Bednarski Igor Aleksander, Ciążyńska Magdalena, Kabziński Jacek, Majsterek Ireneusz, Sobolewska-Sztychny Dorota, Narbutt Joanna, Lesiak Aleksandra
Department of Dermatology, Pediatric Dermatology and Dermatological Oncology, Medical University of Lodz, Lodz, 91-347, Poland.
Nicolaus Copernicus Multidisciplinary Centre for Oncology and Traumatology, Lodz, 93-513, Poland.
Clin Cosmet Investig Dermatol. 2021 Oct 27;14:1561-1568. doi: 10.2147/CCID.S318707. eCollection 2021.
Photoaging is a premature skin aging developing secondarily to the excessive exposure to ultraviolet radiation. Due to its complexity, an exact mechanism of photoaging has not been found yet; however, recent research has shown two new emerging players in this process - cathepsin K and progerin.
To evaluate how different wavelengths of ultraviolet radiation (UVA, narrowband UVB and broadband UVB) influence cathepsin K and progerin protein and mRNA expression in dermal cultured fibroblasts.
Primary human dermal fibroblasts (Detroit 551, ATCC CCL-110) were cultured and irradiated with UVA, narrowband UVB (UVBnb) and broadband UVB (UVBwb). Fibroblasts were irradiated with 2 protocols: single high-dose exposure to UVR with protein/mRNA extraction immediately after exposure, 24 h after exposure and 48 h after exposure, and repeated (0 h, 24 h and 48 h) low-dose exposure to UVR with protein/mRNA extraction 48 h after first exposure.
Single high doses of UVA, UVBwb and UVBnb resulted in decreased expression of cathepsin K and progerin protein/mRNA in all subsequent time points. Repeated exposure to low doses of UVA results in significant increase of progerin mRNA and significant decrease of progerin protein after 48 h, but repeated exposure to UVBwb and UVBnb resulted in decreased progerin mRNA and protein expression. Repeated exposure to UVA, UVBwb and UVBnb resulted in decreased cathepsin K protein and mRNA expression.
The results suggest that there could be another progerin/cathepsin K regulatory pathway, which has not been described yet. Being contradictory with previous research, the influence of ultraviolet radiation on progerin and cathepsin K needs to be further elucidated.
光老化是由于过度暴露于紫外线辐射而继发的皮肤过早老化。由于其复杂性,尚未发现光老化的确切机制;然而,最近的研究表明在此过程中有两个新出现的因素——组织蛋白酶K和早老素。
评估不同波长的紫外线辐射(UVA、窄谱UVB和宽谱UVB)如何影响真皮培养成纤维细胞中组织蛋白酶K和早老素蛋白及mRNA的表达。
培养原代人真皮成纤维细胞(底特律551,ATCC CCL - 110),并用UVA、窄谱UVB(UVBnb)和宽谱UVB(UVBwb)进行照射。成纤维细胞采用两种照射方案:单次高剂量紫外线辐射暴露,暴露后立即、暴露后24小时和暴露后48小时进行蛋白质/mRNA提取;重复(0小时、24小时和48小时)低剂量紫外线辐射暴露,首次暴露后48小时进行蛋白质/mRNA提取。
单次高剂量的UVA、UVBwb和UVBnb在所有后续时间点均导致组织蛋白酶K和早老素蛋白/mRNA表达降低。重复低剂量UVA暴露48小时后,早老素mRNA显著增加,早老素蛋白显著减少,但重复暴露于UVBwb和UVBnb导致早老素mRNA和蛋白表达降低。重复暴露于UVA、UVBwb和UVBnb导致组织蛋白酶K蛋白和mRNA表达降低。
结果表明可能存在另一种尚未被描述的早老素/组织蛋白酶K调节途径。与先前的研究结果相矛盾,紫外线辐射对早老素和组织蛋白酶K的影响需要进一步阐明。