ASK1 modulates the expression of microRNA Let7A in microglia under high glucose in vitro condition

Juhyun Song, Jong Eun Lee

Research output: Contribution to journalArticle

18 Citations (Scopus)

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.

Original languageEnglish
JournalFrontiers in Cellular Neuroscience
Volume9
Issue numberMAY
DOIs
Publication statusPublished - 2015 May 20

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MAP Kinase Kinase Kinase 5
Microglia
MicroRNAs
Glucose
Inflammation
Oxidative Stress
Apoptosis
Cytokines
Central Nervous System Diseases
Hyperglycemia
Interleukin-10
Reverse Transcription
Real-Time Polymerase Chain Reaction
Anti-Inflammatory Agents
Immunohistochemistry
Gene Expression
Polymerase Chain Reaction
In Vitro Techniques
Brain

All Science Journal Classification (ASJC) codes

  • Cellular and Molecular Neuroscience

Cite this

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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.",
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ASK1 modulates the expression of microRNA Let7A in microglia under high glucose in vitro condition. / Song, Juhyun; Lee, Jong Eun.

In: Frontiers in Cellular Neuroscience, Vol. 9, No. MAY, 20.05.2015.

Research output: Contribution to journalArticle

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