Page 6 - Q. Neuroscience
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[Q. Neuroscience-4]
MiR-30 and miR-153 alleviate LPS induced inflammation by
targeting NeuroD1 in microglial cells
Hye-Rim Choi¹, Ji Sun Ha¹˙#, Sung-Woo Cho²˙*, Seung-Ju Yang¹˙*
¹Biomedical Laboratory Science, Konyang University, Daejeon 35365, Korea, ²Biochemistry and Molecular Biology,
University of Ulsan College of Medicine, Seoul 05505, Korea
Neurogenic differentiation 1 (NeuroD1) is a basic helix-loop-helix (bHLH) transcription factor that plays an important
role during neuronal differentiation, maturation and survival. MicroRNA (miRNA) effectively regulates the level of
gene expression at the translation level. The present study assessed the effects of the NeuroD1 targeting miRNAs
against LPS induced inflammation in microglial cells. We confirmed that miR-30 and miR153 decreased NeuroD1
expression induced by LPS. Additionally, miR-30 and miR-153 suppressed pro-inflammatory cytokines, tumor
necrosis factor-α (TNF-α) and interlukin-6 (IL-6), in LPS induced microglial cells. Furthermore, miR-30 and miR-153
inhibited LPS induced phosphorylation of JNK, ERK and p38. Its properties were facilitated via the inhibition of
mitogen-activated protein kinase (MAPK) pathway. Moreover, miR-30 and miR-153 suppressed the expression of
NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome, which is involved in the innate immune
response. These results suggest that miR-30 and miR-153 are novel regulator that suppresses NeuroD1 expression
critical in LPS induced microglial inflammation. [Supported by NRF (2018R1A2B6001743 & 2018R1D1A3A03000692)]
