Hershey, Pa. From the Division of Plastic Surgery, Department of Surgery, Pennsylvania State University, College of Medicine.
Plast Reconstr Surg. 2013 May;131(5):1036-1044. doi: 10.1097/PRS.0b013e3182865c3f.
The prominent inflammatory cell identified in excessive scarring is the mast cell. Hypertrophic scar exhibits myofibroblasts derived from the transformation of fibroblasts, increased collagen synthesis, and stationary nonmigratory resident cells. The co-culture of fibroblasts with an established rat mast cell line (RMC-1) was used to explore the hypothesis of whether mast cells through gap junctional intercellular communications guide fibroblasts in promoting excessive scarring.
Human dermal fibroblasts were cultured alone or co-cultured with RMC-1 cells as is or with either blocked gap junctional intercellular communications or devoid of cytoplasmic granules. Collagen synthesis was analyzed by dot blot analysis; immunohistology identified myofibroblasts, and a cell migration assay measured fibroblast locomotion.
Fibroblasts co-cultured with RMC-1 cells transformed into myofibroblasts, had increased collagen synthesis, and showed retarded cell migration. In contrast, RMC-1 cells unable to form gap junctional intercellular communications were similar to fibroblasts alone, failing to promote these activities. Degranulated RMC-1 cells were as effective as intact RMC-1 cells.
Mast cells induce fibroblast activities associated with hypertrophic scarring through gap junctional intercellular communications. Eliminating the mast cell or its gap junctional intercellular communications with fibroblasts may be a possible approach in preventing hypertrophic scarring or reducing fibrotic conditions.
在过度瘢痕形成中，明显的炎症细胞是肥大细胞。增生性瘢痕表现为成纤维细胞来源的肌成纤维细胞、胶原合成增加和静止的非迁移常驻细胞。将成纤维细胞与已建立的大鼠肥大细胞瘤系（RMC-1）共培养，以探讨肥大细胞是否通过缝隙连接细胞间通讯指导成纤维细胞促进过度瘢痕形成的假说。
单独培养人真皮成纤维细胞或与 RMC-1 细胞共培养，或用阻断缝隙连接细胞间通讯或去除细胞质颗粒的方法处理。通过斑点印迹分析检测胶原合成；免疫组化鉴定肌成纤维细胞，细胞迁移试验测量成纤维细胞的迁移。
与 RMC-1 细胞共培养的成纤维细胞转化为肌成纤维细胞，胶原合成增加，细胞迁移减慢。相比之下，不能形成缝隙连接细胞间通讯的 RMC-1 细胞与单独的成纤维细胞相似，不能促进这些活性。脱颗粒的 RMC-1 细胞与完整的 RMC-1 细胞一样有效。
肥大细胞通过缝隙连接细胞间通讯诱导与增生性瘢痕形成相关的成纤维细胞活性。消除肥大细胞或其与成纤维细胞的缝隙连接细胞间通讯可能是预防增生性瘢痕形成或减少纤维化的一种方法。
