Mechanism of miR-320 in Regulating Biological Characteristics of Ischemic Cerebral Neuron by Mediating Nox2/ROS Pathway

Shen, Wei; Lu, Yigao; Hu, Jun-An; Le, Haiwei; Yu, Wei; Xu, Weihua; Yu, Wangfang; Zheng, Junbao

doi:10.1007/s12031-019-01434-5

Cited by 26 publications

(18 citation statements)

References 27 publications

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“…The levels of the ROS inducer Nox2 and the antioxidant Nrf2 must be counterbalanced in order to overcome lung infection by S. pneumoniae , as demonstrated in WT and MyD88 –/– mice but not in TLR4 –/– mice. Indeed, targeting mitochondrial regulators of NADPH-oxidase production has been evaluated in leukemia cells ( 68 ), ischemic cerebral neurons ( 69 ), and human Nϕ cells after LPS activation ( 70 ). It is tempting to speculate that novel therapies of this type might benefit COPD patients, PRR-immunodeficient subjects, aged recurrent-pneumonia and patients with sepsis as promising alternatives to conventional antibiotic treatments.…”

Section: Discussionmentioning

confidence: 99%

The TLR4-MyD88 Signaling Axis Regulates Lung Monocyte Differentiation Pathways in Response to Streptococcus pneumoniae

et al. 2020

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Streptococcus pneumoniae is the main cause of bacterial pneumonia, a condition that currently produces significant global morbidity and mortality. The initial immune response to this bacterium occurs when the innate system recognizes common motifs expressed by many pathogens, events driven by pattern recognition receptors like the Toll-like family receptors (TLRs). In this study, lung myeloid-cell populations responsible for the innate immune response (IIR) against S. pneumoniae, and their dependence on the TLR4-signaling axis, were analyzed in TLR4 −/− and Myeloid-Differentiation factor-88 deficient (MyD88 −/−) mice. Neutrophils and monocyte-derived cells were recruited in infected mice 3-days post-infection. Compared to wild-type mice, there was an increased bacterial load in both these deficient mouse strains and an altered IIR, although TLR4 −/− mice were more susceptible to bacterial infection. These mice also developed fewer alveolar macrophages, weaker neutrophil infiltration, less Ly6C high monocyte differentiation and a disrupted classical and non-classical monocyte profile. The pro-inflammatory cytokine profile (CXCL1, TNF-α, IL-6, and IL-1β) was also severely affected by the lack of TLR4 and no induction of Th1 was observed in these mice. The respiratory burst (ROS production) after infection was profoundly dampened in TLR4 −/− and MyD88 −/− mice. These data demonstrate the complex dynamics of myeloid populations and a key role of the TLR4-signaling axis in the IIR to S. pneumoniae, which involves both the MyD88 and TRIF (Toll/IL-1R domain-containing adaptor-inducing IFN-β) dependent pathways.

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Section: Discussionmentioning

confidence: 99%

The TLR4-MyD88 Signaling Axis Regulates Lung Monocyte Differentiation Pathways in Response to Streptococcus pneumoniae

et al. 2020

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“…However, in transgenic mice overexpressing Bcl-2, the inflammatory infiltration, demyelination, and axonal injury associated with EAE were significantly decreased [50]. Bcl-2 could protect neurons from apoptosis and reduce ROS-induced injury [51]. The target genes of miR-98 include insulin-like growth factor-(IGF-) 1.…”

Section: Regulation Of Mirs In Exosomes From Mouse Serum By Bsyscmentioning

confidence: 99%

Bu-Shen-Yi-Sui Capsule, an Herbal Medicine Formula, Promotes Remyelination by Modulating the Molecular Signals via Exosomes in Mice with Experimental Autoimmune Encephalomyelitis

Zhao

Liu

et al. 2020

Oxidative Medicine and Cellular Longevity

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Multiple sclerosis (MS) is a common inflammatory demyelinating disorder of the central nervous system. Bu-shen-yi-sui capsule (BSYSC) could significantly reduce the relapse rate, prevent the progression of MS, and enhance remyelination following neurological injury in experimental autoimmune encephalomyelitis (EAE), an established model of MS; however, the mechanism underlying the effect of BSYSC on remyelination has not been well elucidated. This study showed that exosomes carrying biological information are involved in the pathological process of MS and that modified exosomes can promote remyelination by modulating related proteins and microRNAs (miRs). Here, the mechanism by which BSYSC promoted remyelination via exosome-mediated molecular signals was investigated in EAE mice and oligodendrocyte progenitor cells (OPCs) in vitro. The results showed that BSYSC treatment significantly improved the body weight and clinical scores of EAE mice, alleviated inflammatory infiltration and nerve fiber injury, protected the ultrastructural integrity of the myelin sheath, and significantly increased the expression of myelin basic protein (MBP) in EAE mice. In an in vitro OPC study, BSYSC-containing serum, especially 20% BSYSC, promoted the proliferation and migration of OPCs and induced OPCs to differentiate into mature oligodendrocytes that expressed MBP. Furthermore, BSYSC treatment regulated the expression of neuropilin- (NRP-) 1 and GTX, downregulated the expression of miR-16, let-7, miR-15, miR-98, miR-486, and miR-182, and upregulated the level of miR-146 in serum exosomes of EAE mice. In conclusion, these results suggested that BSYSC has a neuroprotective effect and facilitates remyelination and that the mechanism underlying the effect of BSYSC on remyelination probably involves regulation of the NRP-1 and GTX proteins and miRs in serum exosomes, which drive promyelination.

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“…In experiments performed with mice spinal cord in which a decrease in NOX4 level (followed by a decrease of ROS) was induced, the increase in expression levels of the antioxidants GPX3 and TXNL1 was also observed [62]. Similarly, miR-320 overexpression and the subsequent NOX2 decrease was accompanied with increased CAT, SOD and GPX contents in ischemic mice cerebral neurons [59]. In human retinal micro-vascular endothelial cells the increase of NOX4 level obtained by a decrease of miR-590-3p level was accompanied by an increase of TXNIP which is an inhibitor of thioredoxins [67].…”

Section: Unexpected Effects Of Changes In Levels Of Ros Producers and Neutralizersmentioning

confidence: 89%

“…In some cell types the levels of NOX are negatively correlated with the levels of ROS scavengers such as CAT, SOD, GPX and TXNL1 [59,62] and positively correlated with TXNIP levels (which increases ROS levels through inhibition of TXN) [67]. In experiments performed with mice spinal cord in which a decrease in NOX4 level (followed by a decrease of ROS) was induced, the increase in expression levels of the antioxidants GPX3 and TXNL1 was also observed [62].…”

Section: Unexpected Effects Of Changes In Levels Of Ros Producers and Neutralizersmentioning

confidence: 99%

“…Several miRNAs (miR-34a, miR-320, and miR-652) affect ROS production by targeting NOX transcripts. Overexpression of miR-320 in ischemic cerebral neurons reduces NOX2 levels and indirectly increases SOD, CAT, and GPX levels and NOX2 overexpression counteracts these effects; miR-320-mediated NOX2 inhibition causes reduced ROS levels, resulting in induced proliferation and inhibited apoptosis [59]. A second miRNA that impairs ROS production by inhibiting NOX2 expression is miR-652.…”

Section: Nadph Oxidasesmentioning

confidence: 99%

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Micro RNAs in Regulation of Cellular Redox Homeostasis

Ciesielska

Ślęzak-Prochazka

Bil

et al. 2021

IJMS

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In living cells Reactive Oxygen Species (ROS) participate in intra- and inter-cellular signaling and all cells contain specific systems that guard redox homeostasis. These systems contain both enzymes which may produce ROS such as NADPH-dependent and other oxidases or nitric oxide synthases, and ROS-neutralizing enzymes such as catalase, peroxiredoxins, thioredoxins, thioredoxin reductases, glutathione reductases, and many others. Most of the genes coding for these enzymes contain sequences targeted by micro RNAs (miRNAs), which are components of RNA-induced silencing complexes and play important roles in inhibiting translation of their targeted messenger RNAs (mRNAs). In this review we describe miRNAs that directly target and can influence enzymes responsible for scavenging of ROS and their possible role in cellular redox homeostasis. Regulation of antioxidant enzymes aims to adjust cells to survive in unstable oxidative environments; however, sometimes seemingly paradoxical phenomena appear where oxidative stress induces an increase in the levels of miRNAs which target genes which are supposed to neutralize ROS and therefore would be expected to decrease antioxidant levels. Here we show examples of such cellular behaviors and discuss the possible roles of miRNAs in redox regulatory circuits and further cell responses to stress.

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Mechanism of miR-320 in Regulating Biological Characteristics of Ischemic Cerebral Neuron by Mediating Nox2/ROS Pathway

Cited by 26 publications

References 27 publications

The TLR4-MyD88 Signaling Axis Regulates Lung Monocyte Differentiation Pathways in Response to Streptococcus pneumoniae

The TLR4-MyD88 Signaling Axis Regulates Lung Monocyte Differentiation Pathways in Response to Streptococcus pneumoniae

Bu-Shen-Yi-Sui Capsule, an Herbal Medicine Formula, Promotes Remyelination by Modulating the Molecular Signals via Exosomes in Mice with Experimental Autoimmune Encephalomyelitis

Micro RNAs in Regulation of Cellular Redox Homeostasis

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