MicroRNA-152 attenuates neuroinflammation in intracerebral hemorrhage by inhibiting thioredoxin interacting protein (TXNIP)-mediated NLRP3 inflammasome activation

Hu, Liuting; Zhang, Heyu; Wang, Bingyang; Ao, Qiang; He, Zhiwei

doi:10.1016/j.intimp.2019.106141

Cited by 40 publications

(26 citation statements)

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“…These miRNAs can enhance cell viability and inhibit senescence [142,143]. In BV2 microglial cells miR-152 overexpression caused a decrease in neuronal cell death [144]. Luciferase reporter assays confirmed that miR-128 targets TXNIP transcripts in pancreatic beta cells [145].…”

Section: Regulation Of Catalase Glutathione Peroxidases Peroxiredoxins and Thioredoxin System Enzymes By Mirnasmentioning

confidence: 83%

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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Section: Regulation Of Catalase Glutathione Peroxidases Peroxiredoxins and Thioredoxin System Enzymes By Mirnasmentioning

confidence: 83%

Micro RNAs in Regulation of Cellular Redox Homeostasis

Ciesielska

Ślęzak-Prochazka

Bil

et al. 2021

IJMS

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Section: Microrna and Ich-induced Neuroinflammationmentioning

confidence: 99%

“…miR-152, a tumor suppressor microRNA that was mostly associated with cell survival [ 150 , 151 , 152 ], was downregulated in the perihematomal brain tissue of rats on day 1, day 3, and day 5 post-ICH [ 153 ]. In vitro studies revealed that hemin, a hemoglobin metabolite that accumulates in the brain after ICH, is a regulator of miR-152 expression [ 153 ]. Moreover, genetic overexpression of miR-152 attenuated brain water content, neuronal death, hematoma size, and neurological deficits in rats, implicating a neuroprotective role of miR-152 [ 153 ].…”

Section: Microrna and Ich-induced Neuroinflammationmentioning

confidence: 99%

“…In vitro studies revealed that hemin, a hemoglobin metabolite that accumulates in the brain after ICH, is a regulator of miR-152 expression [ 153 ]. Moreover, genetic overexpression of miR-152 attenuated brain water content, neuronal death, hematoma size, and neurological deficits in rats, implicating a neuroprotective role of miR-152 [ 153 ]. Mechanistically, miR-152 regulated NLRP3 inflammasome activation by modulating the expression of thioredoxin interacting protein (TXNIP) after ICH [ 153 ].…”

Section: Microrna and Ich-induced Neuroinflammationmentioning

confidence: 99%

“…Moreover, genetic overexpression of miR-152 attenuated brain water content, neuronal death, hematoma size, and neurological deficits in rats, implicating a neuroprotective role of miR-152 [ 153 ]. Mechanistically, miR-152 regulated NLRP3 inflammasome activation by modulating the expression of thioredoxin interacting protein (TXNIP) after ICH [ 153 ]. Additionally, lentiviral-mediated overexpression of miR-152 attenuated the serum levels of proinflammatory cytokines [ 153 ], suggesting its possible and unexplored role in systemic inflammation.…”

Section: Microrna and Ich-induced Neuroinflammationmentioning

confidence: 99%

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Dysregulation of microRNA and Intracerebral Hemorrhage: Roles in Neuroinflammation

Kashif

Shah

Sukumari‐Ramesh

2021

IJMS

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Intracerebral hemorrhage (ICH) is a major public health problem and devastating subtype of stroke with high morbidity and mortality. Notably, there is no effective treatment for ICH. Neuroinflammation, a pathological hallmark of ICH, contributes to both brain injury and repair and hence, it is regarded as a potential target for therapeutic intervention. Recent studies document that microRNAs, small non-coding RNA molecules, can regulate inflammatory brain response after ICH and are viable molecular targets to alter brain function. Therefore, there is an escalating interest in studying the role of microRNAs in the pathophysiology of ICH. Herein, we provide, for the first time, an overview of the microRNAs that play roles in ICH-induced neuroinflammation and identify the critical knowledge gap in the field, as it would help design future studies.

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