MiR-18a Aggravates Intracranial Hemorrhage by Regulating RUNX1-Occludin/ZO-1 Axis to Increase BBB Permeability

Ren, Siying; Wu, Guofeng; Huang, Yuanxin; Wang, Likun; Li, Yinghui; Zhang, Yan

doi:10.1016/j.jstrokecerebrovasdis.2021.105878

Cited by 11 publications

(5 citation statements)

References 33 publications

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“…We revealed that miR-17-5p could bind to 3’UTR of NFATC3 mRNA and blocked NFATC3 expression in ECs to prompt TJ-related proteins expression. Inconsistent with our finding, miR-18a bound to 3’UTR of TF-RUNX1 mRNA to inhibit RUNX1 expression but ZO-1 and occludin were therefore decreased [ 53 ]. These results implied that TFs and miRNA/TFs interactions played multifarious roles in BBB permeability regulation.…”

Section: Discussionsupporting

confidence: 86%

TARBP2-stablized SNHG7 regulates blood-brain barrier permeability by acting as a competing endogenous RNA to miR-17-5p/NFATC3 in Aβ-microenvironment

et al. 2022

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Breakdown of blood-brain barrier (BBB) is recognized as serious pathological marker of Alzheimer’s disease development. Studies confirmed that β-amyloid (Aβ) deposition induced high BBB permeability by disrupting tight junction (TJ) proteins formed from endothelial cells (ECs). Here, we found TARBP2, SNHG7 and NFATC3 in expressions were increased and miR-17-5p expression was decreased in Aβ(1-42)-incubated ECs. Overexpression of TARBP2, SNHG7 and NFATC3 elevated BBB permeability and knockdown of them had converse results. Agomir-17-5p decreased BBB permeability and antagomir-17-5p increased BBB permeability. TARBP2 as a RNA-binding protein (RBP) bound to SNHG7 and resulted in longer half-life of SNHG7. The decreased expression of miR-17-5p had a negative post-transcriptional regulation to NFATC3, leading to the increased expression of NFATC3. In addition, SNHG7 regulated NFATC3 expression by acting as a molecule sponge targeting to miR-17-5p. NFATC3 inhibited TJ proteins expression by functioning as a transcription factor. TARBP2/SNHG7/miR-17-5p/NFATC3 pathway implied a potential mechanism in studies of BBB changes in AD pathological progression.

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Section: Discussionsupporting

confidence: 86%

TARBP2-stablized SNHG7 regulates blood-brain barrier permeability by acting as a competing endogenous RNA to miR-17-5p/NFATC3 in Aβ-microenvironment

et al. 2022

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“…Of note, emerging evidence indicates that inflammasomes facilitate the disruption of the BBB after cerebral ischemia and reperfusion (12). Consistent with this, inhibition of inflammasomes was shown to reduce postischemic BBB damage, which was related to the upregulated expression of tight junction (TJ) proteins zonule occlusion-1 (ZO-1) and occludin (13,14). Mechanistically, activation of inflammasomes after cerebral ischemia is related to many factors, such as the ROS and thioredoxininteracting protein (TXNIP) pathways (15)(16)(17).…”

Section: Original Articlementioning

confidence: 75%

Interleukin-35 attenuates blood-brain barrier dysfunction caused by cerebral ischemia-reperfusion injury through inhibiting brain endothelial cell injury

Qian¹,

Li²,

Lin³

et al. 2022

Ann Transl Med

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Background: , an anti-inflammatory and antioxidant cytokine, plays a potent immunosuppressive role in various diseases. However, the effects of IL-35 on blood-brain barrier (BBB) dysfunction in ischemic stroke are not well characterized.Methods: A total of 150 male C57BL/6 mice (aged 6-8 weeks and weighing 20-25 g) were used in this study. The protective effects of IL-35 against BBB dysfunction were examined using a mouse model of middle cerebral artery occlusion (MCAO) and an in vitro model of oxygen-glucose deprivation/reoxygenation (OGD/R) injury in mouse brain endothelial cells (bEnd.3).Results: Intracerebroventricular administration of IL-35 (10 μg/g) was found to reduce cerebral edema and Evans blue (EB) leakage, and increase the expression of tight junction (TJ) proteins, thereby attenuating MCAO-induced neurological deficit in mice. Moreover, IL-35 (20 ng/mL) treatment upregulated the expression of TJ proteins in OGD/R-induced bEnd.3 cells. IL-35 also markedly suppressed the expression of caspase-1, IL-1β, and gasdermin D (GSDMD) in vivo and in vitro. In addition, IL-35 decreased the generation of reactive oxygen species (ROS) and inhibited the expression of thioredoxin-interacting protein (TXNIP) in OGD/R-induced bEnd.3 cells.Conclusions: These results indicated that IL-35 exerts a protective effect on the BBB by targeting the ROS/TXNIP/caspase-1 pathway in cerebral ischemia-reperfusion (I/R) injury.

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“…The change in the tightly connected to the protein level may cause the BBB permeability to increase the permeability, and thereby exacerbating BBB dysfunction, therefore the integrity of cells is crucial [ 62 ]. These important proteins include ZO-1, Occludin, and Claudin-5, which can prevent molecules from flowing from blood flow into the brain and closely related to the increased BBB permeability caused by a variety of diseases [ 63 ]. Occludin is the key structural component of BBB, which can regulate the integrity and permeability of BBB, and has become an important focus of BBB damage research.…”

Section: Discussionmentioning

confidence: 99%

Jingfang granules protects against intracerebral hemorrhage by inhibiting neuroinflammation and protecting blood-brain barrier damage

Li,

Yu,

Peng

et al. 2024

Aging

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Intracerebral hemorrhage (ICH) can induce intensive oxidative stress, neuroinflammation, and brain cell apoptosis. However, conventional methods for ICH treatment have many disadvantages. There is an urgent need for alternative, effective therapies with minimal side effects. Pharmacodynamics experiment, molecular docking, network pharmacology, and metabolomics were adopted to investigate the treatment and its mechanism of Jingfang Granules (JFG) in ICH. In this study, we investigated the therapeutic effects of JFG on ICH using behavioral, brain water content and Magnetic resonance imaging experiments. However, the key active component and targets of JFG remain unknown. Here we verified that JFG was beneficial to improve brain

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MiR-18a Aggravates Intracranial Hemorrhage by Regulating RUNX1-Occludin/ZO-1 Axis to Increase BBB Permeability

Cited by 11 publications

References 33 publications

TARBP2-stablized SNHG7 regulates blood-brain barrier permeability by acting as a competing endogenous RNA to miR-17-5p/NFATC3 in Aβ-microenvironment

TARBP2-stablized SNHG7 regulates blood-brain barrier permeability by acting as a competing endogenous RNA to miR-17-5p/NFATC3 in Aβ-microenvironment

Interleukin-35 attenuates blood-brain barrier dysfunction caused by cerebral ischemia-reperfusion injury through inhibiting brain endothelial cell injury

Jingfang granules protects against intracerebral hemorrhage by inhibiting neuroinflammation and protecting blood-brain barrier damage

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