富血小板血浆(PRP)和PRP诱导的细胞增殖和迁移的细胞因子特征:HaCaT细胞中基质金属蛋白酶-1和-9的上调。

The Korean Journal of Hematology Pub Date : 2011-12-01 Epub Date: 2011-12-27 DOI:10.5045/kjh.2011.46.4.265
Hong-Bum Park, Jeong-Hee Yang, Kwang-Hoe Chung
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引用次数: 51

摘要

背景:富血小板血浆(PRP)治疗的基本原理是在损伤部位注射浓缩的PRP可以通过血小板释放细胞因子来促进组织修复。PRP治疗在皮肤伤口愈合过程中的分子机制目前尚不清楚,并将受益于澄清。方法:用血管激动剂刺激PRP 5 min,进行细胞因子谱分析。为了研究PRP的伤口愈合活性,我们在皮肤细胞中进行了细胞增殖和迁移分析。分析PRP对基质金属蛋白酶(matrix metalloproteinase, MMP)-1、-2、-9的表达、活性及转录因子激活的影响。结果:凝血酶是一种强刺激PRP激活释放生长因子和趋化因子。PRP诱导huvec、HaCaT细胞和HDFs的细胞增殖和迁移,以及HaCaT细胞中mmp -1和MMP-9的表达,但PRP对HDFs中MMPs的表达和活性没有显著影响。经PRP处理后,HaCaT细胞中的转录因子,包括信号转导因子和转录激活因子-3 (STAT-3)被磷酸化。结论:在本研究中,我们确定了激动剂刺激后活化的PRP的细胞因子谱。我们已经证明PRP通过调控MMPs在促进皮肤细胞增殖和迁移中发挥积极作用,这可能适用于未来PRP疗法的发展,以促进皮肤伤口愈合。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Characterization of the cytokine profile of platelet rich plasma (PRP) and PRP-induced cell proliferation and migration: Upregulation of matrix metalloproteinase-1 and -9 in HaCaT cells.

Characterization of the cytokine profile of platelet rich plasma (PRP) and PRP-induced cell proliferation and migration: Upregulation of matrix metalloproteinase-1 and -9 in HaCaT cells.

Characterization of the cytokine profile of platelet rich plasma (PRP) and PRP-induced cell proliferation and migration: Upregulation of matrix metalloproteinase-1 and -9 in HaCaT cells.

Characterization of the cytokine profile of platelet rich plasma (PRP) and PRP-induced cell proliferation and migration: Upregulation of matrix metalloproteinase-1 and -9 in HaCaT cells.

Background: The underlying rationale of platelet rich plasma (PRP) therapy is that an injection of concentrated PRP at the site of injury may promote tissue repair via cytokine release from platelets. The molecular mechanisms of PRP therapy in the skin wound healing process are not well understood at present, and would benefit from clarification.

Methods: PRP was stimulated with angonists for 5 min, and cytokine profile analysis was performed. To investigate the wound healing activity of PRP, cell proliferation and migration analyses were performed in skin cells. The effects of PRP were analyzed on the expression and activity of matrix metalloproteinase (MMP)-1, -2, -9, and the activation of transcription factors.

Results: Thrombin was found to be a strong stimulator of PRP activation to release growth factors and chemokines. PRP induced cell proliferation and migration in HUVECs, HaCaT cells, and HDFs, as well as MMP-1and MMP-9 expression in HaCaT cells, but PRP did not have a significant effect on the expression or activity of MMPs in HDFs. The transcription factors, including signal transducer and activator of transcription-3 (STAT-3) were found to be phosphorylated following PRP treatment in HaCaT cells.

Conclusion: In this study, we have identified the cytokine profile of activated PRP after agonist stimulation. We have shown that PRP plays an active role in promoting the proliferation and migration of skin cells via the regulation of MMPs, and this may be applicable to the future development of PRP therapeutics to enhance skin wound healing.

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