UMR5305, Laboratory of Tissue Biology and Therapeutic Engineering, CNRS and University of Lyon, 8 Avenue Rockefeller, F-69373 Lyon, France.
Department of Dermatology, University Hospital of Muenster, D-48149 Muenster, Germany.
Int J Mol Sci. 2022 Jul 5;23(13):7486. doi: 10.3390/ijms23137486.
We evaluated the presence of tight junction (TJ) remnants in the (SC) of in vitro reconstructed human epidermis and human skin explants subjected or not to an aggressive topical treatment with beta-lipohydroxy salicylic acid (LSA) for 24 h. LSA-treated samples showed an increased presence of TJ remnants in the two lowermost layers of the SC, as quantified with standard electron microscopy. The topical aggression-induced overexpression of TJ-like cell-cell envelope fusions may influence SC functions: (1) directly, through an enhanced cohesion, and (2) indirectly, by impeding accessibility of peripheral corneodesmosomes to extracellular hydrolytic enzymes and, thus, slowing down desquamation. Observations of ichthyotic epidermis in peeling skin disease (PSD; corneodesmosin deficiency; two cases) and ichthyosis hypotrichosis sclerosing cholangitis syndrome (IHSC/NISCH; absence of claudin-1; two cases) also demonstrated increased persistence of TJ-like intercellular fusions in pathological SC and contributed to the interpretation of the diseases' pathological mechanisms.
我们评估了体外重建的人表皮和人体皮肤外植体中紧密连接 (TJ) 残余物的存在情况,这些外植体是否接受了贝塔-脂氢水杨酸 (LSA) 的强烈局部治疗 24 小时。用标准电子显微镜定量分析表明,LSA 处理的样本在 SC 的最下面两层中 TJ 残余物的存在增加。局部侵袭性诱导的 TJ 样细胞-细胞包膜融合的过表达可能影响 SC 的功能:(1) 通过增强凝聚力直接影响,(2) 通过阻碍周围桥粒芯糖蛋白对细胞外水解酶的可及性,从而减缓脱屑。在剥落性皮炎 (PSD;桥粒芯糖蛋白缺乏;两例) 和鱼鳞病少毛硬化性胆管炎综合征 (IHSC/NISCH; Claudin-1 缺失;两例) 的剥脱皮肤中也观察到 TJ 样细胞间融合的持续存在增加,这有助于解释疾病的病理机制。