Trabucchi E, Radaelli E, Marazzi M, Foschi D, Musazzi M, Veronesi A M, Montorsi W
Department of General Surgery and Surgical Oncology, University of Milan, Italy.
Int J Tissue React. 1988;10(6):367-72.
Mast cells are known to participate in three phases of wound healing: the inflammatory reaction, angiogenesis and extracellular-matrix reabsorption. The inflammatory reaction is mediated by released histamine and arachidonic acid metabolites. Compound 48/80 and disodium-cromoglycate are both able to increase skin breaking strength shortly after wounding. Under light and electron microscopy we found that small, granule-poor, irregular mast cells (MLMC) accumulate in the wound. This suggests that the small MLMC (mucosal-like mast cells) migrate into the skin during wound healing, and that both CTMC (connective-tissue mast cells) and MLMC are involved in tissue repair. Moreover, there is some evidence that mast cells participate in angiogenesis, since heparin is able to stimulate endothelial-cell migration and proliferation in vitro, and protamine to inhibit these processes and also angiogenesis in vivo. When the effect of protamine on wound breaking strength was examined, we encountered a decrease which was not prevented by heparin administration. Further studies are needed to demonstrate that protamine is specifically involved in inhibiting heparin-mediated angiogenesis in wounded tissue. Finally, mast cells may play a role in the extracellular matrix remodelling, on the basis of in-vitro experiments (but there are still no in-vivo data).
炎症反应、血管生成和细胞外基质重吸收。炎症反应由释放的组胺和花生四烯酸代谢产物介导。化合物48/80和色甘酸钠都能够在受伤后不久增加皮肤断裂强度。在光学显微镜和电子显微镜下,我们发现小的、颗粒少的、不规则的肥大细胞(MLMC)在伤口处聚集。这表明小的MLMC(黏膜样肥大细胞)在伤口愈合过程中迁移到皮肤中,并且结缔组织肥大细胞(CTMC)和MLMC都参与组织修复。此外,有一些证据表明肥大细胞参与血管生成,因为肝素能够在体外刺激内皮细胞迁移和增殖,而鱼精蛋白能够抑制这些过程以及体内的血管生成。当检测鱼精蛋白对伤口断裂强度的影响时,我们发现其降低,且给予肝素并不能阻止这种降低。需要进一步研究来证明鱼精蛋白在受伤组织中特异性地参与抑制肝素介导的血管生成。最后,基于体外实验(但仍没有体内数据),肥大细胞可能在细胞外基质重塑中发挥作用。