AI Article Synopsis

  • Photoaging is skin damage caused primarily by UV radiation, leading to increased reactive oxygen species (ROS) and collagen layer deterioration, which damages cells.
  • The study focuses on the MAPK pathway (specifically p38 and JNK) in Caenorhabditis elegans, demonstrating that mutants lacking p38 MAPK had lower survival rates under UV-A exposure, indicating the pathway's crucial role in photoaging response.
  • Additionally, while the JNK pathway mutants showed no significant lifespan impact from UV-A, this research suggests that the MAPK pathway is vital for the organism's defense against UV-A, offering potential use as a marker for studying photoaging effects.

Article Abstract

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.

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Source
http://dx.doi.org/10.1016/j.jphotobiol.2020.111844DOI Listing

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