Biological Science Research, Kao Corporation, 3-28, 5-chome, Kotobuki-cho, Odawara-shi, Kanagawa, 250-0002, Japan.
Safety Science Research, Kao Corporation, 3-28, 5-chome, Kotobuki-cho, Odawara-shi, Kanagawa, 250-0002, Japan.
Br J Dermatol. 2018 Jul;179(1):136-144. doi: 10.1111/bjd.16335. Epub 2018 May 5.
Hyaluronan (HA) metabolism in skin fibroblasts is mediated by HYBID (hyaluronan binding protein involved in hyaluronan depolymerization, alias CEMIP and KIAA1199) and the HA synthases HAS1 and HAS2. However, photoageing-dependent changes in HA and their molecular mechanisms, and the relationship between HA metabolism and clinical symptoms in photoaged skin remain elusive.
We examined the amount, size and tissue distribution of HA and expression levels of HYBID, HAS1 and HAS2 in photoaged skin, and analysed their relationship with the degree of photoageing.
Photoageing-dependent changes of HA were investigated by studying skin biopsies isolated from photoprotected and photoexposed areas of the same donors, and the relationships between HA and photoageing symptoms such as skin wrinkling and sagging were examined.
Skin biopsy specimens showed that the amount and size of HA are decreased in photoexposed skin compared with photoprotected skin, and this was accompanied by increased expression of HYBID and decreased expression of HAS1 and HAS2. Histologically, HA staining in the papillary dermis was decreased in photoexposed skin, showing reverse correlation with HYBID expression. HYBID expression in the photoexposed skin directly correlated with skin roughness and sagging parameters, and the reduced HA staining in the papillary dermis in the photoexposed skin positively correlated with these symptoms.
These data demonstrate that imbalance between HYBID-mediated HA degradation and HAS-mediated HA synthesis may contribute to enhanced HA catabolism in photoaged skin, and suggest that HYBID-mediated HA reduction in the papillary dermis is related to skin wrinkling and sagging of photoaged skin.
皮肤成纤维细胞中的透明质酸（HA）代谢受 HYBID（参与透明质酸解聚的透明质酸结合蛋白，别名 CEMIP 和 KIAA1199）和 HA 合成酶 HAS1 和 HAS2 介导。然而，HA 的光老化依赖性变化及其分子机制，以及光老化皮肤中 HA 代谢与临床症状之间的关系仍不清楚。
我们研究了 HA 的数量、大小和组织分布以及 HYBID、HAS1 和 HAS2 的表达水平在光老化皮肤中的变化，并分析了它们与光老化程度的关系。
通过研究同一供体的光保护和光暴露区域的皮肤活检，研究 HA 的光老化依赖性变化，并研究 HA 与皮肤皱纹和松弛等光老化症状之间的关系。
皮肤活检标本显示，与光保护皮肤相比，光暴露皮肤中的 HA 含量和大小减少，同时 HYBID 表达增加，HAS1 和 HAS2 表达减少。组织学上，光暴露皮肤的乳头真皮中的 HA 染色减少，与 HYBID 表达呈负相关。光暴露皮肤中的 HYBID 表达与皮肤粗糙度和松弛参数直接相关，光暴露皮肤中乳头真皮中减少的 HA 染色与这些症状呈正相关。
这些数据表明，HYBID 介导的 HA 降解与 HAS 介导的 HA 合成之间的失衡可能导致光老化皮肤中 HA 代谢增强，并提示 HYBID 介导的乳头真皮中 HA 减少与光老化皮肤的皱纹和松弛有关。
