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Effects of miR-21/NLRP3 on Blue Light-Induced Retinal Neurodegeneration in Mice
1Department of Ophthalmology, Changzhou First People's Hospital, Changzhou, China.
Purpose:
Age-related macular degeneration (AMD) is a chronic retinal disease that can lead to blindness. While the NLR family pyrin domain containing 3 (NLRP3) inflammasome is implicated in AMD, the specific roles of miR-21 and NLRP3 in AMD-related inflammation remain unclear. Therefore, this study aimed to investigate the roles of miR-21 and NLRP3 in blue light-induced neurodegeneration in the mouse retina.
Methods:
A mouse model of retinal light damage was established through three months of blue light exposure (BLE). The experimental groups comprised the Control (Ctrl), BLE, BLE + miR-nc, and BLE + miR-21 inhibitor groups. The microRNAs were administered via intravitreal injections once per week. After successful modeling, changes in visual function and retinal morphology were investigated by using electroretinography and hematoxylin and eosin staining, respectively. Photoreceptor apoptosis was assessed using the TdT-mediated dUTP nick-end labeling assay. Immunofluorescence was used to detect and locate microglia and NLRP3 expression in the mouse retina. The expression of miR-21, NLRP3, and downstream factors in the retinas of each group was measured using qRT-PCR and western blotting.
Results:
In the BLE and BLE + miR-nc groups, there was a decrease in visual function and retinal thickness, an increase in retinal ganglion cell injury and photoreceptor cell apoptosis, and elevated microglia activity in the retina, as evidenced by their migration to the outer retinal layer. In addition, the expression of miR-21, NLRP3, and downstream factors was increased in the BLE and BLE + miR-nc groups compared to that in the control group. However, intravitreal injection of the miR-21 inhibitor reduced miR-21 expression in the retina and significantly inhibited the activation of the NLRP3 inflammasome, effectively alleviating retinal photodamage caused by BLE.
Conclusions:
This study indicates that miR-21 may mitigate blue-light-induced retinal neurodegeneration by reducing the activation of the NLRP3 inflammasome in the mouse retina.
Insights
This study shows that miR-21 can reduce blue light-induced retinal damage by inhibiting the NLRP3 inflammasome. This finding offers a potential therapeutic target for age-related macular degeneration (AMD).
Area of Science:
- Ophthalmology
- Neuroscience
- Molecular Biology
Background:
- Age-related macular degeneration (AMD) is a leading cause of blindness.
- The NLRP3 inflammasome is implicated in AMD pathogenesis, but the roles of miR-21 and NLRP3 in AMD-related inflammation are not fully understood.
Purpose of the Study:
- To investigate the roles of miR-21 and NLRP3 in blue light-induced retinal neurodegeneration in a mouse model.
- To explore the therapeutic potential of targeting miR-21 for AMD.
Main Methods:
- Established a mouse model of retinal light damage using blue light exposure (BLE).
- Administered miR-21 inhibitor via intravitreal injections.
- Assessed visual function, retinal morphology, photoreceptor apoptosis, and microglia/NLRP3 expression using electroretinography, H&E staining, TUNEL assay, and immunofluorescence.
- Quantified miR-21, NLRP3, and downstream factor expression via qRT-PCR and western blotting.
Main Results:
- Blue light exposure (BLE) led to decreased visual function, retinal thinning, increased photoreceptor apoptosis, and elevated microglia activation.
- BLE increased the expression of miR-21 and NLRP3 in the retina.
- Inhibition of miR-21 significantly reduced NLRP3 inflammasome activation and alleviated BLE-induced retinal photodamage.
Conclusions:
- miR-21 plays a crucial role in blue light-induced retinal neurodegeneration.
- Inhibiting miR-21 mitigates retinal photodamage by reducing NLRP3 inflammasome activation.
- Targeting the miR-21/NLRP3 pathway presents a potential therapeutic strategy for AMD.
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