RESUMEN
BACKGROUND: Immune and non-immune cells contribute to the pathology of chronic arthritis, and they can contribute to tissue remodeling and repair as well as disease pathogenesis. The present research aimed to analyze inflammation and bone destruction/regeneration biomarkers in patients with psoriatic arthritis (PsA), rheumatoid arthritis (RA), osteoarthritis (OA), and ankylosing spondylitis (AS). METHODS: Samples were obtained from the inflamed knee of patients with knee arthritis who had been referred for undergoing arthroscopies. The synovial membrane was processed for pathological description, IHC analysis, and quantification of mRNA expression ratio by qRT-PCR. Serum levels of TGF-ß1, IL-23, IL-6, IL-17 A, IL-22, Dkk1, Sclerostin, BMP2, BMP4, Wnt1, and Wnt5a were measured by ELISA. All these data were analyzed and compared with the demographic, clinical, blood tests, and radiological characteristics of the patients. RESULTS: The synovial membrane samples were obtained from 42 patients for IHC, extraction, and purification of RNA for synovial mRNA expression analysis, and serum for measuring protein levels from 38 patients. IHC reactivity for TGF-ß1 in the synovial tissue was higher in patients with psoriatic arthritis (p 0.036) and was positively correlated with IL-17 A (r = 0.389, p = 0.012), and Dkk1 (r = 0.388, p = 0.012). Gene expression of the IL-17 A was higher in PsA patients (p = 0.018) and was positively correlated with Dkk1 (r = 0.424, p = 0.022) and negatively correlated with BMP2 (r = -0.396, p = 0.033) and BMP4 (r = -0.472, p = 0.010). It was observed that IHC reactivity for TGF-ß1 was higher in patients with erosive PsA (p = 0.024). CONCLUSIONS: The IHC reactivity of TGF-ß1 in synovial tissue was higher in patients with erosive psoriatic arthritis, and TGF-ß1 was in relation to higher levels of gene expression of IL-17 A and Dkk1.
Asunto(s)
Artritis Psoriásica , Humanos , Factor de Crecimiento Transformador beta1/metabolismo , Interleucina-17/metabolismo , Líquido Sinovial/metabolismo , Inmunohistoquímica , Membrana Sinovial/patología , ARN Mensajero/metabolismoRESUMEN
The establishment of cartilage regenerative medicine is an important clinical issue, but the search for cell sources able to restore cartilage integrity proves to be challenging. Human mesenchymal stromal cells (MSCs) are prone to form epiphyseal or hypertrophic cartilage and have an age-related limited proliferation. On the other hand, it is difficult to obtain functional chondrocytes from human embryonic stem cells (ESCs). Moreover, the ethical issues associated with human ESCs are an additional disadvantage of using such cells. Since their discovery in 2006, induced pluripotent stems cells (iPSCs) have opened many gateways to regenerative medicine research, especially in cartilage tissue engineering therapies. iPSCs have the capacity to overcome limitations associated with current cell sources since large numbers of autologous cells can be derived from small starting populations. Moreover, problems associated with epiphyseal or hypertrophic-cartilage formation can be overcome using iPSCs. iPSCs emerge as a promising cell source for treating cartilage defects and have the potential to be used in the clinical field. For this purpose, robust protocols to induce chondrogenesis, both in vitro an in vivo, are required. This review summarises the recent progress in iPSC technology and its applications for cartilage repair.
Asunto(s)
Cartílago/patología , Células Madre Pluripotentes Inducidas/citología , Cicatrización de Heridas , Animales , Diferenciación Celular , Condrogénesis , Cuerpos Embrioides/citología , Humanos , Trasplante de Células MadreRESUMEN
No disponible
Asunto(s)
Humanos , Tratamiento Basado en Trasplante de Células y Tejidos/métodos , Enfermedades de los Cartílagos/terapia , Cartílago/fisiopatología , BioprótesisRESUMEN
La artrosis (OA) es una patología degenerativa de las articulaciones que se caracteriza por la degradación del cartílago articular hialino. Su progresión es lenta y tiene una etiología múltiple que implica el envejecimiento, la obesidad y la influencia genética como algunos de los factores que favorecen el desarrollo de la OA. En su fase final refleja una insuficiencia de los procesos de reparación del cartílago, resultando en la degradación de la matriz extracellular, muerte del condrocito (por apoptosis) y pérdida total de la integridad del cartílago. El condrocito es el único tipo celular presente en el cartílago maduro y causante de la reparación del tejido dañado. Sin embargo, el desarrollo de esta patología no sólo afecta al cartílago, sino a toda la estructura articular, incluyendo el hueso subcondral y el tejido sinovial. En esta revisión se evaluaran estos cambios desde el punto de vista molecular y celular y se revelará la complejidad de esta patología que incluye múltiples cambios en la estructura articular (AU)
