Lysophosphatidic acid augments fibroblast-mediated contraction of released collagen gels.

The Journal of laboratory and clinical medicine Pub Date : 2002-01-01 DOI:10.1067/MLC.2002.120650

T. Mio, Xiangde Liu, M. Toews, S. Rennard

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引用次数: 21

Abstract

Lysophosphatidic acid (LPA) is a glycerophospholipid released from platelets that has multiple biologic effects. The present study evaluated the potential of LPA to modulate tissue repair and remodeling by modifying human lung fibro-blast-mediated contraction of three-dimensional collagen gels. The contraction of native collagen gels caused by human fetal lung fibroblasts was augmented by LPA in a concentration-dependent manner. The estimated median effective concentration was 3 x 10(-7) mol/L, which was well below the concentrations likely released by platelets in tissues. LPA-augmented contraction was not blocked by pertussis toxin or cholera toxin but was inhibited by inhibition of phospholipase C. Neither calcium mobilization nor protein kinase C appeared to play a role. In contrast, the effect of LPA appeared to depend on a kinase inhibited by staurosporine but not by genistein or GF109203X, suggesting a process that depends on phospholipase C and may involve a novel protein kinase. By modulating fibroblast-mediated remodeling, LPA could play a role in the tissue remodeling that characterizes wound repair.

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溶血磷脂酸增强成纤维细胞介导的释放的胶原凝胶收缩。

溶血磷脂酸(LPA)是一种从血小板释放的甘油磷脂，具有多种生物效应。本研究评估了LPA通过改变人肺成纤维介导的三维胶原凝胶收缩来调节组织修复和重塑的潜力。LPA可增强人胎儿肺成纤维细胞引起的天然胶原凝胶的收缩，并呈浓度依赖性。估计中位有效浓度为3 × 10(-7) mol/L，远低于组织中血小板可能释放的浓度。lpa增强收缩不被百日咳毒素或霍乱毒素阻断，但被磷脂酶C的抑制所抑制。钙动员和蛋白激酶C似乎都不起作用。相反，LPA的作用似乎依赖于一种被staurosporine抑制的激酶，而不是被染料木素或GF109203X抑制的激酶，这表明这一过程依赖于磷脂酶C，可能涉及一种新的蛋白激酶。通过调节成纤维细胞介导的重塑，LPA可能在伤口修复的组织重塑中发挥作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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The Journal of laboratory and clinical medicine

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