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首页> 外文期刊>Annals of Plastic Surgery >Calcimycin Suppresses S100A4 Expression and Inhibits the Stimulatory Effect of Transforming Growth Factor 1 on Keloid Fibroblasts
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Calcimycin Suppresses S100A4 Expression and Inhibits the Stimulatory Effect of Transforming Growth Factor 1 on Keloid Fibroblasts

机译:钙霉素抑制S100A4表达并抑制转化生长因子1对瘢痕疙瘩成纤维细胞的刺激作用

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摘要

Recent researches have indicated that S100A4 participates in tissue fibrosis, whereas calcimycin inhibits this process as a novel S100A4 transcription inhibitor. However, the relationship and mechanisms between calcimycin and S100A4 in keloid fibroblasts (KFs) remain unknown. The present research was aimed to evaluate the effect of calcimycin on S100A4 expression and pathogenesis in KFs. Keloid fibroblasts were cultured and exposed to different concentrations of calcimycin in the absence or presence of transforming growth factor 1 (TGF-1). The results showed that the expression of S100A4 was significantly increased in keloid derived fibroblasts compared with normal skin fibroblasts. Calcimycin depressed S100A4 in a concentration- and time-dependent manner. Moreover, calcimycin suppressed TGF-1-induced collagen type I, fibronectin, and -smooth muscle actin expression and cell viability in cultured KFs. Furthermore, calcimycin modulated expression of TGF-/Smad target genes Smad7 and phosphorylation of TGF-1-induced Smad2/3. This research for the first time confirmed the presence of S100A4 in KFs. Calcimycin inhibits the expression of S100A4, as well as KF proliferation and migration and extracellular matrix (ECM) synthesis. Taken together, these results indicate that calcimycin might be a therapeutic candidate to keloid or other related fibrotic disorders.
机译:最近的研究表明,S100A4参与组织纤维化,而钙霉素抑制该过程作为新型S100A4转录抑制剂。然而,瘢痕疙瘩和瘢痕疙瘩成纤维细胞(KFS)中的钙霉素和S100A4之间的关系和机制仍然未知。本研究旨在评估钙霉素对KFS中S100A4表达和发病机制的影响。在不存在或存在转化生长因子1(TGF-1)的情况下培养并暴露于不同浓度的钙霉素的培养基成纤维细胞。结果表明,与正常皮肤成纤维细胞相比,瘢痕疙瘩衍生的成纤维细胞中S100A4的表达显着增加。钙霉素按下S100A4以浓度和时间依赖的方式。此外,钙霉素抑制了TGF-1诱导的胶原I,纤连蛋白和-Smooth肌肉肌动蛋白的表达和细胞活力在培养的KFS中。此外,钙霉素调节TGF-/ Smad靶基因Smad7的表达和TGF-1诱导的Smad2 / 3的磷酸化。这项研究首次证实了KFS中S100A4的存在。钙霉素抑制S100A4的表达,以及KF增殖和迁移和细胞外基质(ECM)合成。总之,这些结果表明钙霉素可能是瘢痕疙瘩或其他相关纤维化疾病的治疗候选者。

著录项

  • 来源
    《Annals of Plastic Surgery》 |2018年第2期|共7页
  • 作者单位

    Shanghai Jiao Tong Univ Sch Med Shanghai Peoples Hosp 9 Dept Plast &

    Reconstruct Surg 639 Zhi;

    Shanghai Jiao Tong Univ Sch Med Shanghai Peoples Hosp 9 Dept Plast &

    Reconstruct Surg 639 Zhi;

    Shanghai Jiao Tong Univ Sch Med Shanghai Peoples Hosp 9 Dept Plast &

    Reconstruct Surg 639 Zhi;

    Shanghai Jiao Tong Univ Sch Med Shanghai Peoples Hosp 9 Dept Plast &

    Reconstruct Surg 639 Zhi;

    Shanghai Jiao Tong Univ Sch Med Shanghai Peoples Hosp 9 Dept Plast &

    Reconstruct Surg 639 Zhi;

    Shanghai Jiao Tong Univ Sch Med Shanghai Peoples Hosp 9 Dept Plast &

    Reconstruct Surg 639 Zhi;

    Shanghai Jiao Tong Univ Sch Med Shanghai Peoples Hosp 9 Dept Plast &

    Reconstruct Surg 639 Zhi;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 整形外科学(修复外科学);
  • 关键词

    calcimycin; fibroblasts; keloid; S100A4; TGF-1;

    机译:钙霉素;成纤维细胞;瘢痕疙瘩;S100A4;TGF-1;

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