Ehrlich H Paul, Hunt Thomas K
Division of Plastic Surgery, Penn State University College of Medicine , Hershey, Pennsylvania.
Department of Surgery, University of California at San Francisco , San Francisco, California.
Adv Wound Care (New Rochelle). 2012 Feb;1(1):3-9. doi: 10.1089/wound.2011.0311.
Open wound closure by wound contraction produces a healed defect made up mostly of dermis. Generating thicker collagen fibers condenses granulation tissue, which pulls surrounding skin into the defect.
What is the mechanism for open wound contraction? Is it through the generation of contractile force using sustained myosin ATPase, thus causing cell contraction or by rapid myosin ATPase that condenses collagen fibrils into fibers?
BASIC/CLINICAL SCIENCE ADDRESSED: The mechanism for wound contraction is not often debated after the discovery of the myofibroblast. Myofibroblasts are the major cell phenotype in maturing granulation tissue. It is concluded, not quite accurately, that myofibroblasts are responsible for wound contraction. As wound contraction progresses, polarized light microscopy reveals birefringence patterns associated with ever-increasing thickening of collagen fibers. Collagen fibers thicken by eliminating water between fibrils. Wound contraction requires collagen synthesis and granulation tissue compaction. Both myofibroblasts and fibroblasts synthesize collagen, but fibroblasts, not myofibroblasts, compact collagen. Free-floating fibroblast-populated collagen lattices (FPCL) contract by rapid myosin ATPase, thus resulting in thicker collagen fibers by elongated fibroblasts. The release of an attached FPCL, using sustained myosin ATPase, produces rapid lattice contraction, now populated with contracted myofibroblasts in the absence of thick collagen fibers.
and studies show that rapid myosin ATPase is the motor for wound contraction. Myofibroblasts maintain steady mechano-tension through sustained myosin ATPase, which generates cell contraction forces that fail to produce thicker collagen fibers. The hypothesis is that cytoplasmic microfilaments pull collagen fibrils over the fibroblast's plasma membrane surface, bringing collagen fibrils in closer contact with one another. The self-assembly nature of collagen fixes collagen fibrils in regular arrays generating thicker collagen fibers.
Wound contraction progresses through fibroblasts generating thicker collagen fibers, using tractional forces; rather than by myofibroblasts utilizing cell contraction forces.
通过伤口收缩实现开放伤口闭合会产生一个主要由真皮构成的愈合缺损。生成更粗的胶原纤维会使肉芽组织浓缩，从而将周围皮肤拉入缺损处。
开放伤口收缩的机制是什么？是通过利用持续的肌球蛋白ATP酶产生收缩力，从而引起细胞收缩，还是通过快速的肌球蛋白ATP酶将胶原原纤维浓缩成纤维？
基础/临床科学探讨：在肌成纤维细胞被发现后，伤口收缩的机制并不常被争论。肌成纤维细胞是成熟肉芽组织中的主要细胞表型。得出的结论不太准确，即肌成纤维细胞负责伤口收缩。随着伤口收缩的进行，偏振光显微镜显示出与胶原纤维不断增厚相关的双折射模式。胶原纤维通过消除原纤维之间的水分而增厚。伤口收缩需要胶原合成和肉芽组织压实。肌成纤维细胞和成纤维细胞都能合成胶原，但压实胶原的是成纤维细胞，而非肌成纤维细胞。自由漂浮的成纤维细胞填充的胶原晶格（FPCL）通过快速的肌球蛋白ATP酶收缩，从而使成纤维细胞伸长形成更粗的胶原纤维。使用持续的肌球蛋白ATP酶释放附着的FPCL会产生快速的晶格收缩，此时在没有粗胶原纤维的情况下充满了收缩的肌成纤维细胞。
研究表明快速的肌球蛋白ATP酶是伤口收缩的动力。肌成纤维细胞通过持续的肌球蛋白ATP酶维持稳定的机械张力，该酶产生的细胞收缩力无法产生更粗的胶原纤维。假说是细胞质微丝将胶原原纤维拉过成纤维细胞的质膜表面，使胶原原纤维彼此更紧密接触。胶原的自组装性质将胶原原纤维固定成规则排列，形成更粗的胶原纤维。
伤口收缩是通过成纤维细胞利用牵引力产生更粗的胶原纤维来进行的；而不是通过肌成纤维细胞利用细胞收缩力。
