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本文引用的文献

1
CCN2 is necessary for the function of mouse embryonic fibroblasts.CCN2对于小鼠胚胎成纤维细胞的功能是必需的。
Exp Cell Res. 2007 Mar 10;313(5):952-64. doi: 10.1016/j.yexcr.2006.12.006. Epub 2006 Dec 23.
2
All in the CCN family: essential matricellular signaling modulators emerge from the bunker.CCN家族全解析：关键的基质细胞信号调节因子崭露头角。
J Cell Sci. 2006 Dec 1;119(Pt 23):4803-10. doi: 10.1242/jcs.03270.
3
Transforming growth factor-beta signaling through the Smad proteins: role in systemic sclerosis.通过Smad蛋白的转化生长因子-β信号传导：在系统性硬化症中的作用
Autoimmun Rev. 2006 Oct;5(8):563-9. doi: 10.1016/j.autrev.2006.06.001. Epub 2006 Jul 5.
4
New concepts regarding focal adhesion kinase promotion of cell migration and proliferation.关于粘着斑激酶促进细胞迁移和增殖的新概念。
J Cell Biochem. 2006 Sep 1;99(1):35-52. doi: 10.1002/jcb.20956.
5
Constitutive ALK5-independent c-Jun N-terminal kinase activation contributes to endothelin-1 overexpression in pulmonary fibrosis: evidence of an autocrine endothelin loop operating through the endothelin A and B receptors.组成性非ALK5依赖的c-Jun氨基末端激酶激活导致肺纤维化中内皮素-1过表达：通过内皮素A和B受体起作用的自分泌内皮素环的证据。
Mol Cell Biol. 2006 Jul;26(14):5518-27. doi: 10.1128/MCB.00625-06.
6
Scar wars: is TGFbeta the phantom menace in scleroderma?瘢痕之战：转化生长因子β是硬皮病中的幽灵威胁吗？
Arthritis Res Ther. 2006;8(4):213. doi: 10.1186/ar1976.
7
Contribution of activin receptor-like kinase 5 (transforming growth factor beta receptor type I) signaling to the fibrotic phenotype of scleroderma fibroblasts.激活素受体样激酶5（转化生长因子β I型受体）信号传导对硬皮病成纤维细胞纤维化表型的作用。
Arthritis Rheum. 2006 Apr;54(4):1309-16. doi: 10.1002/art.21725.
8
CCN2 is necessary for adhesive responses to transforming growth factor-beta1 in embryonic fibroblasts.CCN2对于胚胎成纤维细胞中对转化生长因子-β1的黏附反应是必需的。
J Biol Chem. 2006 Apr 21;281(16):10715-26. doi: 10.1074/jbc.M511343200. Epub 2006 Feb 16.
9
Matrix contraction by dermal fibroblasts requires transforming growth factor-beta/activin-linked kinase 5, heparan sulfate-containing proteoglycans, and MEK/ERK: insights into pathological scarring in chronic fibrotic disease.真皮成纤维细胞介导的基质收缩需要转化生长因子-β/激活素相关激酶5、含硫酸乙酰肝素的蛋白聚糖和MEK/ERK：对慢性纤维化疾病病理性瘢痕形成的见解
Am J Pathol. 2005 Dec;167(6):1699-711. doi: 10.1016/s0002-9440(10)61252-7.
10
Crosstalk mechanisms between the mitogen-activated protein kinase pathways and Smad signaling downstream of TGF-beta: implications for carcinogenesis.丝裂原活化蛋白激酶途径与转化生长因子-β下游Smad信号之间的串扰机制：对致癌作用的影响
Oncogene. 2005 Aug 29;24(37):5742-50. doi: 10.1038/sj.onc.1208928.

粘着斑激酶（FAK）是成纤维细胞中转化生长因子β（TGFβ）诱导的c-Jun氨基末端激酶（JNK）磷酸化所必需的：对获得基质重塑表型的影响。

FAK is required for TGFbeta-induced JNK phosphorylation in fibroblasts: implications for acquisition of a matrix-remodeling phenotype.

作者信息

Liu Shangxi, Xu Shi-wen, Kennedy Laura, Pala Daphne, Chen Yunliang, Eastwood Mark, Carter David E, Black Carol M, Abraham David J, Leask Andrew

机构信息

Division of Oral Biology and Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON, Canada.

出版信息

Mol Biol Cell. 2007 Jun;18(6):2169-78. doi: 10.1091/mbc.e06-12-1121. Epub 2007 Apr 4.

DOI:10.1091/mbc.e06-12-1121
PMID:17409352
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1877111/
Abstract

Transforming growth factor beta (TGFbeta) plays a critical role in connective tissue remodeling by fibroblasts during development, tissue repair, and fibrosis. We investigated the molecular pathways in the transmission of TGFbeta signals that lead to features of connective tissue remodeling, namely formation of an alpha-smooth muscle actin (alpha-SMA) cytoskeleton, matrix contraction, and expression of profibrotic genes. TGFbeta causes the activation of focal adhesion kinase (FAK), leading to JNK phosphorylation. TGFbeta induces JNK-dependent actin stress fiber formation, matrix contraction, and expression of profibrotic genes in fak+/+, but not fak-/-, fibroblasts. Overexpression of MEKK1, a kinase acting upstream of JNK, rescues TGFbeta responsiveness of JNK-dependent transcripts and actin stress fiber formation in FAK-deficient fibroblasts. Thus we propose a FAK-MEKK1-JNK pathway in the transmission of TGFbeta signals leading to the control of alpha-SMA cytoskeleton reorganization, matrix contraction, and profibrotic gene expression and hence to the physiological and pathological effects of TGFbeta on connective tissue remodeling by fibroblasts.

摘要

转化生长因子β（TGFβ）在发育、组织修复和纤维化过程中，成纤维细胞对结缔组织重塑起着关键作用。我们研究了TGFβ信号转导的分子途径，这些途径导致结缔组织重塑的特征，即α平滑肌肌动蛋白（α-SMA）细胞骨架的形成、基质收缩和促纤维化基因的表达。TGFβ导致粘着斑激酶（FAK）激活，进而导致JNK磷酸化。TGFβ在野生型成纤维细胞中诱导JNK依赖的肌动蛋白应力纤维形成、基质收缩和促纤维化基因表达，但在FAK基因敲除的成纤维细胞中则无此作用。MEKK1是一种作用于JNK上游的激酶，其过表达可恢复FAK缺陷型成纤维细胞中JNK依赖转录本的TGFβ反应性和肌动蛋白应力纤维形成。因此，我们提出了一条FAK-MEKK1-JNK信号通路，该通路参与TGFβ信号转导，从而控制α-SMA细胞骨架重组、基质收缩和促纤维化基因表达，进而介导TGFβ对成纤维细胞结缔组织重塑的生理和病理作用。