The aim of the study was to investigate the role of inflammatory proteins on leukocytes during osteoarthritis (OA) and their effects on joint pathology. Activated monocytes/ macrophages in patients with OA produce high levels of pro-inflammatory proteins driving cartilage and bone destruction. We postulated that the inflammatory state of the joint determines the phenotype and function of the monocytes. We investigated this in vitro using different cell lines and in vivo murine models of osteoarthritis using knockout systems and pharmacological intervention. To translate it to clinical value, we analyzed the expression profiles of monocytes/ macrophages and their functions in humans with osteoarthritis and healthy controls. The transition from pro-inflammatory monocytes towards pro-healing monocytes that promote the resolution of joint inflammation forms an interesting novel therapeutic strategy.

My research focuses on the improvement of wound healing using stem cells and cytoprotective molecules. Hypertrophic scars and ulcers following burns, surgery, or other traumas cause severe morbidity. Stem cell-based adjuvant therapy is considered a novel promising therapeutic target to mediate tissue repair. Following injury, stem cells can migrate towards the injury, where these normally quiescent cells start to multiply, and differentiate into the cells that are needed. However, the migration towards the injury and survival at the injury site can be impaired due to oxidative and inflammatory stressors. Therefore we aim to overexpress cytoprotective proteins to protect the stem cell, and in addition, to create an environment that prevents exacerbation of injury, fibrosis, and hypertrophic scarring, and hence ultimately leading to improved wound regeneration.