For several years we have been researching the mechanisms involved in inflammatory processes. Our activity has focused on a number of aspects such as the study of the mediators that determine the progression of joint injury, the possible protective mechanisms and the main signalling pathways involved, in order to increase knowledge of the pathogenesis of inflammatory-based diseases and find new therapeutic targets. To this end, we conducted in vivo and in vitro studies. We use different animal models of acute inflammation (rat and mouse air pouch, carrageenan oedema, skin inflammation, bowel inflammation) and chronic inflammation, such as rheumatoid arthritis models (adjuvant arthritis, collagen arthritis, serum transfer arthritis from K/BxN transgenic mice). Models of osteoarthritis due to ageing have been developed: such as spontaneous osteoarthritis in STR/ort mice, following the temporal evolution of the disease, with biochemical studies of biomarkers in serum and joint tissues, radiological studies, histological studies, etc. All these findings have made it possible to relate the appearance and progression of the injuries to the age of the animal and to propose various mechanisms that may regulate these processes. Animal models of osteoarthritis/osteoporosis in rats (ACLT+ovariectomy) and arthritis/osteoporosis in mice (CIA+ovariectomy) have also been developed.
We conducted studies on cartilage explants, chondrocytes in normoxia and hypoxia, synoviocytes and osteoblasts from osteoarthritic patients to determine gene and protein expression of factors that may be related to disease progression. We have determined the consequences of over-expression (sometimes by transfection with adenovirus) or inhibition (sometimes by gene silencing with siRNA) of these factors on cellular metabolism, synthesis and degradation of extracellular matrix components, production of cytokines, chemokines, growth and cell differentiation factors, eicosanoids, reactive species, etc. Signalling and transcription pathways related to these factors have also been studied.
One of our lines focuses on cellular senescence and the effects of ageing in different systems, in vivo and in vitro approaches.
We are studying the anti-inflammatory and protective properties of mesenchymal stem cells within in vitro and in vivo models as a source of new therapeutic strategies in inflammatory diseases and joint diseases. In particular, we focus on the properties of extracellular vesicles as potential therapeutic agents, biomarkers and cell communication factors.
We also used culture systems from healthy fibroblasts and keratinocytes and from psoriatic patients to determine the inflammatory mediators and mechanisms involved. In vitro studies have also been conducted in models of human microendothelial cells, fibroblasts and keratinocytes, focusing on adenosine as a target that may lead to new therapeutic strategies for wound healing in highly susceptible population groups such as diabetics, the obese and the elderly.
- Basis of the inflammatory process. Anti-inflammatory drugs
- Cellular senescence and ageing
- Arthritis. Osteoarthritis. Osteoporosis
- Psoriasis and wound healing
- Mesenchymal stem cells
- Extracellular vesicles
- Psoriasis
Skin inflammation, psoriasis, wound healing.
- Inflammation Mechanisms
Basis of the inflammatory process. Anti-inflammatory drugs. New approaches to the treatment of inflammatory diseases. Arthritis. Osteoarthritis. Osteoporosis
- MONTESINOS MEZQUITA, M CARMEN
- PDI-Titular d'Universitat
- FERRANDIZ MANGLANO, MARIA LUISA
- PDI-Catedratic/a d'Universitat
- Vicedega/Vicedegana / Vicedirector/a Ets
- TERENCIO SILVESTRE, MARIA CARMEN
- PDI-Catedratic/a d'Universitat
- SAGRADO VIVES, SALVADOR
- PDI-Catedratic/a d'Universitat
Burjassot/Paterna Campus
Av.Vicent Andrés Estellés, s/n
46100 Burjassot (Valencia)
