@inproceedings {17629, title = {Platelet lysate maintains chondrogenic potential and promotes cartilage regeneration}, journal = {3rd Termis World Congress 2012}, year = {2012}, month = {2012-09-08 00:00:00}, address = {Vienna, Austria}, abstract = {

Platelet rich plasma (PRP), a cocktail of platelet growth factors and bio-active proteins, has\ been proposed as therapeutic agent to restore damaged articular cartilage. We report the\ biological effect of the platelet lysate (PL), a PRP derivative, on primary human articular\ chondrocytes cultured under both physiological and inflammatory condition. When added to the\ culture medium, PL induced a strong mitogenic response in the chondrocytes.\ The in vitro expanded cell population maintained a chondrogenic re-differentiation potential as\ revealed by micromass culture in vitro and ectopic cartilage formation in vivo.\ Furthermore, in chondrocytes cultured in the presence of the pro-inflammatory cytokine IL-1α,\ the PL induced a drastic enhancement of the synthesis of the cytokines IL-6 and IL-8 and of\ NGAL, a lipocalin expressed in cells of the chondrogenic lineage. These events were\ controlled by the p38 MAP kinase and NF-κΒ pathways. The pro-inflammatory effect of the PL\ was a transient phenomenon. In fact, after an initial up regulation, we observed a significant\ reduction of the NF-κΒ activity together with the repression of the inflammatory enzyme\ ciclooxygenase-2 (COX-2).\ Moreover, the medium of chondrocytes cultured in the contemporary presence of PL and IL-1α,\ showed a significant enhancement of the chemoattractant activity versus untreated\ chondrocytes.\ On the whole, our findings support the concept that the platelet products have a direct\ beneficial effect on articular chondrocytes and at the same time could drive in sequence a\ transient activation and the resolution of the inflammatory process, thus providing a rational for\ their use as therapeutic agents in cartilage inflammation and damage.

}, keywords = {cartilage, Inflammation}, author = {Pereira, R. C. and Scaranari, M. and Strada, P. and Reis, R. L. and Cancedda, R. and Gentili, C.} }