Protective Effect of BLED-exposed Conditioned Media on Cell Injury

Photochem Photobiol. 2018 May;94(3):583-588. doi: 10.1111/php.12887. Epub 2018 Mar 2.

Abstract

Previous studies have reported that 450 nm blue light emitting diode (BLED) induces apoptosis through a mitochondria-mediated pathway in cancer cells and reduces the early stage tumor growth. This study was performed to determine the effects of BLED-irradiated cell metabolites on cell injury. Our results showed that conditioned medium (CM) from cells irradiated with low-dose BLED (LCM) inhibited apoptosis and increased cell survival. Cell protection-related proteins were identified in cell metabolites of CM and LCM using 2-DE and MALDI-TOF analysis. Treatment with LCM inhibited apoptotic cell death and increased the live cell population. The cellular protective effect of LCM was associated with keratin and collagen type VI secretion from cells after low dose of BLED irradiation. Interestingly, expression of endoplasmic reticulum stress proteins was dose dependently increased after 4 h BLED irradiation. Only levels of BiP, CHOP and ERO1-Lα were decreased significantly after 24 h incubation, indicating their anti-apoptotic property in these cells. These results indicated that cell metabolites stimulated by low-dose BLED irradiation have a cytoprotective effect on cell injury via increasing transient intracellular ER stress. Further studies remain to provide the molecular mechanisms of LCM for cytoprotective activity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / radiation effects
  • Cell Line, Tumor
  • Culture Media, Conditioned / pharmacology
  • Dose-Response Relationship, Radiation
  • Electrophoresis, Gel, Two-Dimensional
  • Endoplasmic Reticulum Stress / radiation effects
  • Humans
  • Light*
  • Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization

Substances

  • Culture Media, Conditioned

Associated data

  • GENBANK/EAW71104.1
  • GENBANK/NP_002267.2
  • GENBANK/AAB50217.1
  • GENBANK/CAA28444.1