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碱性成纤维细胞生长因子通过调控 PI3-激酶-Rac1-JNK 通路促进创面愈合中纤维母细胞的迁移。

bFGF regulates PI3-kinase-Rac1-JNK pathway and promotes fibroblast migration in wound healing.

机构信息

Department of Plastic Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.

出版信息

PLoS One. 2010 Aug 17;5(8):e12228. doi: 10.1371/journal.pone.0012228.

DOI:10.1371/journal.pone.0012228
PMID:20808927
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2923192/
Abstract

Fibroblast proliferation and migration play important roles in wound healing. bFGF is known to promote both fibroblast proliferation and migration during the process of wound healing. However, the signal transduction of bFGF-induced fibroblast migration is still unclear, because bFGF can affect both proliferation and migration. Herein, we investigated the effect of bFGF on fibroblast migration regardless of its effect on fibroblast proliferation. We noticed involvement of the small GTPases of the Rho family, PI3-kinase, and JNK. bFGF activated RhoA, Rac1, PI3-kinase, and JNK in cultured fibroblasts. Inhibition of RhoA did not block bFGF-induced fibroblast migration, whereas inhibition of Rac1, PI3-kinase, or JNK blocked the fibroblast migration significantly. PI3-kinase-inhibited cells down-regulated the activities of Rac1 and JNK, and Rac1-inhibited cells down-regulated JNK activity, suggesting that PI3-kinase is upstream of Rac1 and that JNK is downstream of Rac1. Thus, we concluded that PI3-kinase, Rac1, and JNK were essential for bFGF-induced fibroblast migration, which is a novel pathway of bFGF-induced cell migration.

摘要

成纤维细胞增殖和迁移在伤口愈合中起着重要作用。bFGF 已知在伤口愈合过程中促进成纤维细胞增殖和迁移。然而，bFGF 诱导的成纤维细胞迁移的信号转导仍不清楚，因为 bFGF 可以影响增殖和迁移。在此，我们研究了 bFGF 对成纤维细胞迁移的影响，而不考虑其对成纤维细胞增殖的影响。我们注意到 Rho 家族的小 GTPases、PI3-激酶和 JNK 的参与。bFGF 激活了培养的成纤维细胞中的 RhoA、Rac1、PI3-激酶和 JNK。RhoA 的抑制并没有阻止 bFGF 诱导的成纤维细胞迁移，而 Rac1、PI3-激酶或 JNK 的抑制则显著阻止了成纤维细胞的迁移。PI3-激酶抑制的细胞下调 Rac1 和 JNK 的活性，而 Rac1 抑制的细胞下调 JNK 活性，表明 PI3-激酶是 Rac1 的上游，而 JNK 是 Rac1 的下游。因此，我们得出结论，PI3-激酶、Rac1 和 JNK 是 bFGF 诱导的成纤维细胞迁移所必需的，这是 bFGF 诱导的细胞迁移的新途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5010/2923192/a06b31348f3e/pone.0012228.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5010/2923192/27b4b3ba4055/pone.0012228.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5010/2923192/d0ef88fe8173/pone.0012228.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5010/2923192/bd6989c05047/pone.0012228.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5010/2923192/cb49da777be6/pone.0012228.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5010/2923192/9188bcbee077/pone.0012228.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5010/2923192/8bd027bce863/pone.0012228.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5010/2923192/698760523af0/pone.0012228.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5010/2923192/a06b31348f3e/pone.0012228.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5010/2923192/27b4b3ba4055/pone.0012228.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5010/2923192/d0ef88fe8173/pone.0012228.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5010/2923192/bd6989c05047/pone.0012228.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5010/2923192/cb49da777be6/pone.0012228.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5010/2923192/9188bcbee077/pone.0012228.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5010/2923192/8bd027bce863/pone.0012228.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5010/2923192/698760523af0/pone.0012228.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5010/2923192/a06b31348f3e/pone.0012228.g008.jpg

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