PLATELET RICH PLASMA (PRP) STIMULATES OSTEOBLAST PRECURSORS THROUGH AUTOPHAGY INDUCTION

SERGIO A. CARMINATI; MARÍA VICTORIA BERTOLDI; CLAUDIO M. FADER

Salta

Congreso; SAIB-PABMB; 2019

Platelet-rich plasma (PRP) is a preparation containing a higher concentration of platelets, isolated from autologous blood, which contains numerous different growth factors and cytokines that activates several cellular signaling cascades. Some of these signalings are wound healing and osteogenesis promotion by stimulation of homeostatic responses to injury. Autophagy is an essential cellular homeostatic mechanism by which intracellular components are delivered into the lysosomes for degradation and recycling. Autophagy has been related to a diversity of pathological or physiological dentary processes such as bone remodeling, skeletal aging, osteoclastogenesis, osteoblastogenesis, and different types of oral cancer. Bone homeostasis is a tightly controlled mechanism in which osteoblasts (OB, the cells responsible for bone formation), osteoclasts (OC,the cells specialized for bone resorption) and osteocytes (the multifunctional mechanosensing cells embedded in the bone matrix), are the main actors in bone remodeling. Osteoblast and adipocytes originate from common mesenchymal stem cells (MSCs), and several transcription factorscontrol the differentiation of the two lineages. It is known that 3T3-L1 cells, an immortalized preadipocyte cell line, are able to differentiate into bone-forming osteoblasts by transdifferentiation. This differentiation produces an increase of alkaline phosphatase (ALP) activity and expression of osteocalcin (OC), some known osteoblast factors. These data indicate that 3T3-L1 cells are a good model to study the molecular mechanisms of osteoblast function and differentiation. This report aimed to show whether PRP was able to induce autophagy in osteoblast precursors 3T3-L1 cells. Our results showed that PRP can increase the number of autophagic structures in 3T3-L1 and HeLa (cervical cancer cells) cells. Moreover, we have determined by Western blot a rise in the lipidated form of the autophagic protein LC3 (i.e. LC3-II) upon PRP treatment. Taken together, our results suggest that PRP is able to induce a strong autophagy response in osteoblast precursor and, to a lesser extent, in non-related osteoblastic cells, suggesting that PRP could be a potential therapeutic tool for some autophagy-related diseases associated with bone homeostasis.