Platelet-Rich Fibrin Decreases the Inflammatory Response of Mesenchymal Cells
Chronic inflammation is a pathological process where cells of the mesenchymal lineage become a major source of inflammatory mediators. Platelet-rich fibrin (PRF) has been shown to possess potent anti-inflammatory activity in macrophages, but its impact on mesenchymal cells has not been investigated....
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2021
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oai:doaj.org-article:5f2fe166ded343b2b4daf0b3a7ab13842021-11-11T16:48:58ZPlatelet-Rich Fibrin Decreases the Inflammatory Response of Mesenchymal Cells10.3390/ijms2221113331422-00671661-6596https://doaj.org/article/5f2fe166ded343b2b4daf0b3a7ab13842021-10-01T00:00:00Zhttps://www.mdpi.com/1422-0067/22/21/11333https://doaj.org/toc/1661-6596https://doaj.org/toc/1422-0067Chronic inflammation is a pathological process where cells of the mesenchymal lineage become a major source of inflammatory mediators. Platelet-rich fibrin (PRF) has been shown to possess potent anti-inflammatory activity in macrophages, but its impact on mesenchymal cells has not been investigated. The aim of this study was, therefore, to expose mesenchymal cells to inflammatory cytokines together with lysates generated from liquid platelet-poor plasma (PPP), the cell-rich buffy coat layer (BC; concentrated-PRF or C-PRF), and the remaining red clot layer (RC), following centrifugation of blood. Heating PPP generates an albumin gel (Alb-gel) that when mixed back with C-PRF produces Alb-PRF. Membranes prepared from solid PRF were also subjected to lysis. We report here that lysates of PPP, BC, and PRF decreased the cytokine-induced expression of interleukin 6 (IL6) and nitric oxide synthase (iNOS) in the bone marrow-derived ST2 cells. Consistently, PPP, BC, and PRF greatly decreased the phosphorylation and nuclear translocation of p65 in ST2 cells. The inflammatory response caused by Pam3CSK4 was reduced accordingly. Moreover, PPP, BC, and PRF reduced the enhanced expression of inflammatory mediators IL6 and iNOS in 3T3-L1 pre-adipocyte mesenchymal cells, and iNOS and CCL5 in murine calvarial cells. Surprisingly, PRF lysates were not effective in reducing the inflammatory response of human gingival fibroblasts and HSC2 epithelial cells. The data from the present study suggest that both liquid PRF and solid PRF exert potent anti-inflammatory activity in murine mesenchymal cells.Zahra KargarpourJila NasirzadeLayla PanahipourRichard J. MironReinhard GruberMDPI AGarticleplatelet-rich fibrininflammationToll-like receptormesenchymal cellscytokineBiology (General)QH301-705.5ChemistryQD1-999ENInternational Journal of Molecular Sciences, Vol 22, Iss 11333, p 11333 (2021) |
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platelet-rich fibrin inflammation Toll-like receptor mesenchymal cells cytokine Biology (General) QH301-705.5 Chemistry QD1-999 |
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platelet-rich fibrin inflammation Toll-like receptor mesenchymal cells cytokine Biology (General) QH301-705.5 Chemistry QD1-999 Zahra Kargarpour Jila Nasirzade Layla Panahipour Richard J. Miron Reinhard Gruber Platelet-Rich Fibrin Decreases the Inflammatory Response of Mesenchymal Cells |
description |
Chronic inflammation is a pathological process where cells of the mesenchymal lineage become a major source of inflammatory mediators. Platelet-rich fibrin (PRF) has been shown to possess potent anti-inflammatory activity in macrophages, but its impact on mesenchymal cells has not been investigated. The aim of this study was, therefore, to expose mesenchymal cells to inflammatory cytokines together with lysates generated from liquid platelet-poor plasma (PPP), the cell-rich buffy coat layer (BC; concentrated-PRF or C-PRF), and the remaining red clot layer (RC), following centrifugation of blood. Heating PPP generates an albumin gel (Alb-gel) that when mixed back with C-PRF produces Alb-PRF. Membranes prepared from solid PRF were also subjected to lysis. We report here that lysates of PPP, BC, and PRF decreased the cytokine-induced expression of interleukin 6 (IL6) and nitric oxide synthase (iNOS) in the bone marrow-derived ST2 cells. Consistently, PPP, BC, and PRF greatly decreased the phosphorylation and nuclear translocation of p65 in ST2 cells. The inflammatory response caused by Pam3CSK4 was reduced accordingly. Moreover, PPP, BC, and PRF reduced the enhanced expression of inflammatory mediators IL6 and iNOS in 3T3-L1 pre-adipocyte mesenchymal cells, and iNOS and CCL5 in murine calvarial cells. Surprisingly, PRF lysates were not effective in reducing the inflammatory response of human gingival fibroblasts and HSC2 epithelial cells. The data from the present study suggest that both liquid PRF and solid PRF exert potent anti-inflammatory activity in murine mesenchymal cells. |
format |
article |
author |
Zahra Kargarpour Jila Nasirzade Layla Panahipour Richard J. Miron Reinhard Gruber |
author_facet |
Zahra Kargarpour Jila Nasirzade Layla Panahipour Richard J. Miron Reinhard Gruber |
author_sort |
Zahra Kargarpour |
title |
Platelet-Rich Fibrin Decreases the Inflammatory Response of Mesenchymal Cells |
title_short |
Platelet-Rich Fibrin Decreases the Inflammatory Response of Mesenchymal Cells |
title_full |
Platelet-Rich Fibrin Decreases the Inflammatory Response of Mesenchymal Cells |
title_fullStr |
Platelet-Rich Fibrin Decreases the Inflammatory Response of Mesenchymal Cells |
title_full_unstemmed |
Platelet-Rich Fibrin Decreases the Inflammatory Response of Mesenchymal Cells |
title_sort |
platelet-rich fibrin decreases the inflammatory response of mesenchymal cells |
publisher |
MDPI AG |
publishDate |
2021 |
url |
https://doaj.org/article/5f2fe166ded343b2b4daf0b3a7ab1384 |
work_keys_str_mv |
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_version_ |
1718432241716035584 |