Downregulation of microRNA-9-5p promotes synaptic remodeling in the chronic phase after traumatic brain injury

Wu, Junqi; Li, Hui; He, Junchi; Tian, Xingui; Luo, Shuilian; Li, Jiankang; Li, Wei; Zhong, Jian; Zhang, Hongrong; Huang, Zhijian; Sun, Xiaochuan; Jiang, Tao

doi:10.1038/s41419-020-03329-5

Cited by 25 publications

(14 citation statements)

References 52 publications

(75 reference statements)

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“…The qPCR results were presented as a heat map of mRNA expression and obtained via the method of Ma et al. ( 19 ).…”

Section: Methodsmentioning

confidence: 99%

“…Until now, a total of four types of Notch receptors (Notch protein) has been identified: Notch-1, Notch-2, Notch-3 and Notch-4 ( 17 ). Five kinds of Notch’s ligands, DLL1, DLL3, DLL4, Jagged1 and Jagged2 bind to Notch protein to activate Notch pathway ( 18 , 19 ). The Notch-protein is featured as single trans-transmembrane with an extracellular ligand-binding domain and an intracellular domains (NICD) ( 20 ).…”

Section: Introductionmentioning

confidence: 99%

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miR-27-3p Enhances the Sensitivity of Triple-Negative Breast Cancer Cells to the Antitumor Agent Olaparib by Targeting PSEN-1, the Catalytic Subunit of Γ-Secretase

et al. 2021

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Olaparib has been used in the treatment of triple-negative breast cancer (TNBC) with BRCA mutations. In the present study, we demonstrated the effect of miR-27-3p on the γ-secretase pathway by regulating the sensitivity of TNBC cells to olaparib. miR-27-3p, a microRNA with the potential to target PSEN-1, the catalytic subunit of γ-secretase mediating the second step of the cleavage of the Notch protein, was identified by the online tool miRDB and found to inhibit the expression of PSEN-1 by directly targeting the 3’-untranslated region (3’-UTR) of PSEN-1. The overexpression of miR-27-3p inhibited the activation of the Notch pathway via the inhibition of the cleavage of the Notch protein, mediated by γ-secretase, and, in turn, enhanced the sensitivity of TNBC cells to the antitumor agent olaparib. Transfection with PSEN-1 containing mutated targeting sites for miR-27-3p or the expression vector of the Notch protein intracellular domain (NICD) almost completely blocked the effect of miR-27-3p on the Notch pathway or the sensitivity of TNBC cells to olaparib, respectively. Therefore, our results suggest that the miR-27-3p/γ-secretase axis participates in the regulation of TNBC and that the overexpression of miR-27-3p represents a potential approach to enhancing the sensitivity of TNBC to olaparib.

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“…The qPCR results were presented as a heat map of mRNA expression and obtained via the method of Ma et al. ( 19 ).…”

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

miR-27-3p Enhances the Sensitivity of Triple-Negative Breast Cancer Cells to the Antitumor Agent Olaparib by Targeting PSEN-1, the Catalytic Subunit of Γ-Secretase

et al. 2021

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“…This is not surprising since astrocytes alongside microglia have been found promoting neuroinflammation for several decades by now. Finally, downregulation of miR-9-5p promote the proliferation of astrocytes and evoke the release of astrocytederived neurotrophic factors that promotes overall brain cell survival (Wu et al, 2021). The astrocytic proliferation during TBI also contributes to monocyte invasion due to alterations in the vasculature and contributing to immune response (Frik et al, 2018).…”

Section: Traumatic Brain Injury and The Astrocytic Responsementioning

confidence: 99%

Traumatic Brain Injury: Mechanisms of Glial Response

2021

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Traumatic brain injury (TBI) is a heterogeneous disorder that involves brain damage due to external forces. TBI is the main factor of death and morbidity in young males with a high incidence worldwide. TBI causes central nervous system (CNS) damage under a variety of mechanisms, including synaptic dysfunction, protein aggregation, mitochondrial dysfunction, oxidative stress, and neuroinflammation. Glial cells comprise most cells in CNS, which are mediators in the brain’s response to TBI. In the CNS are present astrocytes, microglia, oligodendrocytes, and polydendrocytes (NG2 cells). Astrocytes play critical roles in brain’s ion and water homeostasis, energy metabolism, blood-brain barrier, and immune response. In response to TBI, astrocytes change their morphology and protein expression. Microglia are the primary immune cells in the CNS with phagocytic activity. After TBI, microglia also change their morphology and release both pro and anti-inflammatory mediators. Oligodendrocytes are the myelin producers of the CNS, promoting axonal support. TBI causes oligodendrocyte apoptosis, demyelination, and axonal transport disruption. There are also various interactions between these glial cells and neurons in response to TBI that contribute to the pathophysiology of TBI. In this review, we summarize several glial hallmarks relevant for understanding the brain injury and neuronal damage under TBI conditions.

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“…CircRNAs are a type of long RNA formed by covalent binding of the 3′ and 5′ ends after reverse splicing [207,208]. The junction between two related exons in the opposite order is called the back-sliced junction (BSJ), which represent a molecular signature of circRNA [28,57].…”

Section: Characteristics Of Lncrna and Circrnamentioning

confidence: 99%

The role of noncoding RNAs in Parkinson’s disease: biomarkers and associations with pathogenic pathways

et al. 2021

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The discovery of various noncoding RNAs (ncRNAs) and their biological implications is a growing area in cell biology. Increasing evidence has revealed canonical and noncanonical functions of long and small ncRNAs, including microRNAs, long ncRNAs (lncRNAs), circular RNAs, PIWI-interacting RNAs, and tRNA-derived fragments. These ncRNAs have the ability to regulate gene expression and modify metabolic pathways. Thus, they may have important roles as diagnostic biomarkers or therapeutic targets in various diseases, including neurodegenerative disorders, especially Parkinson’s disease. Recently, through diverse sequencing technologies and a wide variety of bioinformatic analytical tools, such as reverse transcriptase quantitative PCR, microarrays, next-generation sequencing and long-read sequencing, numerous ncRNAs have been shown to be associated with neurodegenerative disorders, including Parkinson’s disease. In this review article, we will first introduce the biogenesis of different ncRNAs, including microRNAs, PIWI-interacting RNAs, circular RNAs, long noncoding RNAs, and tRNA-derived fragments. The pros and cons of the detection platforms of ncRNAs and the reproducibility of bioinformatic analytical tools will be discussed in the second part. Finally, the recent discovery of numerous PD-associated ncRNAs and their association with the diagnosis and pathophysiology of PD are reviewed, and microRNAs and long ncRNAs that are transported by exosomes in biofluids are particularly emphasized.

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Downregulation of microRNA-9-5p promotes synaptic remodeling in the chronic phase after traumatic brain injury

Cited by 25 publications

References 52 publications

miR-27-3p Enhances the Sensitivity of Triple-Negative Breast Cancer Cells to the Antitumor Agent Olaparib by Targeting PSEN-1, the Catalytic Subunit of Γ-Secretase

miR-27-3p Enhances the Sensitivity of Triple-Negative Breast Cancer Cells to the Antitumor Agent Olaparib by Targeting PSEN-1, the Catalytic Subunit of Γ-Secretase

Traumatic Brain Injury: Mechanisms of Glial Response

The role of noncoding RNAs in Parkinson’s disease: biomarkers and associations with pathogenic pathways

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