MicroRNA-421 suppresses the apoptosis and autophagy of hippocampal neurons in epilepsy mice model by inhibition of the TLR/MYD88 pathway.
Xin WenXin-Rui HanYong-Jian WangShan WangMin ShenZi-Feng ZhangShao-Hua FanQun ShanLiang WangMeng-Qiu LiBin HuChun-Hui SunDong-Mei WuJun LuYuan-Lin ZhengPublished in: Journal of cellular physiology (2018)
Epilepsy is a group of neurological disorders characterized by epileptic seizures. In this study, we aim to explore the role of microRNA-421 (miR-421) in hippocampal neurons of epilepsy mice via the TLR/MYD88 pathway. Forty mice were randomly served as the normal and model (established as epilepsy model) groups. Hippocampal neurons were assigned into seven groups with different transfections. The RT-qPCR and western blotting were conducted to examine the expression of miR-421 TLR2, TLR4, MYD88, Bax, Bcl-2, p53, Beclin-1, and LC3II/LC3I. Cell proliferation and apoptosis were detected by MTT and flow cytometry.MYD88 is a target gene of miR-421. Model mice showed elevated expression of TLR2, TLR4, MYD88, Bax, p53, Beclin-1, and LC3II/LC3I but reduced expression of miR-421 and Bcl-2. In vitro experiments reveals that overexpression of miR-421 inhibited the TLR/MYD88 pathway. Besides, overexpressed miR-421 declined cell apoptosis but increased cell proliferation. It reveals that miR-421 targeting MYD88 could inhibit the apoptosis and autophagy of hippocampal neurons in epilepsy mice by down-regulating the TLR/MYD88 pathway.
Keyphrases
- toll like receptor
- cell proliferation
- inflammatory response
- long non coding rna
- nuclear factor
- poor prognosis
- immune response
- endoplasmic reticulum stress
- cell cycle
- long noncoding rna
- oxidative stress
- high fat diet induced
- cell death
- temporal lobe epilepsy
- pi k akt
- spinal cord
- signaling pathway
- induced apoptosis
- flow cytometry
- cell cycle arrest
- insulin resistance
- transcription factor
- type diabetes
- south africa
- gene expression
- dna methylation
- genome wide