Carrión Caballo, Mar; Pérez García, Selene; Villanueva Romero, Raúl; Castro Moreno, David; Lamana, Amalia; Mellado, Mario; González Álvaro, Isidoro; Gomáriz, Rosa P.
The neuroendocrine and immune systems are coordinated to maintain the homeostasis of the organism, generating bidirectional communication through shared mediators and receptors. Vasoactive intestinal peptide (VIP) is the paradigm of an endogenous neuropeptide produced by neurons and endocrine and immune cells, involved in the control of both innate and adaptive immune responses. Exogenous administration of VIP exerts therapeutic effects in models of autoimmune/inflammatory diseases mediated by G-protein-coupled receptors (VPAC1 and VPAC2). Currently, there are no curative therapies for inflammatory and autoimmune diseases, and patients present complex diagnostic, therapeutic, and prognostic problems in daily clinical practice due to their heterogeneous nature. This review focuses on the biology of VIP and VIP receptor signaling, as well as its protective effects as an immunomodulatory factor. Recent progress in improving the stability, selectivity, and effectiveness of VIP/receptors analogues and new routes of administration are highlighted, as well as important advances in their use as biomarkers, contributing to their potential application in precision medicine. On the 50th anniversary of VIP’s discovery, this review presents a spectrum of potential clinical benefits applied to inflammatory and autoimmune diseases.
Vasoactive intestinal peptide axis is dysfunctional in patients with Graves’ disease
(Nature Research, 2020-08-03) Carrión Caballo, Mar; Ramos-Levi, A. M.; Valiño Seoane, Iria; Martínez Hernández, R.; Serrano-Somavilla, A.; Castro Vázquez, David; Juarranz Moratilla, Yasmina; González Álvaro, I.; Gomáriz, Rosa P.; Marazuela, Mónica
Vasoactive intestinal peptide (VIP) is a neuropeptide with potent immunoregulatory properties. Reduced serum VIP levels and alterations in VIP receptors/signaling on immune cells have been associated with diferent infammatory/autoimmune diseases. However, its role in autoimmune thyroid diseases (AITD) remains unknown. This study examined the interrelationship between VIP system, autoimmune background and thyroid hormones in peripheral immune cells in patients with AITD. Only Graves’ disease (GD) patients showed signifcantly lower serum VIP levels when compared to healthy subjects and to Hashimoto’s thyroiditis patients. Serum VIP levels were lower at the onset of GD, showing a signifcant negative correlation with thyroid hormone levels. The expression of VIP receptors, VPAC1 and VPAC2, was signifcantly upregulated in peripheral blood mononuclear cells (PBMC) from GD patients. There was an impairment of VIP signalling in these patients, probably attributable to a dysfunction of VPAC1 with preservation of VPAC2. The correlation between VPAC1 and thyroid hormone receptor expression in PBMC from healthy subjects was lost in GD patients. In summary, the VIP system is altered in peripheral immune cells of GD patients and this fnding is associated with diferent thyroid hormone receptor patterns, showing a dynamic inter-regulation and a prominent role of VIP in this setting.
The Adipokine network in rheumatic joint diseases
(MDPI, 2019-08-22) Carrión Caballo, Mar; Frommer, Klaus W.; Pérez García, Selene; Müller-Ladner, Ulf; Gomáriz, Rosa P.; Neumann, Elena
Rheumatic diseases encompass a diverse group of chronic disorders that commonly affect musculoskeletal structures. Osteoarthritis (OA) and rheumatoid arthritis (RA) are the two most common, leading to considerable functional limitations and irreversible disability when patients are unsuccessfully treated. Although the specific causes of many rheumatic conditions remain unknown, it is generally accepted that immune mechanisms and/or uncontrolled inflammatory responses are involved in their etiology and symptomatology. In this regard, the bidirectional communication between neuroendocrine and immune system has been demonstrated to provide a homeostatic network that is involved in several pathological conditions. Adipokines represent a wide variety of bioactive, immune and inflammatory mediators mainly released by adipocytes that act as signal molecules in the neuroendocrine-immune interactions. Adipokines can also be synthesized by synoviocytes, osteoclasts, osteoblasts, chondrocytes and inflammatory cells in the joint microenvironment, showing potent modulatory properties on different effector cells in OA and RA pathogenesis. Effects of adiponectin, leptin, resistin and visfatin on local and systemic inflammation are broadly described. However, more recently, other adipokines, such as progranulin, chemerin, lipocalin-2, vaspin, omentin-1 and nesfatin, have been recognized to display immunomodulatory actions in rheumatic diseases. This review highlights the latest relevant findings on the role of the adipokine network in the pathophysiology of OA and RA.
Activation of Th lymphocytes alters pattern expression and cellular location of VIP receptors in healthy donors and early arthritis patients
(Nature Research, 2019-05-14) Villanueva Romero, Raúl; Gutiérrez Cañas, Irene; Carrión Caballo, Mar; González Álvaro, Isidoro; Rodríguez Frade, José Miguel; Mellado, Mario; Martínez, Carmen; Gomáriz, Rosa P.; Juarranz Moratilla, Yasmina
Vasoactive Intestinal Peptide (VIP) is an important immunomodulator of CD4+ cells in normal and pathological conditions, which exerts its anti-infammatory and immunomodulatory actions through VPAC receptors, VPAC1 and VPAC2. Only a decrease in the expression of VPAC1 mRNA on Th cells upon activation has been reported. Thus, the deepening in the knowledge of the behavior of these receptors may contribute to the design of new therapies based on their activation and/or blockade. In this study, we describe the expression pattern, cellular location and functional role of VIP receptors during the activation of human Th cells in healthy conditions and in early arthritis (EA). The protein expression pattern of VPAC1 did not change with the activation of Th lymphocytes, whereas VPAC2 was up-regulated. In resting cells, VPAC1 was located on the plasma membrane and nucleus, whereas it only appeared in the nucleus in activated cells. VPAC2 was always found in plasma membrane location. VIP receptors signaled through a PKA-dependent pathway in both conditions, and also by a PKAindependent pathway in activated cells. Both receptors exhibit a potent immunomodulatory capacity by controlling the pathogenic profle and the activation markers of Th cells. These results highlight a novel translational view in infammatory/autoimmune diseases.