Division of Plastic Surgery, Penn State University College of Medicine, Hershey, Pennsylvania, USA.
Ann N Y Acad Sci. 2012 Oct;1269:74-8. doi: 10.1111/j.1749-6632.2012.06730.x.
In previous studies, granulation tissue from subcutaneous sponge implants in rats receiving thymosin β4, a 43-amino acid actin-binding protein that advances wound repair, produced the unexpected absence of myofibroblast populations, along with uniform organized collagen fibers within the newly deposited connective tissue matrix. This result raised the question of whether the Tβ4 effect on blocking fibroblasts transformation into myofibroblasts a direct or indirect one. We report here work in progress to address this question. When human dermal fibroblasts are plated at low density, upon reaching confluence, they all express α smooth muscle actin (αSMA) within their cytoplasmic stress fibers, morphologically defining them as myofibroblasts. Treating low-density plated fibroblasts with Tβ4 prevents their expression of αSMA, as well as the generation an uneven distribution of microtubules within the cytoplasm. The speculation is that Tβ4 disruption of the distribution of microtubules alters the TGF-β-Smad signaling pathway, thus blocking fibroblast transformation into myofibroblasts.
在以前的研究中，在接受胸腺素 β4（一种 43 个氨基酸的肌动蛋白结合蛋白，可促进伤口修复）的大鼠皮下海绵植入物的肉芽组织中，出乎意料地没有出现肌成纤维细胞群体，而新沉积的结缔组织基质内则存在均匀的有组织胶原纤维。这一结果提出了一个问题，即 Tβ4 阻止成纤维细胞向肌成纤维细胞转化的作用是直接的还是间接的。我们在此报告正在进行的工作，以解决这个问题。当人真皮成纤维细胞以低密度铺板时，当达到汇合时，它们都在细胞质应力纤维中表达α平滑肌肌动蛋白（αSMA），从形态上定义为肌成纤维细胞。用 Tβ4 处理低密度铺板的成纤维细胞，可阻止它们表达αSMA，以及细胞质中微管的不均匀分布。推测是 Tβ4 破坏微管的分布改变了 TGF-β-Smad 信号通路，从而阻止成纤维细胞向肌成纤维细胞的转化。
