MircoRNA-29a in Astrocyte-derived Extracellular Vesicles Suppresses Brain Ischemia Reperfusion Injury via TP53INP1 and the NF-κB/NLRP3 Axis

Liu, Xin; Lv, Xinghua; Liu, Zhenzhen; Zhang, Mengjie; Leng, Yufang

doi:10.1007/s10571-021-01040-3

Cited by 25 publications

(20 citation statements)

References 43 publications

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“…miR-29a-5p and NLRP3 can regulate inflammatory diseases together. miR-29a in astrocyte-derived extracellular vesicles inhibits cerebral ischemia-reperfusion injury through TP53INP1 and NF- κ B/NLRP3 [ 39 ]. The expression level of NLRP3 in sepsis patients was significantly increased [ 40 ].…”

Section: Discussionmentioning

confidence: 99%

17β-Estradiol Attenuates LPS-Induced Macrophage Inflammation In Vitro and Sepsis-Induced Vascular Inflammation In Vivo by Upregulating miR-29a-5p Expression

Zhang

Chen

Yang

et al. 2021

Mediators of Inflammation

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Excessive release of cytokines such as IL-1β and other inflammatory mediators synthesized and secreted by macrophages is the fundamental link of uncontrolled inflammatory response in sepsis. 17β-Estradiol (E2) plays anti-inflammatory and vascular protective effects by regulating leukocyte infiltration and the expression of chemokines or cytokines induced by injury. However, the role of E2 in the inflammatory response of macrophages in sepsis and its mechanism are still not fully understood. In the present study, we show that E2 alleviates vascular inflammation in sepsis mice induced by cecal ligation puncture (CLP). E2 significantly decreases RAW 264.7 cell inflammation response by downregulating the expression of NLRP3. Furthermore, we found that miR-29a-5p was significantly downregulated in LPS-treated macrophages. Treating RAW 264.7 cells with E2 markedly upregulated the miR-29a-5p expression level. More importantly, we demonstrated that miR-29a-5p repressed NLRP3 expression by directly targeting its 3 ′ -UTR. Loss- and gain-of-function experiments revealed that transfection of the miR-29a-5p mimic abrogates LPS-induced macrophage inflammation. Moreover, depletion of miR-29a-5p by its inhibitor largely promotes LPS-induced macrophage inflammation. In summary, miR-29a-5p upregulation induced by E2 alleviated RAW 264.7 cell inflammation response by aggravating miR-29a-5p repression of NLRP3 expression. E2 exerts significant anti-inflammatory efficacy in macrophages by regulating the miR-29a-5p/NLRP3 axis. Targeting miR-29a-5p may be a novel therapeutic strategy to suppress sepsis-induced vascular inflammation.

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Section: Discussionmentioning

confidence: 99%

17β-Estradiol Attenuates LPS-Induced Macrophage Inflammation In Vitro and Sepsis-Induced Vascular Inflammation In Vivo by Upregulating miR-29a-5p Expression

Zhang

Chen

Yang

et al. 2021

Mediators of Inflammation

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“…The process was repeated until no further studies would be obtained. A total of 29 studies were identified in this section ( Frühbeis et al, 2013 ; Fröhlich et al, 2014 ; Guitart et al, 2016 ; Xin et al, 2017 ; Xu et al, 2017 ; Hira et al, 2018 ; Yang et al, 2018 ; Song et al, 2019a ; Song et al, 2019b ; Pei et al, 2019 ; Tian et al, 2019 ; Xu et al, 2019 ; Chen et al, 2020b ; Bu et al, 2020 ; Frühbeis et al, 2020 ; Huang et al, 2020 ; Pei et al, 2020 ; Wu et al, 2020 ; Xie et al, 2020 ; Zang et al, 2020 ; Liu et al, 2021a ; Yang et al, 2021a ; Zhang et al, 2021a ; Li et al, 2021b ; Liu et al, 2021b ; Zhang et al, 2021b ; Chiang et al, 2021 ; Du et al, 2021 ; Raffaele et al, 2021 ), conducted from 2016 to 2021. The most extensively adopted species and associated stroke models are mice and middle cerebral artery occlusion, respectively.…”

Section: The Role Of Extracellular Vesicles-derived From Neurons/neur...mentioning

confidence: 99%

“…The most extensively adopted species and associated stroke models are mice and middle cerebral artery occlusion, respectively. Among these 29 publications, 10 focused on microglia-EVs ( Yang et al, 2018 ; Song et al, 2019a ; Tian et al, 2019 ; Xie et al, 2020 ; Zang et al, 2020 ; Liu et al, 2021a ; Zhang et al, 2021a ; Li et al, 2021b ; Zhang et al, 2021b ; Raffaele et al, 2021 ), 11 focused on astrocyte-EVs ( Guitart et al, 2016 ; Xin et al, 2017 ; Hira et al, 2018 ; Pei et al, 2019 ; Xu et al, 2019 ; Chen et al, 2020b ; Bu et al, 2020 ; Pei et al, 2020 ; Wu et al, 2020 ; Liu et al, 2021b ; Du et al, 2021 ), 3 focused on oligodendrocytes ( Frühbeis et al, 2013 ; Fröhlich et al, 2014 ; Frühbeis et al, 2020 ) and 5 focused on neuron-EVs ( Xu et al, 2017 ; Song et al, 2019b ; Huang et al, 2020 ; Yang et al, 2021a ; Chiang et al, 2021 ), demonstrating that it is sufficient to suggest that EVs derived from neurons/glial cells play an important role in regulating the progress and prognosis of ischemic stroke.…”

Section: The Role Of Extracellular Vesicles-derived From Neurons/neur...mentioning

confidence: 99%

“…In addition to EVs derived from normoxic astrocytes, Xu et al (2019) indicated that EVs released from ischemic preconditioned astrocytes ameliorated OGD-induced cell death and apoptosis. Concerning the regulation of inflammation and functional recovery, Liu et al (2021b) established an OGD N9 microglial model and an MCAO rat model. These findings revealed that astrocyte-derived EVs inhibited OGD-induced injury and inflammation by regulating NLPR3, oxidative stress, and inflammatory factors (IL-1β and IL-18) in N9 microglia; reduced brain infarction; and improved MCAO rat neural functions.…”

Section: The Role Of Extracellular Vesicles-derived From Neurons/neur...mentioning

confidence: 99%

“…It has been shown to promote multiple pro-inflammatory mediators, and suppression of NF-κB signaling correlates with beneficial effects in ischemic stroke by EV-miRNAs. Liu et al (2021b) reported that miR-29a in astrocyte-derived EVs inhibits brain ischemia-reperfusion injury by downregulating the NF-κB/NLRP3 axis. Wu et al (2020) indicated that astrocytes-EVs transported miR-34c downregulates the NF-κB/MAPK axis and relieves neurological damage in ischemic stroke.…”

Section: The Role Of Extracellular Vesicles-derived From Neurons/neur...mentioning

confidence: 99%

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The Emerging Role of Extracellular Vesicle Derived From Neurons/Neurogliocytes in Central Nervous System Diseases: Novel Insights Into Ischemic Stroke

Kang

Xin

et al. 2022

Front. Pharmacol.

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Neurons and neurogliocytes (oligodendrocytes, astrocytes, and microglia) are essential for maintaining homeostasis of the microenvironment in the central nervous system (CNS). These cells have been shown to support cell-cell communication via multiple mechanisms, most recently by the release of extracellular vesicles (EVs). Since EVs carry a variety of cargoes of nucleic acids, lipids, and proteins and mediate intercellular communication, they have been the hotspot of diagnosis and treatment. The mechanisms underlying CNS disorders include angiogenesis, autophagy, apoptosis, cell death, and inflammation, and cell-EVs have been revealed to be involved in these pathological processes. Ischemic stroke is one of the most common causes of death and disability worldwide. It results in serious neurological and physical dysfunction and even leads to heavy economic and social burdens. Although a large number of researchers have reported that EVs derived from these cells play a vital role in regulating multiple pathological mechanisms in ischemic stroke, the specific interactional relationships and mechanisms between specific cell-EVs and stroke treatment have not been clearly described. This review aims to summarize the therapeutic effects and mechanisms of action of specific cell-EVs on ischemia. Additionally, this study emphasizes that these EVs are involved in stroke treatment by inhibiting and activating various signaling pathways such as ncRNAs, TGF-β1, and NF-κB.

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Extracellular vesicles with diagnostic and therapeutic potential for prion diseases

et al. 2022

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Prion diseases (PrD) or transmissible spongiform encephalopathies (TSE) are invariably fatal and pathogenic neurodegenerative disorders caused by the self-propagated misfolding of cellular prion protein (PrPC) to the neurotoxic pathogenic form (PrPTSE) via a yet undefined but profoundly complex mechanism. Despite several decades of research on PrD, the basic understanding of where and how PrPC is transformed to the misfolded, aggregation-prone and pathogenic PrPTSE remains elusive. The primary clinical hallmarks of PrD include vacuolation-associated spongiform changes and PrPTSE accumulation in neural tissue together with astrogliosis. The difficulty in unravelling the disease mechanisms has been related to the rare occurrence and long incubation period (over decades) followed by a very short clinical phase (few months). Additional challenge in unravelling the disease is implicated to the unique nature of the agent, its complexity and strain diversity, resulting in the heterogeneity of the clinical manifestations and potentially diverse disease mechanisms. Recent advances in tissue isolation and processing techniques have identified novel means of intercellular communication through extracellular vesicles (EVs) that contribute to PrPTSE transmission in PrD. This review will comprehensively discuss PrPTSE transmission and neurotoxicity, focusing on the role of EVs in disease progression, biomarker discovery and potential therapeutic agents for the treatment of PrD.

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MircoRNA-29a in Astrocyte-derived Extracellular Vesicles Suppresses Brain Ischemia Reperfusion Injury via TP53INP1 and the NF-κB/NLRP3 Axis

Cited by 25 publications

References 43 publications

17β-Estradiol Attenuates LPS-Induced Macrophage Inflammation In Vitro and Sepsis-Induced Vascular Inflammation In Vivo by Upregulating miR-29a-5p Expression

17β-Estradiol Attenuates LPS-Induced Macrophage Inflammation In Vitro and Sepsis-Induced Vascular Inflammation In Vivo by Upregulating miR-29a-5p Expression

The Emerging Role of Extracellular Vesicle Derived From Neurons/Neurogliocytes in Central Nervous System Diseases: Novel Insights Into Ischemic Stroke

Extracellular vesicles with diagnostic and therapeutic potential for prion diseases

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