MicroRNA‑381/Hes1 is a potential therapeutic target for spinal cord injury

Abstract

The aim of the present study was to investigate whether microRNA‑381 is a potential therapeutic target for spinal cord injury (SCI) and its possible mechanism. Reverse transcription quantitative polymerase chain reaction (qPCR) for mRNA expression was used to analyze the changes of microRNA-381 expression. Cell viability and cell apoptosis were measured using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry. Caspase‑3 activity was measured using caspase‑3 activity kit, and western blot analysis was used to measure the protein expression of neurogenic locus notch homolog protein 1 (Notch1), notch 1 intracellular domain (NICD) and transcription factor HES-1 (Hes1). The data showed that microRNA‑381 expression of model SCI rats was downregulated compared with that of control rats. Overexpression of microRNA‑381 promoted cell proliferation, and inhibited apoptosis and caspase‑3 and apoptosis regulator BAX (Bax) protein expression in neurocytes. Overexpression of microRNA‑381 also increased Wnt and β‑catenin protein expression, and suppressed the protein expression of Notch1, NICD and Hes1 in neurocytes. Wnt inhibitor, Wnt‑C59 (1 µmol/l), inhibited cell proliferation, promoted apoptosis and caspase‑3 and Bax protein expression, suppressed β‑catenin protein expression and induced Hes1 protein expression in neurocytes following microRNA‑381 overexpression. Notch inhibitor, FLI‑06 (1 µmol/l), promoted cell proliferation, inhibited apoptosis and caspase‑3 and Bax protein expression, and suppressed NICD and Hes1 protein expression in neurocytes following microRNA‑381 overexpression. Thus, this study showed that overexpression of microRNA‑381 promotes cell proliferation of neurocytes in SCI via Hes1 expression, which may be a novel important mechanism for SCI in clinical applications.

The neuroprotective mechanism of sevoflurane in rats with traumatic brain injury via FGF2

“…Besides, the HES1 upregulation has been detected in mice with TB1 by the research of Wang et al [ 33 ]. Consistently, a prior research suggested that HES1 overexpression was involved in promotion of neuronal apoptosis in rats with spinal cord injury [ 34 ].…”

Identification of Novel Hypothalamic MicroRNAs as Promising Therapeutics for SARS-CoV-2 by Regulating ACE2 and TMPRSS2 Expression: An In Silico Analysis

“…Moreover, a high-throughput screening study was able to identify the expression pattern of additional hypothalamic sets of miRNAs, including let-7a, miR-9, miR-30e, miR-132, miR-145, miR-200a, and miR-218, which were altered by caloric restriction and/or a high-fat diet [ 39 , 40 ]. Moreover, association of miR-96/182/183 cluster, miR-141/200c cluster, miR-200a/200b/429 cluster [ 41 ], miR-142 and miR-376c [ 42 ], microRNA 381/Hes1 [ 43 ], miR-361-3p [ 44 ], and miR-219 [ 45 ] was linked with the development of hypothalamic abnormalities in various studies. Furthermore, recent studies found that hypothalamic miR-141 [ 46 ], miR-326 [ 47 ], miR-34b, miR-326, miR-432, miR-548c-3p, miR-570, miR-603 [ 48 ], miR-488, miR-144, miR-542-5p, miR-421, miR-376b-5p [ 49 ], miR-543-5p [ 50 ] [ 51 ], and miR-363-3p [ 52 ] are potential contributors in different neurodegenerative diseases.…”

Effect of M2 macrophage adoptive transfer on transcriptome profile of injured spinal cords in rats

“…Though still in animal experiment stage, an increasing number of studies have confirmed this hypothesis. 34–40 In this study, the transferred M2 cells could promote ncRNA metabolic process and ncRNA processing. This may be a reasonable explanation for the adoptive immunization of M2 cells to promote SCI repair.…”