From the Laboratory for Tissue Repair and Regenerative Surgery and the Division of Plastic and Reconstructive Surgery, Northwestern University, Feinberg School of Medicine.
Plast Reconstr Surg. 2020 Jul;146(1):43e-53e. doi: 10.1097/PRS.0000000000006922.
Skeletal muscle trauma can produce grave functional deficits, but therapeutic options remain limited. The authors studied whether a decellularized skeletal muscle scaffold would provide benefits in inducing skeletal muscle regeneration over acellular dermal matrices.
Eighty-two rat muscle defects were surgically created and assigned to no intervention or implantation of AlloDerm, Strattice, decellularized rat muscle, or decellularized rat dermis to 30 or 60 days. Decellularized rat muscle and dermis were prepared using a negative pressure-assisted protocol. Assessment for cellularity, neovascularization, myogenesis, inflammation and fibrosis were done histologically and by polymerase chain reaction.
Histology showed relative hypercellularity of AlloDerm (p < 0.003); Strattice appeared encapsulated. Immunofluorescence for CD31 and myosin heavy chain in decellularized rat muscle revealed dense microvasculature and peripheral islands of myogenesis. MyoD expression in muscle scaffolds was 23-fold higher than in controls (p < 0.01). Decellularized rat muscle showed no up-regulation of COX-2 (p < 0.05), with less expression than decellularized rat dermis and Strattice (p < 0.002). Decellularized rat muscle scaffolds expressed tumor necrosis factor-α less than Strattice, AlloDerm, and decellularized rat dermis (p < 0.01); collagen-1a less than decellularized rat dermis and Strattice (p < 0.04); α-smooth muscle actin 7-fold less than AlloDerm (p = 0.04); and connective tissue growth factor less than Strattice, AlloDerm, and decellularized rat dermis (p < 0.02).
Decellularized muscle matrix appears to reduce inflammation and fibrosis in an animal muscle defect as compared with dermal matrices and promotes greater expression of myocyte differentiation-inducing genes.
骨骼肌创伤可导致严重的功能障碍，但治疗选择仍然有限。作者研究了脱细胞骨骼肌支架在诱导骨骼肌再生方面是否优于脱细胞真皮基质。
通过手术在 82 只大鼠的肌肉缺损处造成损伤，然后将这些大鼠分为不干预组和植入 AlloDerm、Strattice、脱细胞大鼠肌肉或脱细胞大鼠真皮组，分别在 30 天或 60 天进行检测。使用负压辅助法制备脱细胞大鼠肌肉和真皮。通过组织学和聚合酶链反应评估细胞、新生血管、肌生成、炎症和纤维化情况。
组织学显示 AlloDerm 具有相对较高的细胞密度（p<0.003）；Strattice 表现为被包裹。脱细胞大鼠肌肉的 CD31 和肌球蛋白重链免疫荧光显示出密集的微血管和周围肌生成小岛。肌肉支架中的 MyoD 表达水平比对照组高 23 倍（p<0.01）。脱细胞大鼠肌肉中 COX-2 没有上调（p<0.05），其表达水平低于脱细胞大鼠真皮和 Strattice（p<0.002）。脱细胞大鼠肌肉支架的肿瘤坏死因子-α表达水平低于 Strattice、AlloDerm 和脱细胞大鼠真皮（p<0.01）；胶原-1a 低于脱细胞大鼠真皮和 Strattice（p<0.04）；α-平滑肌肌动蛋白低 7 倍（p=0.04）；结缔组织生长因子低于 Strattice、AlloDerm 和脱细胞大鼠真皮（p<0.02）。
与真皮基质相比，脱细胞肌肉基质似乎在动物肌肉缺损中减少了炎症和纤维化，并促进了更多的肌细胞分化诱导基因表达。
