Ultraviolet-A triggers photoaging in model nematode Caenorhabditis elegans in a DAF-16 dependent pathway

• Published in: AGE 2016-02, Vol.38 (1), p.27-27, Article 27
• Main Authors: Prasanth, Mani Iyer, Santoshram, Gunasekaran Santhi, Bhaskar, James Prabhanand, Balamurugan, Krishnaswamy
• Format: Article
• Language: English
• Subjects: Age; Aging; Animal cognition; Animals; Biomedical and Life Sciences; Caenorhabditis elegans - genetics; Caenorhabditis elegans - growth & development; Caenorhabditis elegans - radiation effects; Caenorhabditis elegans Proteins - biosynthesis; Caenorhabditis elegans Proteins - genetics; Cell Biology; Collagen; E coli; Forkhead Transcription Factors - biosynthesis; Forkhead Transcription Factors - genetics; Gene Expression Regulation, Developmental - radiation effects; Geriatrics/Gerontology; Life Sciences; Longevity - genetics; Longevity - radiation effects; Microscopy, Confocal; Molecular Medicine; Nematodes; Physiology; Polymerase Chain Reaction; RNA - genetics; Signal Transduction - radiation effects; Skin Aging - genetics; Skin Aging - pathology; Skin Aging - radiation effects; Skin cancer; Ultraviolet radiation; Ultraviolet Rays; Vitamin D; Worms; Young adults
• ISSN: 0161-9152; 2509-2715; 1574-4647; 2509-2723
• DOI: 10.1007/s11357-016-9889-y

Ultraviolet radiations (UV) are the primary causative agent for skin aging (photoaging) and cancer, especially UV-A. The mode of action and the molecular mechanism behind the damages caused by UV-A is not well studied, in vivo. The current study was employed to investigate the impact of UV-A exposure using the model organism, Caenorhabditis elegans. Analysis of lifespan, healthspan, and other cognitive behaviors were done which was supported by the molecular mechanism. UV-A exposure on collagen damages the synthesis and functioning which has been monitored kinetically using engineered strain, col-19:: GFP. The study results suggested that UV-A accelerated the aging process in an insulin-like signaling pathway dependent manner. Mutant ( daf-2 )-based analysis concrete the observations of the current study. The UV-A exposure affected the usual behavior of the worms like pharyngeal movements and brood size. Quantitative PCR profile of the candidate genes during UV-A exposure suggested that continuous exposure has damaged the neural network of the worms, but the mitochondrial signaling and dietary restriction pathway remain unaffected. Western blot analysis of HSF-1 evidenced the alteration in protein homeostasis in UV-A exposed worms. Outcome of the current study supports our view that C. elegans can be used as a model to study photoaging, and the mode of action of UV-A-mediated damages can be elucidated which will pave the way for drug developments against photoaging.