Department of Biotechnology, Science Campus, Alagappa University, Karaikudi 630 003, Tamil Nadu, India.
ITC - Life Sciences & Technology Centre, Peenya Industrial Area, 1st Phase, Bengaluru 560058, Karnataka, India.
J Photochem Photobiol B. 2020 Apr;205:111844. doi: 10.1016/j.jphotobiol.2020.111844. Epub 2020 Mar 2.
Premature aging of the skin, principally induced by the UV radiations is called as photoaging, characterized by an increase in the level of ROS and the damage of the collagen layer leading to the damage of the cells. Mitogen activated Protein kinase (MAPK) pathway is known to mediate photoaging by controlling the level of ROS and initiating detoxification. Caenorhabditis elegans, a known model to analyze photoaging was used to understand the role of MAPK pathway (p38 and JNK) during UV-A mediated photoaging. Gene specific mutants of p38 MAPK pathway showed reduced survival when exposed to UV-A suggesting that UV-A mediated photoaging was dependent on this pathway. Also, the role of SKN-1 in eliciting response against UV-A was analyzed with the help of GFP tagged strains and qPCR analysis. Further, UV-A did not have any impact on the lifespan of JNK pathway mutants suggesting the importance of the pathway in eliciting a response against UV-A exposure, which was further validated by Western blot analysis. Overall, this study suggests that MAPK pathway could play an important part in initiating and eliciting a response by the host against UV-A exposure, by which it could be used as a marker to analyze the effects of photoaging.
皮肤的过早老化，主要是由紫外线辐射引起的，被称为光老化，其特征是 ROS 水平的增加和胶原蛋白层的损伤，导致细胞损伤。丝裂原活化蛋白激酶（MAPK）途径被认为通过控制 ROS 水平和启动解毒来介导光老化。秀丽隐杆线虫是一种已知的分析光老化的模型，用于了解 MAPK 途径（p38 和 JNK）在 UV-A 介导的光老化过程中的作用。p38 MAPK 途径的基因特异性突变体在暴露于 UV-A 时表现出存活率降低，这表明 UV-A 介导的光老化依赖于该途径。此外，还利用 GFP 标记菌株和 qPCR 分析来分析 SKN-1 在引发对 UV-A 反应中的作用。此外，UV-A 对 JNK 途径突变体的寿命没有任何影响，这表明该途径在引发对 UV-A 暴露的反应中很重要，这一结论通过 Western blot 分析进一步得到验证。总的来说，这项研究表明，MAPK 途径可能在宿主对 UV-A 暴露的起始和引发反应中发挥重要作用，可作为分析光老化影响的标志物。
