牙周韧带干细胞在 PAR1 激活下产生的细胞膜可改善成骨分化。

IF 1.5 4区 医学 Q3 DENTISTRY, ORAL SURGERY & MEDICINE
Brazilian oral research Pub Date : 2024-09-02 eCollection Date: 2024-01-01 DOI:10.1590/1807-3107bor-2024.vol38.0079
Letícia Miquelitto Gasparoni, Tomaz Alves, Bruno Nunes de França, Danilo Balzarini, Emmanuel Albuquerque-Souza, Ana Clara Fagundes Pedroni, Emanuel da Silva Rovai, Aldrin Huamán Mendoza, Carla Renata Sipert, Marinella Holzhausen
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引用次数: 0

摘要

牙周再生是一项挑战,而以牙周韧带干细胞(PDLSCs)为基础的组织工程学已被证明是这一过程的一种有前途的替代方法。然而,对支架的需求限制了牙周韧带干细胞的治疗用途。在这种情况下,使用细胞片(CS)技术的无支架组织工程已被开发为一种改善组织再生的替代方法。此前,我们发现蛋白酶激活受体-1(PAR1)可以调控 PDLSCs。在此,我们评估了 PAR1 是否会影响由 PDLSCs 制成的 CS 的成骨过程,而无需使用支架。我们分离了 PDLSCs 并对其进行了免疫分型。然后,通过在培养基中添加抗坏血酸(50 µg/mL)获得CSs,并通过其激动剂肽(100 nM)激活PAR1。无支架三维CSs成功地从PDLSCs中产生,与分离的PDLSCs相比,它们显示出更高的增殖潜力。此外,PAR1 的激活还能通过增加矿化结节沉积和碱性磷酸酶浓度来减少 CSs 的衰老并改善其成骨分化;PAR1 还能在基因和蛋白水平上调节成骨标志物。我们进一步证实,这种效应受 PDLSCs 中 Wnt、TGF-βI、MEK、p38 MAPK 和 FGF/VEGF 信号通路的调控(p < 0.05%)。总之,PAR1 的激活提高了 CSs 的成骨活性,是一种很有前景的牙周再生无支架治疗方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Cell sheet produced from periodontal ligament stem cells activated by PAR1 improves osteogenic differentiation.

Periodontal regeneration is a challenge, and tissue engineering based on periodontal ligament stem cells (PDLSCs) has been shown to be a promising alternative to this process. However, the need for scaffolds has limited the therapeutic use of PDLSCs. In this context, scaffold-free tissue engineering using the cell sheet (CS) technique has been developed as an alternative approach to improve tissue regeneration. Previously, we showed that Protease-activated receptor-1 (PAR1) can regulate PDLSCs. Herein, we evaluate whether PAR1 influences osteogenesis in CSs produced from PDLSCs, without the use of scaffolds. PDLSCs were isolated and immunophenotyped. Then, CSs were obtained by supplementing the culture medium with ascorbic acid (50 µg/mL), and PAR1 was activated through its agonist peptide (100 nM). Scaffold-free 3D CSs were successfully produced from PDLSCs, and they showed higher proliferation potential than isolated PDLSCs. Also, PAR1 activation decreased senescence and improved osteogenic differentiation of CSs by increasing mineralized nodule deposition and alkaline phosphatase concentration; PAR1 also modulated osteogenic markers at the gene and protein levels. We further demonstrated that this effect was regulated by Wnt, TGF-βI, MEK, p38 MAPK, and FGF/VEGF signaling pathways in PDLSCs (p < 0.05%). Overall, PAR1 activation increased osteogenic activity in CSs, emerging as a promising scaffold-free therapeutic approach for periodontal regeneration.

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来源期刊
CiteScore
3.70
自引率
4.00%
发文量
107
审稿时长
12 weeks
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