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PRP具有預防肌膚纖維化效果

PRP具有預防肌膚纖維化效果 

PRP可消除TGF-β1誘導的電壓依賴性細胞間隙連接(gap junction)電流出現,亦可同時防止連結蛋白43(connexin 43)增加並促進連結蛋白26(connexin 26) 表達。這項研究增加了對調節成纖維細胞-肌成纖維細胞轉變的分子和功能機制的見解,並支持 PRP 的抗纖維化潛力;進一步證明PRP能夠阻礙細胞間隙連接(gap junction)的肌成纖維細胞生成。
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PRP科技新知- PRP具有預防肌膚纖維化效果

文章背景:
由於PRP的促肌原和抗纖維化作用,PRP治療對於骨骼肌修復與再生可能有所助益,但是PRP的抗纖維化作用仍存在爭議;這篇於2020年所發表的國際性期刊文章主要探討PRP對於體外轉化生長因子 (TGF)-β1誘導的成纖維細胞分化為肌成纖維細胞(纖維化的效應細胞)的抑制作用的研究。

結果簡介:
PRP可消除TGF-β1誘導的電壓依賴性細胞間隙連接(gap junction)電流出現,亦可同時防止連結蛋白43(connexin 43)增加並促進連結蛋白26(connexin 26) 表達。這項研究增加了對調節成纖維細胞-肌成纖維細胞轉變的分子和功能機制的見解,並支持 PRP 的抗纖維化潛力;進一步證明PRP能夠阻礙細胞間隙連接(gap junction)的肌成纖維細胞生成。

結論: PRP能達成抗纖維化效果。

原文摘要:
Skeletal muscle repair/regeneration may benefit by Platelet-Rich Plasma (PRP) treatment owing to PRP pro-myogenic and anti-fibrotic effects. However, PRP anti-fibrotic action remains controversial. Here, we extended our previous researches on the inhibitory effects of PRP on in vitro transforming growth factor (TGF)-β1-induced differentiation of fibroblasts into myofibroblasts, the effector cells of fibrosis, focusing on gap junction (GJ) intercellular communication. The myofibroblastic phenotype was evaluated by cell shape analysis, confocal fluorescence microscopy and Western blotting analyses of α-smooth muscle actin and type-1 collagen expression, and electrophysiological recordings of resting membrane potential, resistance, and capacitance. PRP negatively regulated myofibroblast differentiation by modifying all the assessed parameters. Notably, myofibroblast pairs showed an increase of voltage-dependent GJ functionality paralleled by connexin (Cx) 43 expression increase. TGF-β1-treated cells, when exposed to a GJ blocker, or silenced for Cx43 expression, failed to differentiate towards myofibroblasts. Although a minority, myofibroblast pairs also showed not-voltage-dependent GJ currents and coherently Cx26 expression. PRP abolished the TGF-β1-induced voltage-dependent GJ current appearance while preventing Cx43 increase and promoting Cx26 expression. This study adds insights into molecular and functional mechanisms regulating fibroblast-myofibroblast transition and supports the anti-fibrotic potential of PRP, demonstrating the ability of this product to hamper myofibroblast generation targeting GJs.
文章出處:
Squecco R, Chellini F, Idrizaj E, Tani A, Garella R, Pancani S, Pavan P, Bambi F, Zecchi-Orlandini S, Sassoli C: Platelet-Rich Plasma Modulates Gap Junction Functionality and Connexin 43 and 26 Expression During TGF-beta1-Induced Fibroblast to Myofibroblast Transition: Clues for Counteracting Fibrosis. Cells 2020, 9(5).