The Expression and Significance of the Plasma Let-7 Family in Anti-N-methyl-d-aspartate Receptor Encephalitis

Abstract

The study aimed to investigate the expression and significance of the plasma let-7 family in anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis. Blood samples from 5 anti-NMDAR encephalitis patients and 5 negative controls were collected for microarray analysis. Blood samples from10 anti-NMDAR encephalitis patients, 10 anti-NMDAR encephalitis patients whose physical conditions have improved after 3 months of immunotherapy, 20 virus (meningitis) encephalitis patients, 20 tuberculosis (meningitis) encephalitis patients, 10 purulent (meningitis) encephalitis patients, 20 cerebral cysticercosis patients, 20 ischemic stroke patients, 20 intracerebral hemorrhage patients, 15 neuromyelitis optica patients, 15 multiple sclerosis patients, 15 moyamoya disease patients, and 20 negative controls were collected for real-time quantitative PCR (qRT-PCR) analysis. The expression levels of let-7a, let-7b, let-7d, and let-7f were significantly down-regulated in anti-NMDAR encephalitis compared with the negative controls (NC). The expression levels of let-7a, let-7d, and let-7f were significantly down-regulated in other nervous system diseases compared with the NC group while the expression level of let-7b was statistically insignificant in other nervous system diseases compared with the NC group. In addition, there was no significant dysregulation of let-7b in the anti-NMDAR encephalitis treatment group compared with the NC. Let-7b may be a potential diagnostic marker and an indicator that reflected the molecular mechanism of anti-NMDAR encephalitis.

Analysis of microRNA and Gene Expression Profiles in Multiple Sclerosis: Integrating Interaction Data to Uncover Regulatory Mechanisms

“…In MS, it has been demonstrated that there is a significant increase in the number of CD19 + cells in the blood 36 . Therefore, it would be of interest to perform cell type-specific studies to validate miR-345 as a biomarker for the diagnosis and prognosis of MS. Two recent studies did not observe different let-7b levels between individuals with MS and HCs 37 38 . This miRNA has however been linked to neurodegeneration; elevated amounts of let-7b were found in the cerebrospinal fluid (CSF) of patients with Alzheimer’s disease 39 .…”

Anti-NMDA Receptor Encephalitis and Vaccination

“…For Japanese encephalitis virus (JEV), miR-19b-3p and miR-155 were shown in regulating the JEV-induced inflammatory response [ 25 , 26 ]; miR-146a suppresses the cellular immune response in human microglial cells during JEV infection [ 27 ], and miR-33a-5p contributes to viral replication by targeting eukaryotic translation elongation factor 1A1 during JEV infection [ 30 ]. For the miRNAs associated with anti-NMDA receptor encephalitis, the let-7 family has been discovered in the literature, and the expression levels of let-7a, let-7b, let-7d, and let-7f were shown to be significantly downregulated in anti-NMDAR encephalitis compared with the negative controls [ 28 ].…”

“…The let-7 family was reported to be related to anti-NMDA receptor encephalitis [ 2 , 28 ]. let-7f is the only common miRNA of vaccine and anti-NMDA receptor encephalitis from Table 1 .…”

MicroRNAs and Apoptosis in Colorectal Cancer

“…The miRNAs are also related to the development of Parkinson’s disease (PD) [ 49 , 50 ], frontotemporal dementia [ 51 ], Alzheimer’s disease [ 52 ], and spinal muscular atrophy [ 53 ]. Additionally, let-7b is a miRNA biomarker for anti-NMDA receptor encephalitis [ 54 , 55 , 56 ]. In addition to being a useful disease biomarker, miRNA can be used to explore the association between two diseases or between disease and vaccination.…”

“…Overexpression of miR-378-5p was found to induce cell cycle arrest and promote apoptosis in CRC cells. In addition, miR-378-5p was shown to down-regulate gene BRAF in CRC cells [ 54 ]. Ectopic expression of miR-18a was found to inhibit the repair of DNA damage induced by etoposide, leading to the accumulation of DNA damage and increasing colon cancer cell apoptosis [ 70 ].…”