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ASK1 modulates the expression of microRNA Let7A in microglia under high glucose in vitro condition
1Department of Anatomy, Yonsei University College of Medicine Seoul, South Korea.
Abstract:
Hyperglycemia results in oxidative stress and leads to neuronal apoptosis in the brain. Diabetes studies show that microglia participate in the progression of neuropathogenesis through their involvement in inflammation in vivo and in vitro. In high-glucose-induced inflammation, apoptosis signal regulating kinase 1 (ASK1) triggers the release of apoptosis cytokines and apoptotic gene expression. MicroRNA-Let7A (miR-Let7A) is reported to be a regulator of inflammation. In the present study, we investigated whether miR-Let7A regulates the function of microglia by controlling ASK1 in response to high-glucose-induced oxidative stress. We performed reverse transcription (RT) polymerase chain reaction, Taqman assay, real-time polymerase chain reaction, and immunocytochemistry to confirm the alteration of microglia function. Our results show that miR-Let7A is associated with the activation of ASK1 and the expression of anti-inflammatory cytokine (interleukin (IL)-10) and Mycs (c-Myc and N-Myc). Thus, the relationship between Let-7A and ASK1 could be a novel target for enhancing the beneficial function of microglia in central nervous system (CNS) disorders.
Insights
MicroRNA-Let7A (miR-Let7A) may regulate microglia function by controlling apoptosis signal regulating kinase 1 (ASK1) in response to high glucose. This finding offers a potential target for treating central nervous system disorders.
Area of Science:
- Neuroscience
- Molecular Biology
- Immunology
Background:
- Hyperglycemia induces oxidative stress and neuronal apoptosis, contributing to neuropathogenesis.
- Microglia play a key role in diabetes-related brain inflammation and neuronal damage.
- Apoptosis signal regulating kinase 1 (ASK1) is implicated in high-glucose-induced inflammation and apoptosis.
Purpose of the Study:
- To investigate the role of microRNA-Let7A (miR-Let7A) in regulating microglia function.
- To determine if miR-Let7A controls ASK1 activity in microglia under high-glucose conditions.
- To explore the potential of the miR-Let7A-ASK1 pathway as a therapeutic target for CNS disorders.
Main Methods:
- Reverse transcription polymerase chain reaction (RT-PCR)
- Taqman assay
- Real-time polymerase chain reaction (RT-PCR)
- Immunocytochemistry
Main Results:
- miR-Let7A expression was found to be associated with ASK1 activation in microglia.
- The study observed a correlation between miR-Let7A and the expression of anti-inflammatory cytokine IL-10.
- Associations were also found between miR-Let7A, ASK1, and the expression of Mycs (c-Myc and N-Myc).
Conclusions:
- The miR-Let7A-ASK1 pathway is a potential regulator of microglia function in response to high-glucose-induced oxidative stress.
- Targeting the relationship between miR-Let7A and ASK1 may offer a novel therapeutic strategy for central nervous system (CNS) disorders.
- This research highlights a new molecular mechanism influencing microglia's beneficial functions in neurological conditions.
