Abstract

Modern life is full of artificial light in day and night. Smart phones, laptops, televisions, and high definition monitors provide unnatural human light source into human eye and cause ocular defects in modern human being. Understanding the molecular mechanism of the interplay between artificial light and ocular cells may help researcher society understanding the methods that preventing artificial light‐induced visual impairment. Here, we reported a short‐term exposure at short wavelength light source from blue and green light‐emitting diode (LED) could cause the murine photoreceptor cells 661W cells death, but not in red LED. However, the molecular mechanism remaining unclear. Using the molecular probe of caspase 3 reporter, we found the blue and green LED caused caspase 3 activation even as short as 10 minutes exposure and subsequently cell death at 16 hours later. We further confirmed 661W cells apoptosis by cleavage form caspase 3 and PARP formation. Moreover, we found the decreasing of mitochondria membrane potential and increasing of cellular relative‐oxygen species in 661W cells both indicate early cell apoptosis under short‐term exposure. Up to our knowledge, there was no transcriptome analysis which revealed immediately early gene expression in light‐induced cell death. Thus, we analyzed the 661W transcriptome at 2 hours after 10 minutes’ short wavelength light exposure and validated the candidate genes expression by RT‐Q‐PCR. Using the ingenuity pathway analysis, we found valuable up‐stream regulators, pathways, and potential mechanisms in short wavelength induced photoreceptor cell death and may provide novel therapy niches. In conclusion, our preliminary results prove that short wavelength light exposure can cause the photoreceptor cells death and the potential molecular clues. Further pathohistological analysis of key protein expression in the animal models may help us to prove the mechanism inside the eye damage from short wavelength light in future.Support or Funding InformationThis study was support by Shu Zen College of Medicine and Management with grant number (SZL10800012) and Academia Sinica

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