Hershey, Pa. From the Wound Healing Laboratory, Division of Plastic Surgery, The Pennsylvania State University, College of Medicine, M. S. Hershey Medical Center.
Plast Reconstr Surg. 2011 Apr;127(4):1478-1486. doi: 10.1097/PRS.0b013e318208d0bb.
Mast cells' association with fibrosis is known, but the mechanics of that association are unclear. The hypothesis is that mast cells promote fibroblast profibrotic activities through heterocellular gap junctional intercellular communications. Casting populated collagen lattices with both human mastocytoma cell line (HMC-1), an established mast cell line, and fibroblasts enhances lattice contraction via gap junctional intercellular communications. Unfortunately, in monolayer culture, HMC-1 cells and fibroblasts do not form heterocellular gap junctional intercellular communications. Freshly isolated rat peritoneal mast cells, however, establish these communications with fibroblasts in monolayer culture. Isolated rat peritoneal mast cells, however, survive only 7 days. Establishing a rat mast cell line that grows in the same medium as fibroblasts advances the study of mast cell-fibroblast interactions. HMC-1 cells thrive without supplements, suggesting that they release the factor(s) necessary for their viability. Spent HMC-1 medium may contain the factor(s) that generate a viable rat mast cell line.
Rat peritoneal-isolated mast cells grew in culture medium containing spent HMC-1 medium for 4 weeks. At 4 weeks, rat mast cells (RMC-1) were successfully maintained in Dulbecco's Modified Eagle Medium with 10% serum.
RMC-1 cells formed heterocellular gap junctional intercellular communications with fibroblasts, enhancing both fibroblast proliferation and co-cultured RMC-1/fibroblast/populated collagen lattice contraction. Enhanced fibroblast proliferation and lattice contraction failed to occur by including RMC-1 cells unable to establish gap junctional intercellular communications with fibroblasts, but cell proliferation was not affected by including degranulated RMC-1 cells.
Heterocellular gap junctional intercellular communications with mast cells increase in fibroblast proliferation and fibroblast PCL contraction, two hypertrophic scar fibroblast activities.
已知肥大细胞与纤维化有关，但这种关联的机制尚不清楚。假说认为，肥大细胞通过异细胞缝隙连接细胞间通讯促进成纤维细胞的促纤维化活性。用已建立的肥大细胞瘤株 HMC-1（人肥大细胞瘤株）和成纤维细胞铸造富含胶原蛋白的格子会通过缝隙连接细胞间通讯增强格子收缩。不幸的是，在单层培养中，HMC-1 细胞和成纤维细胞不会形成异细胞缝隙连接细胞间通讯。然而，新鲜分离的大鼠腹腔肥大细胞在单层培养中与成纤维细胞建立这些通讯。然而，分离的大鼠腹腔肥大细胞仅存活 7 天。建立一种与成纤维细胞在相同培养基中生长的大鼠肥大细胞瘤株可推进肥大细胞和成纤维细胞相互作用的研究。HMC-1 细胞无需补充即可茁壮成长，这表明它们释放了维持其生存所需的因子。用过的 HMC-1 培养基可能含有产生可行的大鼠肥大细胞系的因子。
大鼠腹腔分离的肥大细胞在含有用过的 HMC-1 培养基的培养基中培养 4 周。在第 4 周，大鼠肥大细胞（RMC-1）成功地在含 10%血清的 Dulbecco 改良 Eagle 培养基中维持。
RMC-1 细胞与成纤维细胞形成异细胞缝隙连接细胞间通讯，增强了成纤维细胞增殖和共培养的 RMC-1/成纤维细胞/富含胶原蛋白格子的收缩。未能通过包括不能与成纤维细胞建立缝隙连接细胞间通讯的 RMC-1 细胞来实现增强的成纤维细胞增殖和格子收缩，但细胞增殖不受包括脱颗粒的 RMC-1 细胞的影响。
与肥大细胞的异细胞缝隙连接细胞间通讯增加了成纤维细胞的增殖和成纤维细胞 PCL 的收缩，这是两种肥大瘢痕成纤维细胞的活性。
