Pooled Platelet-Rich Plasma Lysate Therapy Increases Synoviocyte Proliferation and Hyaluronic Acid Production While Protecting Chondrocytes From Synoviocyte-Derived Inflammatory Mediators.
Pooled Platelet-Rich Plasma Lysate Therapy Increases Synoviocyte Proliferation and Hyaluronic Acid Production While Protecting Chondrocytes From Synoviocyte-Derived Inflammatory Mediators.
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DOI：
10.3389/fvets.2018.00150
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发表时间：
2018
影响因子：
3.2
通讯作者：
Schnabel LV
中科院分区：
文献类型：
--
作者：
Gilbertie JM;Long JM;Schubert AG;Berglund AK;Schaer TP;Schnabel LV
富含血小板血浆（PRP）制剂用于治疗人类和兽医的骨关节炎（OA），并取得了一定的成功。然而，此类制剂由于本质上是自体的并且受到巨大的患者和加工变异性的影响而受到阻碍。因此，人们对使用血小板裂解物制剂代替传统 PRP 越来越感兴趣。血小板裂解物制剂是无细胞的，因此减少了对免疫原性的担忧，并且含有高浓度的生长因子和细胞因子。此外，血小板裂解物制剂可以冷冻保存以备随时使用。本研究的目的是评估混合同种异体富血小板血浆裂解物 (PRP-L) 制剂对体外炎症介质刺激的马滑膜细胞和软骨细胞的影响，以模拟 OA 关节环境。我们的假设是，PRP-L 治疗发炎的滑膜细胞可以通过减少滑膜细胞促炎细胞因子的产生同时增加滑膜细胞抗炎细胞因子的产生来保护受到滑膜细胞条件培养基攻击的软骨细胞。用白介素-1β (IL-1β) 或脂多糖 (LPS) 刺激滑膜细胞 24 小时，然后不处理或用贫血小板血浆裂解物 (PPP-L) 或 PRP-L 处理 48 小时。在治疗期结束时评估滑膜细胞生长，并评估滑膜细胞条件培养基中透明质酸（HA）、IL-1β、肿瘤坏死因子α（TNF-α）和白细胞介素6（IL-6）的浓度。然后用每个刺激组和治疗组的滑膜细胞条件培养基攻击软骨细胞 48 小时，并检查 I 型胶原蛋白 (COL1A1)、II 型胶原蛋白 (COL2A1) 和 III 型胶原蛋白 (COL3A1)、聚集蛋白聚糖 (ACAN)、润滑素 (PRG4) 以及基质金属肽酶 3 (MMP-3) 和 13 (MMP-13) 的基因表达。用 PRP-L 处理发炎的滑膜细胞会导致滑膜细胞生长增加以及滑膜细胞 HA 和 IL-6 的产生增加。用来自 PRP-L 处理的滑膜细胞的条件培养基攻击软骨细胞，导致 II 型胶原和聚集蛋白聚糖基因表达增加，以及 MMP-13 基因表达减少。这项研究的结果支持继续研究使用混合 PRP-L 治疗骨关节炎，并需要进一步的体外研究来辨别 PRP-L 的作用机制。
Platelet-rich plasma (PRP) preparations are being used with moderate success to treat osteoarthritis (OA) in humans and in veterinary species. Such preparations are hindered, however, by being autologous in nature and subject to tremendous patient and processing variability. For this reason, there has been increasing interest in the use of platelet lysate preparations instead of traditional PRP. Platelet lysate preparations are acellular, thereby reducing concerns over immunogenicity, and contain high concentrations of growth factors and cytokines. In addition, platelet lysate preparations can be stored frozen for readily available use. The purpose of this study was to evaluate the effects of a pooled allogeneic platelet-rich plasma lysate (PRP-L) preparation on equine synoviocytes and chondrocytes challenged with inflammatory mediators in-vitro to mimic the OA joint environment. Our hypothesis was that PRP-L treatment of inflamed synoviocytes would protect chondrocytes challenged with synoviocyte conditioned media by reducing synoviocyte pro-inflammatory cytokine production while increasing synoviocyte anti-inflammatory cytokine production. Synoviocytes were stimulated with either interleukin-1β (IL-1β) or lipopolysaccharide (LPS) for 24 h followed by no treatment or treatment with platelet-poor plasma lysate (PPP-L) or PRP-L for 48 h. Synoviocyte growth was evaluated at the end of the treatment period and synoviocyte conditioned media was assessed for concentrations of hyaluronic acid (HA), IL-1β, tumor necrosis factor alpha (TNF-α), and interleukin-6 (IL-6). Chondrocytes were then challenged for 48 h with synoviocyte conditioned media from each stimulation and treatment group and examined for gene expression of collagen types I (COL1A1), II (COL2A1), and III (COL3A1), aggrecan (ACAN), lubricin (PRG4), and matrix metallopeptidase 3 (MMP-3) and 13 (MMP-13). Treatment of inflamed synoviocytes with PRP-L resulted in increased synoviocyte growth and increased synoviocyte HA and IL-6 production. Challenge of chondrocytes with conditioned media from PRP-L treated synoviocytes resulted in increased collagen type II and aggrecan gene expression as well as decreased MMP-13 gene expression. The results of this study support continued investigation into the use of pooled PRP-L for the treatment of osteoarthritis and warrant further in-vitro studies to discern the mechanisms of action of PRP-L.
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影响因子：
7.5
作者：
Bussche L;Harman RM;Syracuse BA;Plante EL;Lu YC;Curtis TM;Ma M;Van de Walle GR
通讯作者：
Van de Walle GR
影响因子：
5
作者：
Bennell, Kim L.;Hunter, David J.;Paterson, Kade L.
通讯作者：
Paterson, Kade L.
影响因子：
3.3
作者：
Andersen, Mette Bisgaard;Pingel, Jessica;Langberg, Henning
通讯作者：
Langberg, Henning
影响因子：
3.7
作者：
Broeckx S;Zimmerman M;Crocetti S;Suls M;Mariën T;Ferguson SJ;Chiers K;Duchateau L;Franco-Obregón A;Wuertz K;Spaas JH
通讯作者：
Spaas JH
DOI：
10.1073/pnas.1514854113
发表时间：
2016-05-10
影响因子：
11.1
作者：
Bouaziz, Wafa;Sigaux, Johanna;Hay, Eric
通讯作者：
Hay, Eric