• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法，用中文像聊天一样搜索，搜遍4000万医学文献。AI智能推荐，让科研检索更轻松。

立即免费搜索

文件翻译

保留排版，准确专业，支持PDF/Word/PPT等文件格式，支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述，25分钟生成高质量综述，智能提取关键信息，辅助科研写作。

立即免费体验

肿瘤坏死因子-α抑制人皮肤成纤维细胞中α-平滑肌肌动蛋白的表达：对异常伤口愈合的一种启示。

TNF-alpha suppresses alpha-smooth muscle actin expression in human dermal fibroblasts: an implication for abnormal wound healing.

作者信息

Goldberg Mytien T, Han Yuan-Ping, Yan Chunli, Shaw Michael C, Garner Warren L

机构信息

Division of Plastic Surgery, Keck School of Medicine, University of Southern California, Los Angeles, California, USA.

出版信息

J Invest Dermatol. 2007 Nov;127(11):2645-55. doi: 10.1038/sj.jid.5700890. Epub 2007 May 31.

DOI:10.1038/sj.jid.5700890
PMID:17554369
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2366884/
Abstract

Abnormal wound healing encompasses a wide spectrum, from chronic wounds to hypertrophic scars. Both conditions are associated with an abnormal cytokine profile in the wound bed. In this study, we sought to understand the dynamic relationships between myofibroblast differentiation and mechanical performance of the collagen matrix under tissue growth factor-beta (TGF-beta) and tumor necrosis factor-alpha (TNF-alpha) stimulation. We found TGF-beta increased alpha-smooth muscle actin (alpha-SMA) and TNF-alpha alone decreased the basal alpha-SMA expression. When TGF-beta1 and TNF-alpha were both added, the alpha-SMA expression was suppressed below the baseline. Real-time PCR showed that TNF-alpha suppresses TGF-beta1-induced myofibroblast (fibroproliferative) phenotypic genes, for example, alpha-SMA, collagen type 1A, and fibronectin at the mRNA level. TNF-alpha suppresses TGF-beta1-induced gene expression by affecting its mRNA stability. Our results further showed that TNF-alpha inhibits TGF-beta1-induced Smad-3 phosphorylation via Jun N-terminal kinase signaling. Mechanical testing showed that TNF-alpha decreases the stiffness and contraction of the lattices after 5 days in culture. We proposed that changes in alpha-SMA, collagen, and fibronectin expression result in decreased contraction and stiffness of collagen matrices. Therefore, the balance of cytokines in a wound defines the mechanical properties of the extracellular matrix and optimal wound healing.

摘要

异常伤口愈合涵盖范围广泛，从慢性伤口到增生性瘢痕。这两种情况均与伤口床中细胞因子谱异常有关。在本研究中，我们试图了解在组织生长因子-β（TGF-β）和肿瘤坏死因子-α（TNF-α）刺激下，肌成纤维细胞分化与胶原基质力学性能之间的动态关系。我们发现TGF-β增加α-平滑肌肌动蛋白（α-SMA），而单独的TNF-α降低基础α-SMA表达。当同时添加TGF-β1和TNF-α时，α-SMA表达被抑制至基线以下。实时PCR显示，TNF-α在mRNA水平抑制TGF-β1诱导的肌成纤维细胞（纤维增生性）表型基因，例如α-SMA、1A型胶原和纤连蛋白。TNF-α通过影响其mRNA稳定性来抑制TGF-β1诱导的基因表达。我们的结果进一步表明，TNF-α通过Jun N末端激酶信号传导抑制TGF-β1诱导的Smad-3磷酸化。力学测试表明，培养5天后，TNF-α降低晶格的硬度和收缩性。我们提出，α-SMA、胶原和纤连蛋白表达的变化导致胶原基质收缩和硬度降低。因此，伤口中细胞因子的平衡决定了细胞外基质的力学性能和最佳伤口愈合。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b53/2366884/f06fe63d99ba/nihms46527f10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b53/2366884/56eace9ca42b/nihms46527f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b53/2366884/f11fcf90119b/nihms46527f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b53/2366884/046d411d87fe/nihms46527f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b53/2366884/b04d4e05e770/nihms46527f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b53/2366884/6aa0c225b152/nihms46527f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b53/2366884/a6d2eda1faab/nihms46527f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b53/2366884/03db1f8b5870/nihms46527f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b53/2366884/db3c62c36a19/nihms46527f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b53/2366884/7ac99aabe7fe/nihms46527f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b53/2366884/f06fe63d99ba/nihms46527f10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b53/2366884/56eace9ca42b/nihms46527f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b53/2366884/f11fcf90119b/nihms46527f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b53/2366884/046d411d87fe/nihms46527f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b53/2366884/b04d4e05e770/nihms46527f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b53/2366884/6aa0c225b152/nihms46527f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b53/2366884/a6d2eda1faab/nihms46527f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b53/2366884/03db1f8b5870/nihms46527f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b53/2366884/db3c62c36a19/nihms46527f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b53/2366884/7ac99aabe7fe/nihms46527f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b53/2366884/f06fe63d99ba/nihms46527f10.jpg

相似文献

1
TNF-alpha suppresses alpha-smooth muscle actin expression in human dermal fibroblasts: an implication for abnormal wound healing.肿瘤坏死因子-α抑制人皮肤成纤维细胞中α-平滑肌肌动蛋白的表达：对异常伤口愈合的一种启示。
J Invest Dermatol. 2007 Nov;127(11):2645-55. doi: 10.1038/sj.jid.5700890. Epub 2007 May 31.
2
Wnt4 negatively regulates the TGF-β1-induced human dermal fibroblast-to-myofibroblast transition via targeting Smad3 and ERK.Wnt4 通过靶向 Smad3 和 ERK 负调控 TGF-β1 诱导的人真皮成纤维细胞向肌成纤维细胞转化。
Cell Tissue Res. 2020 Mar;379(3):537-548. doi: 10.1007/s00441-019-03110-x. Epub 2019 Nov 27.
3
In vitro cultured fetal fibroblasts have myofibroblast-associated characteristics and produce a fibrotic-like environment upon stimulation with TGF-β1: Is there a thin line between fetal scarless healing and fibrosis?体外培养的胎儿成纤维细胞具有肌成纤维细胞相关特征，并在转化生长因子-β1刺激下产生类似纤维化的环境：胎儿无瘢痕愈合与纤维化之间是否存在细微差别？
Arch Dermatol Res. 2017 Mar;309(2):111-121. doi: 10.1007/s00403-016-1710-3. Epub 2016 Dec 21.
4
Role of vitronectin and fibronectin receptors in oral mucosal and dermal myofibroblast differentiation.玻连蛋白和纤连蛋白受体在口腔黏膜和真皮肌成纤维细胞分化中的作用
Biol Cell. 2007 Nov;99(11):601-14. doi: 10.1042/BC20070008.
5
[Effects of silencing Smad ubiquitination regulatory factor 2 on the function of human hypertrophic scar-derived fibroblasts].沉默Smad泛素化调节因子2对人增生性瘢痕来源成纤维细胞功能的影响
Zhonghua Shao Shang Za Zhi. 2017 Mar 20;33(3):145-151. doi: 10.3760/cma.j.issn.1009-2587.2017.03.004.
6
Ligand-activated PPARδ upregulates α-smooth muscle actin expression in human dermal fibroblasts: A potential role for PPARδ in wound healing.配体激活的过氧化物酶体增殖物激活受体δ上调人皮肤成纤维细胞中α平滑肌肌动蛋白的表达：过氧化物酶体增殖物激活受体δ在伤口愈合中的潜在作用。
J Dermatol Sci. 2015 Dec;80(3):186-95. doi: 10.1016/j.jdermsci.2015.10.005. Epub 2015 Oct 9.
7
[Tofacitinib inhibits the transformation of lung fibroblasts into myofibroblasts through JAK/STAT3 pathway].托法替布通过JAK/STAT3信号通路抑制肺成纤维细胞向肌成纤维细胞的转化。
Beijing Da Xue Xue Bao Yi Xue Ban. 2024 Jun 18;56(3):505-511. doi: 10.19723/j.issn.1671-167X.2024.03.018.
8
[Effects of mechanical tension on the formation of hypertrophic scars in rabbit ears and transforming growth factor-β/Smad signaling pathway].[机械张力对兔耳增生性瘢痕形成及转化生长因子-β/Smad信号通路的影响]
Zhonghua Shao Shang Yu Chuang Mian Xiu Fu Za Zhi. 2022 Dec 20;38(12):1162-1169. doi: 10.3760/cma.j.cn501120-20211213-00412.
9
[Influences of human dermis derived mesenchymal stem cells on α-SMA and DCN expressions of hypertrophic scars fibroblasts].人真皮来源间充质干细胞对增生性瘢痕成纤维细胞α-SMA及DCN表达的影响
Zhonghua Zheng Xing Wai Ke Za Zhi. 2016 Jul;32(4):285-92.
10
Simvastatin inhibits transforming growth factor-β1-induced expression of type I collagen, CTGF, and α-SMA in keloid fibroblasts.辛伐他汀抑制瘢痕成纤维细胞中转化生长因子-β1 诱导的 I 型胶原、结缔组织生长因子和 α-SMA 的表达。
Wound Repair Regen. 2014 Jan-Feb;22(1):125-33. doi: 10.1111/wrr.12136. Epub 2013 Dec 13.

引用本文的文献

1
Anti-Inflammatory and Antimicrobial Effect of Ellagic Acid and Punicalagin in Dermal Fibroblasts.鞣花酸和石榴皮苷对真皮成纤维细胞的抗炎和抗菌作用
Int J Mol Sci. 2025 Sep 5;26(17):8681. doi: 10.3390/ijms26178681.
2
M2-like macrophages derived from THP-1 cells promote myofibroblast differentiation of synovial fibroblasts in association with the TGF-β1/SMAD2/3 signaling pathway.源自THP-1细胞的M2样巨噬细胞与TGF-β1/SMAD2/3信号通路相关，促进滑膜成纤维细胞向肌成纤维细胞分化。
Sci Rep. 2025 Jul 15;15(1):25505. doi: 10.1038/s41598-025-10858-6.
3
Effect of Hydrothermal Coatings of Magnesium AZ31 Alloy on Osteogenic Differentiation of hMSCs: From Gene to Protein Analysis.

本文引用的文献

1
Cell adaptation to a physiologically relevant ECM mimic with different viscoelastic properties.细胞对具有不同粘弹性特性的生理相关细胞外基质模拟物的适应性。
Biomaterials. 2007 Feb;28(4):671-9. doi: 10.1016/j.biomaterials.2006.09.038. Epub 2006 Oct 17.
2
Focal adhesion size controls tension-dependent recruitment of alpha-smooth muscle actin to stress fibers.粘着斑大小控制α-平滑肌肌动蛋白向应力纤维的张力依赖性募集。
J Cell Biol. 2006 Jan 16;172(2):259-68. doi: 10.1083/jcb.200506179. Epub 2006 Jan 9.
3
Local administration of TGF-beta1 to reinforce the anterior abdominal wall in a rat model of incisional hernia.
镁合金AZ31水热涂层对人骨髓间充质干细胞成骨分化的影响：从基因到蛋白质分析
Materials (Basel). 2025 Mar 12;18(6):1254. doi: 10.3390/ma18061254.
4
Electrospinning strategies targeting fibroblast for wound healing of diabetic foot ulcers.针对成纤维细胞的静电纺丝策略用于糖尿病足溃疡的伤口愈合
APL Bioeng. 2025 Feb 25;9(1):011501. doi: 10.1063/5.0235412. eCollection 2025 Mar.
5
Next-Generation Biomaterials for Wound Healing: Development and Evaluation of Collagen Scaffolds Functionalized with a Heparan Sulfate Mimic and Fibroblast Growth Factor 2.用于伤口愈合的下一代生物材料：用硫酸乙酰肝素模拟物和成纤维细胞生长因子2功能化的胶原蛋白支架的开发与评估
J Funct Biomater. 2025 Feb 7;16(2):51. doi: 10.3390/jfb16020051.
6
Corneal protective effects of a new ophthalmic formulation based on vitamin B12 and sodium hyaluronate.基于维生素B12和透明质酸钠的新型眼科制剂对角膜的保护作用
Front Pharmacol. 2025 Jan 31;16:1548213. doi: 10.3389/fphar.2025.1548213. eCollection 2025.
7
Molecular insights and efficacy of guava leaf oil emulgel in managing non diabetic as well as diabetic wound healing by reducing inflammation and oxidative stress.番石榴叶油乳胶在通过减轻炎症和氧化应激来管理非糖尿病及糖尿病伤口愈合方面的分子见解与功效。
Inflammopharmacology. 2025 Mar;33(3):1491-1503. doi: 10.1007/s10787-025-01648-7. Epub 2025 Feb 8.
8
Therapeutic potential of phloridzin carbomer gel for skin inflammatory healing in atopic dermatitis.根皮苷卡波姆凝胶对特应性皮炎皮肤炎症愈合的治疗潜力。
Arch Dermatol Res. 2025 Feb 6;317(1):352. doi: 10.1007/s00403-025-03866-z.
9
Immunological Regulation of Fibrosis During Heart Failure: It Takes Two to Tango.心力衰竭期间纤维化的免疫调节：两人才能跳探戈。
Biomolecules. 2025 Jan 3;15(1):58. doi: 10.3390/biom15010058.
10
Regulation of fibronectin and collagens type I, III and VI by TNF-α, TGF-β, IL-13, and tofacitinib.肿瘤坏死因子-α、转化生长因子-β、白细胞介素-13及托法替布对纤连蛋白以及Ⅰ型、Ⅲ型和Ⅵ型胶原蛋白的调控
Sci Rep. 2025 Jan 7;15(1):1087. doi: 10.1038/s41598-024-84151-3.
在大鼠切口疝模型中局部给予转化生长因子β1以加强腹壁。
Hernia. 2005 Oct;9(3):252-8. doi: 10.1007/s10029-005-0341-y. Epub 2005 May 24.
4
Transcriptional interactions of transforming growth-factor-beta with pro-inflammatory cytokines.转化生长因子-β与促炎细胞因子的转录相互作用。
Curr Biol. 1993 Dec 1;3(12):822-31. doi: 10.1016/0960-9822(93)90216-b.
5
Smad7 is required for TGF-beta-induced activation of the small GTPase Cdc42.转化生长因子β（TGF-β）诱导小GTP酶Cdc42激活需要Smad7。
J Cell Sci. 2004 Apr 1;117(Pt 9):1835-47. doi: 10.1242/jcs.01036.
6
On and off: proteasome and TGF-beta signaling.断断续续：蛋白酶体与转化生长因子-β信号传导
Exp Cell Res. 2003 Dec 10;291(2):275-81. doi: 10.1016/j.yexcr.2003.07.007.
7
Interference with transforming growth factor-beta/ Smad3 signaling results in accelerated healing of wounds in previously irradiated skin.干扰转化生长因子-β/ Smad3信号传导可加速先前受辐照皮肤伤口的愈合。
Am J Pathol. 2003 Dec;163(6):2247-57. doi: 10.1016/s0002-9440(10)63582-1.
8
Cell and molecular mechanics of biological materials.生物材料的细胞与分子力学
Nat Mater. 2003 Nov;2(11):715-25. doi: 10.1038/nmat1001.
9
The myofibroblast in wound healing and fibrocontractive diseases.伤口愈合和纤维收缩性疾病中的肌成纤维细胞。
J Pathol. 2003 Jul;200(4):500-3. doi: 10.1002/path.1427.
10
Smad3: a key player in pathogenetic mechanisms dependent on TGF-beta.Smad3：依赖转化生长因子-β的致病机制中的关键因子。
Ann N Y Acad Sci. 2003 May;995:1-10. doi: 10.1111/j.1749-6632.2003.tb03205.x.