• 主题
高级搜索  >
历史搜索 清空历史
首页> 美国卫生研究院文献>Cells Tissues Organs >Diminished Type III Collagen Promotes Myofibroblast Differentiation and Increases Scar Deposition in Cutaneous Wound Healing
【2h】

Diminished Type III Collagen Promotes Myofibroblast Differentiation and Increases Scar Deposition in Cutaneous Wound Healing

机译：减少的III型胶原蛋白促进肌成纤维细胞分化并增加皮肤伤口愈合中的疤痕沉积

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务，本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文，但由于OA文献来源多样且变更频繁，仍可能出现获取不到、文献不完整或与标题不符等情况，如果获取不到我们将提供退款服务。请知悉。
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The repair of cutaneous wounds in the postnatal animal is associated with the development of scar tissue. Directing cell activities to efficiently heal wounds while minimizing the development of scar tissue is a major goal of wound management and the focus of intensive research efforts. Type III collagen (Col3), expressed in early granulation tissue, has been proposed to play a prominent role in cutaneous wound repair, although little is known about its role in this process. To establish the role of Col3 in cutaneous wound repair, we examined the healing of excisional wounds in a previously described murine model of Col3 deficiency. Col3 deficiency (Col3+/–) in aged mice resulted in accelerated wound closure with increased wound contraction. In addition, Col3-deficient mice had increased myofibroblast density in the wound granulation tissue as evidenced by an increased expression of the myofibroblast marker, α-smooth muscle actin. In vitro, dermal fibroblasts obtained from Col3-deficient embryos (Col3+/– and –/–) were more efficient at collagen gel contraction and also displayed increased myofibroblast differentiation compared to those harvested from wild-type (Col3+/+) embryos. Finally, wounds from Col3-deficient mice also had significantly more scar tissue area on day 21 postwounding compared to wild-type mice. The effect of Col3 expression on myofibroblast differentiation and scar formation in this model suggests a previously undefined role for this ECM protein in tissue regeneration and repair.
机译：产后动物皮肤伤口的修复与疤痕组织的发展有关。指导细胞活动以有效治愈伤口，同时最大程度地减少疤痕组织的形成是伤口管理的主要目标，也是深入研究工作的重点。有人提出在早期肉芽组织中表达的III型胶原蛋白（Col3）在皮肤伤口修复中起着重要作用，尽管鲜为人知。为了建立Col3在皮肤伤口修复中的作用，我们在先前描述的Col3缺乏小鼠模型中检查了切除伤口的愈合。老年小鼠的Col3缺乏症（Col3 +/–）导致伤口闭合加速，伤口收缩增加。另外，Col3缺陷型小鼠的伤口肉芽组织中的成纤维细胞密度增加，这是由成纤维细胞标志物α-平滑肌肌动蛋白表达增加所证明的。在体外，与从野生型（Col3 + / +）胚胎收获的真皮成纤维细胞相比，从Col3缺陷型胚胎（Col3 +/–和– / –）获得的真皮成纤维细胞在胶原蛋白凝胶收缩方面更有效，并且还显示出增加的成纤维细胞分化。最后，与野生型小鼠相比，Col3缺陷小鼠的伤口在受伤后第21天的疤痕组织面积也明显增加。在此模型中，Col3表达对成肌纤维细胞分化和瘢痕形成的影响表明，该ECM蛋白在组织再生和修复中的作用尚不确定。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号