Kishimoto Tatsuma, Ishida Waka, Nakajima Isana, Taguchi Osamu, Sugioka Koji, Kusaka Shunji, Fukuda Ken
Department of Ophthalmology and Visual Science, Kochi Medical School, Kochi University, Nankoku City, Kochi, Japan.
Department of Ophthalmology, Kindai University Nara Hospital, Ikoma City, Nara, Japan; Department of Ophthalmology, Kindai University Faculty of Medicine, Osakasayama City, Osaka, Japan.
Exp Eye Res. 2022 May;218:108980. doi: 10.1016/j.exer.2022.108980. Epub 2022 Feb 9.
Mast cells and conjunctival fibroblasts contribute to conjunctival wound healing and allergic ocular inflammation. The number of mast cells in the conjunctiva is increased in individuals with cicatricial fibrosis-causing ocular surface diseases and after glaucoma filtering surgery, suggesting that these cells may contribute to the scarring observed after such surgery. We studied the potential mechanism of fibroblast-mast cell interaction in the healing of conjunctival wounds using a three-dimensional collagen gel culture system. We found that mast cells derived from the bone marrow of mice embedded in a collagen gel did not induce gel contraction. However, an increase in mast cells was associated with increased collagen gel contraction mediated by mouse conjunctival fibroblasts. The extent of collagen degradation was not affected by the co-culture of mast cells and conjunctival fibroblasts. Gelatin zymography disclosed that mast cells increased the amounts of both the pro form of matrix metalloproteinase (MMP)-9 and the active form of MMP-2 in supernatants of conjunctival fibroblast cultures. Furthermore, the potentiating effect of mast cells on contraction of the collagen gel through conjunctival fibroblasts was attenuated by the addition of a synthetic MMP inhibitor. Thus, current results suggest that mast cells accelerate the conjunctival fibroblast-dependent contraction of collagen gel by increasing the release as well as activation of MMPs. Therefore, the interaction between mast cells and conjunctival fibroblasts may contribute to conjunctival scar formation after glaucoma filtering surgery.
肥大细胞和结膜成纤维细胞参与结膜伤口愈合和过敏性眼部炎症。在患有导致瘢痕性纤维化的眼表疾病的个体以及青光眼滤过手术后,结膜中肥大细胞的数量会增加,这表明这些细胞可能与该手术后观察到的瘢痕形成有关。我们使用三维胶原凝胶培养系统研究了结膜伤口愈合过程中,成纤维细胞与肥大细胞相互作用的潜在机制。我们发现,嵌入胶原凝胶中的源自小鼠骨髓的肥大细胞不会诱导凝胶收缩。然而,肥大细胞数量的增加与小鼠结膜成纤维细胞介导的胶原凝胶收缩增加有关。胶原降解的程度不受肥大细胞与结膜成纤维细胞共培养的影响。明胶酶谱分析显示,肥大细胞增加了结膜成纤维细胞培养上清液中基质金属蛋白酶(MMP)-9的前体形式和MMP-2的活性形式的含量。此外,添加合成MMP抑制剂可减弱肥大细胞通过结膜成纤维细胞对胶原凝胶收缩的增强作用。因此,目前的结果表明,肥大细胞通过增加MMP的释放以及激活来加速结膜成纤维细胞依赖的胶原凝胶收缩。所以,肥大细胞与结膜成纤维细胞之间的相互作用可能导致青光眼滤过手术后结膜瘢痕形成。