Out of the Shadow: Blue Light Exposure Induces Apoptosis in Müller Cells

Abstract

Awareness toward the risks of blue light (BL) exposure is rising due to increased use of BL-enriched LEDs in displays. Short-wave BL (400–500 nm) has a high photochemical energy, leading to the enhanced production of reactive oxygen species (ROS). BL potentially plays a role in causing dry eye, cataracts, and age-related macular degeneration (AMD). The effect of BL on retinal pigment epithelium cells (RPEs) or photoreceptors has been extensively investigated. In contrast, only a few studies have investigated the effects of BL exposure on Müller cells (MCs). This is mainly due to their lack of photosensitive elements and the common assumption that their reaction to stress is only secondary in disease development. However, MCs perform important supportive, secretory, and immune functions in the retina, making them essential for retinal survival. Increased oxidative stress is a key player in many retinal diseases such as AMD or glaucoma. We hypothesize that increased oxidative stress can also affect MCs. Thus, we simulated oxidative stress levels by exposing primary porcine MCs and human MIO-M1 cells to BL. To confirm the wavelength-specificity, the cells were further exposed to red (RL), purple (PL), and white light (WL). BL and WL exposure increased ROS levels, but only BL exposure led to apoptosis in primary MCs. Thus, BL accounted for the harmful part of WL exposure. When cells were simultaneously exposed to BL and RL (i.e., PL), cell damage due to BL could be partly prevented, as could the inhibition of p53, demonstrating the protective effect of RL and p53 dependency. In contrast, BL hardly induced apoptosis in MIO-M1 cells, which is likely due to the immortalization of the cells. Therefore, enhanced oxidative stress levels can significantly harm MC function, probably leading to decreased retinal survival and, thus, further enhancing the progression of retinal diseases. Preventing the cell death of these essential retinal cells represents a promising therapy option to enhance retinal survival.

Blue Light Exposure: Ocular Hazards and Prevention—A Narrative Review

“…In laboratory settings on animal subjects and tissues, blue–violet light causes cumulative and lasting damage to retinal structures [ 15 – 17 ]. In particular, it causes oxidative stress that leads to the destruction of photoreceptor cells, which process light to create vision, and leads to apoptosis in primary Müller cells [ 18 ]. Most of the blue light research has studied varying blue–violet wavelengths from 405 to 455 nm.…”

Establishment of a primary porcine retinal pigment epithelium monolayer to complement retinal ex vivo cultures

“…As already reported previously, especially Müller cells react very sensitive to BL exposure 3 and they are thought to play a role in oxidative-stress based retinal diseases like AMD. 3 , 4 , 5 , 6 To investigate, whether co-cultivation with a functional ppRPE-monolayer could have a beneficial effect in the BL-damage model and, more precisely on BL damaged Müller cells, we evaluated the expression of Glial Fibrillary Acid Protein (GFAP), indicating activated and thus stressed Müller cells. Enhanced activation of Müller cells ( GFAP expression) due to BL exposure dropped to control levels in co-cultivated explants, as demonstrated via qRT-PCR ( Figures 9 A and 9B).…”

Low-Intensity Blue Light Exposure Reduces Melanopsin Expression in Intrinsically Photosensitive Retinal Ganglion Cells and Damages Mitochondria in Retinal Ganglion Cells in Wistar Rats

“…Although it had previously been shown that exposure of pigmented rats to high-intensity blue light (8000 lx) [ 3 ] caused Müller cell hypertrophy and GFAP overexpression, our study shows that exposure to much less intense blue light causes similar effects. Although retinal neurons are more sensitive to blue-light-induced damage in vitro than Müller cells [ 54 ], recent studies have shown that exposure of Müller cells (in vitro) to low-intensity blue light can also cause apoptosis [ 55 ].…”