El-Ghazaly, Mona ARashed, Engy REl-Sabbagh, Walaa AEl-Hazek, Rania M.Rashed, Rasha ROmar, Nesreen Nabil2019-11-272019-11-272018-031011-1344https://doi.org/https://www.ncbi.nlm.nih.gov/pubmed/29413698Accession Number: WOS:000428490800003BACKGROUND: Platelet-rich plasma (PRP) is a source of natural growth factors and is emerging as a treatment modality to mitigate radiotherapy- induced adverse effects. Activin A (ACTA) is a member of the transforming growth factor-β (TGF-β) superfamily, which has been shown to modulate the inflammatory response and macrophages polarization between different phenotypes. The aim of this study is to determine the value of PRP in preventing radiation-induced malignancies in light of the cross-talk between PRP and activin A type II receptors (ActR-IIA)/follistatin (FST) signaling pathways where the inflammatory responses at 2 different time points were evaluated. MATERIAL AND METHODS: Male albino rats were exposed to radiation and given PRP over the course of 6 days. Rats were sacrificed on day 7 or day 28 post radiation. RESULTS: Quantitative real-time reverse transcriptase polymerase chain reaction (QRT-PCR) and western-blot showed that after 7 days of administrating of PRP, ActR-IIA/FST signaling was markedly induced and was associated with the expressions of inflammatory, natural killer and M1 macrophages markers, TNF-α, IL-1β, IFN-γ and IL-12. By contrast, on day 28 of PRP administration, ActR-IIA/FST signaling and the expressions of proinflammatory cytokines were downregulated in parallel with inducing M2 macrophages phenotype as indicated by arginase-1, IL-10 and dectin-1. CONCLUSION: The suppression of inflammation and induction of M2 macrophages phenotype in response to PRP administration were found significantly linked to ActR-IIA/FST signaling downregulation. Furthermore, the specific M2 macrophage subtype was found to express dectin-1 receptors which have high affinity for tumor cells thereby is expected to reduce the potential for developing tumors after radiotherapy.en-USACTIVATIONREGENERATIONFOLLISTATINMACROPHAGESCANCERIMMUNITYWOUND REPAIRGROWTH-FACTORSRADIATION-THERAPYSTEM-CELLSMacrophages polarizationInflammationMalignancyRadiationActivin A/follistatin signalingPlatelet-rich plasmaArticlehttps://doi.org/