635 nm LED irradiation may prevent endoplasmic reticulum stress in MC3T3-E1 cells.
Hyejoung ChoOk-Su KimByunggook KimYing YangJianan SongDanyang LiuYoung KimSangmi JeonOk-Joon KimPublished in: Journal of molecular histology (2021)
Although endoplasmic reticulum (ER) stress is thought to be involved in various diseases such as cancer, metabolic, and inflammatory disorders, the relationship between ER stress and bone diseases, are remains unclear. Tunicamycin-treated MC3T3-E1 osteoblasts were used as the ER stress model in this study. 635 nm light-emitting diode irradiation (635 nm-IR) was carried out for 1 h before and after inducing ER stress. To investigate the effects of 635 nm-IR on ER stress-induced MC3T3-E1 osteoblasts and the underlying mechanism, western blot, reverse transcription polymerase chain reaction, alkaline phosphatase and Alizarin red staining, 2',7'-dichlorodyhydrofluorescein diacetate assay, Fluo-3AM and immunocytochemistry were performed. Pretreatment with 635 nm-IR effectively prevented intracellular reactive oxygen species production and alleviated ER stress through the pancreatic ER kinase (PERK)-eukaryotic initiation factor 2 (eIF2)-activating transcription factor 4 (ATF4)-nuclear factor-like 2 (Nrf2) signaling pathway. Hence, 635 nm-IR may serve a protective role in the treatment of ER stress-related bone diseases.
Keyphrases
- light emitting
- endoplasmic reticulum stress
- induced apoptosis
- endoplasmic reticulum
- photodynamic therapy
- transcription factor
- signaling pathway
- stress induced
- nuclear factor
- reactive oxygen species
- oxidative stress
- toll like receptor
- bone mineral density
- epithelial mesenchymal transition
- south africa
- soft tissue
- cell cycle arrest
- body composition
- dna binding
- radiation induced
- protein kinase
- smoking cessation
- newly diagnosed
- tyrosine kinase
- lymph node metastasis
- bone regeneration