Open Access
ARTICLE
Platelet rich plasma (PRP) induces autophagy in osteoblast precursor 3T3-L1
Sergio Andrés CARMINATI1,2, María Carolina BARBOSA2, Claudio Marcelo FADER1,2*
1
Universidad Nacional de Cuyo, Facultad de Odontología, Mendoza, Argentina
2
Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET). Instituto de Histología y Embriología (IHEM), Facultad de Ciencias Médicas, Universidad Nacional de Cuyo, Mendoza, Argentin
* Address correspondence to: Claudio M. Fader,
BIOCELL 2018, 42(1), 13-16. https://doi.org/10.32604/biocell.2018.07008
Abstract
Autophagy is an essential cellular homeostatic mechanism by which intracellular components
are delivered into the lysosomes for degradation and recycling. Autophagy has been related with a
diversity of pathological or physiological dentary processes such as bone remodeling, skeletal aging,
osteoclastogenesis, osteoblastogenesis and different types of oral cancer. Platelet-rich plasma (PRP),
isolated from autologous blood, is a plasma preparation containing a higher concentration of platelets
which contains numerous different growth factors and cytokines that activate several cellular signaling
cascades. The purpose of this study is to investigate the effect of PRP on autophagy stimulation in
both osteoblast precursor 3T3-L1 and non-related osteoblastic 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
strongly 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.
Keywords
Cite This Article
CARMINATI, S. A., BARBOSA, M. C., FADER, C. M. (2018). Platelet rich plasma (PRP) induces autophagy in osteoblast precursor 3T3-L1.
BIOCELL, 42(1), 13–16. https://doi.org/10.32604/biocell.2018.07008
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