Targeting CCL20 inhibits subarachnoid hemorrhage-related neuroinflammation in mice

Liao, Lishang; Zhang, Mingwei; Gu, Yingjiang; Sun, Xiaochuan

doi:10.18632/aging.103548

Cited by 20 publications

(16 citation statements)

References 32 publications

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“…CCL20 gene expression in neurons and microglia was significantly upregulated in the acute stage after subarachnoid hemorrhage, and participated in the pathological process of early brain injury, such as the inflammatory response and neuronal apoptosis. Inhibition of CCL20 activity could significantly inhibit the pathological process of the inflammatory response and neuronal apoptosis, and alleviate the neurological dysfunction [45]. Based on the key Cytoscape findings, 20(R)-Rg3 may exert protective effect in regulating the expression of these genes, which is worthy of further investigation.…”

Section: Discussionmentioning

confidence: 98%

Comprehensive analysis of lncRNA expression profiles in rats with cerebral ischemia-reperfusion injury after treatment with 20(R)-ginsenoside Rg3

Yang¹,

He²,

Yang³

et al. 2022

J. Integr. Neurosci.

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This study was aimed at investigating the di ferentially expressions of long noncoding RNAs (lncRNAs) and mRNAs in the brains of a middle cerebral artery occlusion/reperfusion (MCAO/R) group and a MCAO/R + 20(R)-Rg3 group. Biological enrichment analysis was performed, and a lncRNA-mRNA coexpression network was constructed, to reveal the targets and pathways of 20(R)-Rg3 involved in the regulation of cerebral ischemia-reperfusion injury (CIRI). The RNA-seq high-throughput sequencing method was employed to detect di ferentially-expressed genes between the groups, which were verified by RT-PCR. Functional enrichment analyses of Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway were performed to explore the biological functions and relevant pathways. The coexpression network of the screened lncRNAs and mRNAs was built by using Cytoscape so tware. The results identified 77 upregulated lncRNAs, 162 downregulated lncRNAs, 66 upregulated mRNAs and 472 downregulated mRNAs in the MCAO/R + 20(R)-Rg3 group, compared with those in the MCAO/R group. GO enrichment analysis showed that the GO terms were mainly enriched in stimulation response, cellular response, and stress response. KEGG pathways were mainly related to the tumor necrosis factor (TNF), NF-κB, cytokine, and other receptor signaling pathways. In addition, the coexpression analysis between lncRNA and mRNA identified 314 nodes and 515 connections between 6 lncR-NAs and 308 mRNAs, of which 511 were positive and 4 were negative. Among them, ENSRNOG-00000059555 was strongly correlated with AABR07001160.1. This study revealed multiple lncRNAs were involved in the neuroprotection of 20(R)-Rg3 against CIRI and thereby provided new insights into the use of 20(R)-Rg3 as a novel neuro protectant in ischemic stroke management.

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Section: Discussionmentioning

confidence: 98%

Comprehensive analysis of lncRNA expression profiles in rats with cerebral ischemia-reperfusion injury after treatment with 20(R)-ginsenoside Rg3

Yang¹,

He²,

Yang³

et al. 2022

J. Integr. Neurosci.

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“…However, CCL20 localized on microglia and neurons promotes inflammation via its cognate CCR6 receptor also expressed on microglia. CCL20/CCR6 induces microglial activation and pro-inflammatory mediator release, thereby increasing neuronal apoptosis [ 344 ]. There is some evidence that not only cytokines but also the release of carbon monoxide (CO), one of the products of heme catabolism by HO-1, contributes to the neuroprotective and antiapoptotic effects of HO-1 after SAH [ 341 , 345 ].…”

Section: Reaction To Sah Of Neurovascular Unit Cellsmentioning

confidence: 99%

The blood–brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments

Solar

Zamani

Lakatosová

et al. 2022

Fluids Barriers CNS

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The response of the blood–brain barrier (BBB) following a stroke, including subarachnoid hemorrhage (SAH), has been studied extensively. The main components of this reaction are endothelial cells, pericytes, and astrocytes that affect microglia, neurons, and vascular smooth muscle cells. SAH induces alterations in individual BBB cells, leading to brain homeostasis disruption. Recent experiments have uncovered many pathophysiological cascades affecting the BBB following SAH. Targeting some of these pathways is important for restoring brain function following SAH. BBB injury occurs immediately after SAH and has long-lasting consequences, but most changes in the pathophysiological cascades occur in the first few days following SAH. These changes determine the development of early brain injury as well as delayed cerebral ischemia. SAH-induced neuroprotection also plays an important role and weakens the negative impact of SAH. Supporting some of these beneficial cascades while attenuating the major pathophysiological pathways might be decisive in inhibiting the negative impact of bleeding in the subarachnoid space. In this review, we attempt a comprehensive overview of the current knowledge on the molecular and cellular changes in the BBB following SAH and their possible modulation by various drugs and substances.

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“…In the acute phase, microglia are more sensitive to stimuli and are first activated into the proinflammatory M1 phenotype. Activated microglia secrete cytokines and chemokines to trigger reactive astrocytes, such as IL-1β, TNF-α, and HMGB1 ( 18 , 51 , 101 , 102 ). In turn, proliferated and activated astrocytes also participate in the regulation of the activation of microglia, possibly via the release of molecular signals and the action of cellular connexin channels ( 90 , 100 ).…”

Section: Alterative Crosstalk Between Astrocytes and Other Cerebral C...mentioning

confidence: 99%

The role of the astrocyte in subarachnoid hemorrhage and its therapeutic implications

Zhao²,

Yao³

et al. 2022

Front. Immunol.

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Subarachnoid hemorrhage (SAH) is an important public health concern with high morbidity and mortality worldwide. SAH induces cell death, blood−brain barrier (BBB) damage, brain edema and oxidative stress. As the most abundant cell type in the central nervous system, astrocytes play an essential role in brain damage and recovery following SAH. This review describes astrocyte activation and polarization after SAH. Astrocytes mediate BBB disruption, glymphatic–lymphatic system dysfunction, oxidative stress, and cell death after SAH. Furthermore, astrocytes engage in abundant crosstalk with other brain cells, such as endothelial cells, neurons, pericytes, microglia and monocytes, after SAH. In addition, astrocytes also exert protective functions in SAH. Finally, we summarize evidence regarding therapeutic approaches aimed at modulating astrocyte function following SAH, which could provide some new leads for future translational therapy to alleviate damage after SAH.

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Targeting CCL20 inhibits subarachnoid hemorrhage-related neuroinflammation in mice

Cited by 20 publications

References 32 publications

Comprehensive analysis of lncRNA expression profiles in rats with cerebral ischemia-reperfusion injury after treatment with 20(R)-ginsenoside Rg3

Comprehensive analysis of lncRNA expression profiles in rats with cerebral ischemia-reperfusion injury after treatment with 20(R)-ginsenoside Rg3

The blood–brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments

The role of the astrocyte in subarachnoid hemorrhage and its therapeutic implications

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