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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, email

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.

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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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cc This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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