Publication: El sinoviocito fibroblástico en la artrosis. Efecto protector de VIP y CRF
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2017-05-29
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Universidad Complutense de Madrid
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Abstract
La artrosis (OA) es una enfermedad reumática crónica degenerativa y multifactorial. Es la artropatía más frecuente y la principal causa de daño y disfunción entre la población de mediana edad y anciana, caracterizada por una pérdida progresiva de la función de las articulaciones sinoviales (Bondeson et al., 2010; Loeser et al., 2012). Aunque la artritis reumatoide (AR) es la enfermedad reumática autoinmune inflamatoria por excelencia, más del 50% de los pacientes artrósicos también poseen signos de inflamación (Monfort, 2010; Pelletier et al., 2001; Scanzello y Goldring, 2012). Durante la sinovitis, el sinoviocito fibroblástico (SF) juega un papel esencial mediante la liberación de mediadores inflamatorios (Benito et al., 2005; Bottini y Firestein, 2013), entre los que se incluyen citocinas como la IL‐1β (Goldring et al., 2011; Stylianou y Saklatvala, 1998). Por otro lado, durante el proceso de destrucción articular se liberan componentes de la matriz extracelular (MEC) con propiedades potencialmente inflamatorios, incluyendo a la fibronectina y sus fragmentos de degradación (Fn‐fs) (Homandberg et al., 1998; Zack et al., 2006). Estos mediadores contribuyen a la destrucción del cartílago articular, rompiendo el balance entre degradación y síntesis de la MEC, como consecuencia de una expresión alterada de las proteinasas (Attur et al., 2002; Kato et al., 2014; Pelletier et al., 2001; Troeberg y Nagase, 2012)...
Osteoarhthritis (OA) is a chronic, degenerative and multifactorial disease. OA is the most frequent arthropathy being the main cause of pain and dysfunction among middle age and elder people, characterized by a progressive loss of the synovial joints function (Bondeson et al., 2010; Loeser et al., 2012). Despite that rheumatoid arthritis (RA) is considered the key inflammatory and autoimmune rheumatic disease, more than 50% of the OA patients, also present signs of inflammation (Monfort, 2010; Pelletier et al., 2001; Scanzello y Goldring, 2012). During synovitis, the synovial fibroblast (SF) plays a key role releasing inflammatory mediators (Benito et al., 2005; Bottini y Firestein, 2013), including cytokines as IL‐1β (Goldring et al., 2011; Stylianou y Saklatvala, 1998). On the other hand, during joint destruction, components with inflammatory properties are released from the extracellular matrix (ECM), including fibronectin and its degradation fragments (Fn‐fs). These mediators contribute to the articular cartilage ECM destruction, breaking the balance between synthesis and degradation, as a consequence of the altered expression of proteinases (Attur et al., 2002; Kato et al., 2014; Pelletier et al., 2001; Troeberg y Nagase, 2012). The urokinase plasminogen activator (uPA) contributes to the activation of other proteinases such as matrix metalloproteinases (MMPs), including MMP‐13 and MMP‐9 (Smith y Marshall, 2010). A disintegrin and metalloproteinases with thrombospondin motifs (ADAMTS) are also involved in the ECM degradation (Kelwick et al., 2015; Porter et al., 2005; Takeda, 2009)...
Osteoarhthritis (OA) is a chronic, degenerative and multifactorial disease. OA is the most frequent arthropathy being the main cause of pain and dysfunction among middle age and elder people, characterized by a progressive loss of the synovial joints function (Bondeson et al., 2010; Loeser et al., 2012). Despite that rheumatoid arthritis (RA) is considered the key inflammatory and autoimmune rheumatic disease, more than 50% of the OA patients, also present signs of inflammation (Monfort, 2010; Pelletier et al., 2001; Scanzello y Goldring, 2012). During synovitis, the synovial fibroblast (SF) plays a key role releasing inflammatory mediators (Benito et al., 2005; Bottini y Firestein, 2013), including cytokines as IL‐1β (Goldring et al., 2011; Stylianou y Saklatvala, 1998). On the other hand, during joint destruction, components with inflammatory properties are released from the extracellular matrix (ECM), including fibronectin and its degradation fragments (Fn‐fs). These mediators contribute to the articular cartilage ECM destruction, breaking the balance between synthesis and degradation, as a consequence of the altered expression of proteinases (Attur et al., 2002; Kato et al., 2014; Pelletier et al., 2001; Troeberg y Nagase, 2012). The urokinase plasminogen activator (uPA) contributes to the activation of other proteinases such as matrix metalloproteinases (MMPs), including MMP‐13 and MMP‐9 (Smith y Marshall, 2010). A disintegrin and metalloproteinases with thrombospondin motifs (ADAMTS) are also involved in the ECM degradation (Kelwick et al., 2015; Porter et al., 2005; Takeda, 2009)...
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Tesis inédita de la Universidad Complutense de Madrid, Facultad de Ciencias Biológicas, Departamento de Biología Celular leída el 17-06-2016