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MGF E peptide pretreatment improves collagen synthesis and cell proliferation of injured human ACL fibroblasts via MEK-ERK1/2 signaling pathway

机译:MGF E肽预处理通过MEK-ERK1 / 2信号通路改善了受伤人ACL成纤维细胞的胶原合成和细胞增殖

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摘要

Injured anterior cruciate ligament (ACL) is hard to heal due to the poor proliferative potential of ACL fibroblasts. To verify whether mechano-growth factor (MGF) E peptide can restore the cell proliferation of injured ACL fibroblasts, ACL fibroblasts pretreated with MGF E peptide were subjected to injurious stretch and the outcomes were evaluated at 0 and 24 h. After injured, the type III collagen synthesis was increased at 0 h while inhibited at 24 h. The matrix metalloproteinase-2 (MMP-2) activity/expression was up-regulated, but the cell proliferation was inhibited. Fortunately, exogenous MGF E peptide decreased the type I/III collagen synthesis at 0 h but improved the type III collagen synthesis at 24 h. It decreased the MMP-2 activity/expression of injured ACL fibroblasts. Besides, MGF E peptide accelerated the cell proliferation via MEK-ERK1/2 signaling pathway. Our results implied that MGF E peptide pretreatment could provide a new efficient approach for ACL regeneration.
机译:由于ACL成纤维细胞的增殖潜力差,受伤的前令韧带(ACL)难以愈合。 为了验证机械生长因子(MGF)E肽是否可以恢复受伤的ACL成纤维细胞的细胞增殖,用MGF E肽预处理的ACL成纤维细胞受到伤害拉伸,并在0和24小时评估结果。 受伤后,III型胶原蛋白合成在0小时升高,同时在24小时抑制。 基质金属蛋白酶-2(MMP-2)活性/表达上调,但抑制细胞增殖。 幸运的是,外源性MgF E肽在0小时下降低I / III型胶原蛋白合成,但在24小时时改善了III型胶原合成。 它降低了受损ACL成纤维细胞的MMP-2活性/表达。 此外,MGF E肽通过MEK-ERK1 / 2信号传导途径加速了细胞增殖。 我们的结果暗示MGF E肽预处理可以为ACL再生提供新的有效方法。

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