MicroRNA-107 prevents amyloid-beta induced blood-brain barrier disruption and endothelial cell dysfunction by targeting Endophilin-1

Liu, Wenjing; Cai, Heng; Miao, Lin; Zhu, Lu; Gao, Lili; Zhong, Renjia; Bi, Siwei; Xue, Yixue; Shang, Xiuli

doi:10.1016/j.yexcr.2016.03.026

Cited by 47 publications

(45 citation statements)

References 42 publications

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“…46,47 For instance, miR-34a is enriched in the cerebral cortex of AD mouse models and contributes to the pathogenesis of AD. 29 In the present study, we demonstrated that miR-224-5p/miR-497-5p was highly expressed in Abeta 1-42 -incubated ECs and miR-224-5p/miR-497-5p over-expression reduced BBB permeability in AD microenvironment by promoting TJs expression. Over-expression of miR-107 could alleviate BBB permeability and protect BBB integrity by up-regulating TJs.…”

Section: Discussionsupporting

confidence: 54%

“…29 Human embryonic kidney 293 (HEK293T) cells were acquired from Shanghai Institutes for Biological Sciences Cell Resource Center and the cell culture has been previously detailed. ECs were limited from 28 to 32 passages.…”

Section: Cell Culturesmentioning

confidence: 99%

“…The in vitro co-culturing BBB model was established following Liu et al 29 First, pericytes were seeded (2 × 10 5 cells/cm 2 ) onto the lower chamber of Transwell inserts (0.4 μm pore size; Corning, NY, USA). After pericytes cells were cultured overnight, 2 × 10 5 cells/cm 2 hCMEC/D3 cells were subsequent placed on the upper chambers of Transwell inserts.…”

Section: In Vitro Bbb Model Establishmentmentioning

confidence: 99%

“…The cells were cultured as described previously. 29 Human embryonic kidney 293 (HEK293T) cells were acquired from Shanghai Institutes for Biological Sciences Cell Resource Center and the cell culture has been previously detailed. 30 All cells were cultured in a humidified incubator at 37°C with 5% CO 2 .…”

Section: Cell Culturesmentioning

confidence: 99%

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The role of LINC00094/miR‐224‐5p (miR‐497‐5p)/Endophilin‐1 axis in Memantine mediated protective effects on blood‐brain barrier in AD microenvironment

Zhu

Miao

et al. 2019

J Cellular Molecular Medi

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The dysfunction of the blood‐brain barrier ( BBB ) is one of the main pathological features of Alzheimer's disease ( AD ). Memantine ( MEM ), an N ‐methyl‐ d ‐aspartate ( NMDA ) receptor antagonist, has been reported that been used widely for AD therapy. This study was performed to demonstrate the role of the MEM in regulating BBB permeability in AD microenvironment as well as its possible mechanisms. The present study showed that LINC 00094 was dramatically increased in Abeta 1‐42 ‐incubated microvascular endothelial cells ( EC s) of BBB model in vitro. Besides, it was decreased in MEM ‐incubated EC s. Silencing LINC 00094 significantly decreased BBB permeability, meanwhile up‐regulating the expression of ZO ‐1, occludin and claudin‐5. Furthermore, silencing LINC 00094 enhance the effect of MEM on decreasing BBB permeability in AD microenvironment. The analysis of the mechanism demonstrated that reduction of LINC 00094 inhibited Endophilin‐1 expression by up‐regulating miR‐224‐4p/miR‐497‐5p, promoted the expression of ZO ‐1, occludin and claudin‐5, and ultimately alleviated BBB permeability in AD microenvironment. Taken together, the present study suggests that the MEM / LINC 00094/miR‐224‐5p (miR‐497‐5p)/Endophilin‐1 axis plays a crucial role in the regulation of BBB permeability in AD microenvironment. Silencing LINC 00094 combined with MEM provides a novel target for the therapy of AD .

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Section: Discussionsupporting

confidence: 54%

Section: Cell Culturesmentioning

confidence: 99%

Section: In Vitro Bbb Model Establishmentmentioning

confidence: 99%

Section: Cell Culturesmentioning

confidence: 99%

See 2 more Smart Citations

The role of LINC00094/miR‐224‐5p (miR‐497‐5p)/Endophilin‐1 axis in Memantine mediated protective effects on blood‐brain barrier in AD microenvironment

Zhu

Miao

et al. 2019

J Cellular Molecular Medi

Self Cite

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“…3-UTR assay showed that endophilin-1 mRNA is the direct target of miR-107, which further affected endothelial junction by upregulation of ZO-1, occludin, and claudin-5 [4]. The rat permanent middle cerebral artery occlusion (MCAO) model showed that MCAO significantly increased BBB permeability in MCAO area.…”

Section: Tight Junction Proteinsmentioning

confidence: 99%

MicroRNA Regulation of Endothelial Junction Proteins and Clinical Consequence

Zhuang

Mastej

et al. 2016

Mediators of Inflammation

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Cellular junctions play a critical role in structural connection and signal communication between cells in various tissues. Although there are structural and functional varieties, cellular junctions include tight junctions, adherens junctions, focal adhesion junctions, and tissue specific junctions such as PECAM-1 junctions in endothelial cells (EC), desmosomes in epithelial cells, and hemidesmosomes in EC. Cellular junction dysfunction and deterioration are indicative of clinical diseases. MicroRNAs (miRNA) are ~20 nucleotide, noncoding RNAs that play an important role in posttranscriptional regulation for almost all genes. Unsurprisingly, miRNAs regulate junction protein gene expression and control junction structure integrity. In contrast, abnormal miRNA regulation of junction protein gene expression results in abnormal junction structure, causing related diseases. The major components of tight junctions include zonula occluden-1 (ZO-1), claudin-1, claudin-5, and occludin. The miRNA regulation of ZO-1 has been intensively investigated. ZO-1 and other tight junction proteins such as claudin-5 and occludin were positively regulated by miR-126, miR-107, and miR21 in different models. In contrast, ZO-1, claudin-5, and occludin were negatively regulated by miR-181a, miR-98, and miR150. Abnormal tight junction miRNA regulation accompanies cerebral middle artery ischemia, brain trauma, glioma metastasis, and so forth. The major components of adherens junctions include VE-cadherin, β-catenin, plakoglobin, P120, and vinculin. VE-cadherin and β-catenin were regulated by miR-9, miR-99b, miR-181a, and so forth. These regulations directly affect VE-cadherin-β-catenin complex stability and further affect embryo and tumor angiogenesis, vascular development, and so forth. miR-155 and miR-126 have been shown to regulate PECAM-1 and affect neutrophil rolling and EC junction integrity. In focal adhesion junctions, the major components are integrin β4, paxillin, and focal adhesion kinase (FAK). Integrin β4 has been regulated by miR-184, miR-205, and miR-9. Paxillin has been regulated by miR-137, miR-145, and miR-218 in different models. FAK has been regulated by miR-7, miR-138, and miR-135. Deregulation of miRNAs is caused by viral infections, tumorigenesis, and so forth. By regulation of posttranscription, miRNAs manipulate junction protein expression in all cellular processes and further determine cellular fate and development. Elucidation of these regulatory mechanisms will become a new alternative therapy for many diseases, such as cancers and inflammatory diseases.

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MiR‐128‐1‐5p regulates tight junction induced by selenium deficiency via targeting cell adhesion molecule 1 in broilers vein endothelial cells

Pan

Liu

et al. 2018

Journal Cellular Physiology

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Vein endothelial cells (VECs) constitute an important barrier for macromolecules and circulating cells from the blood to the tissues, stabilizing the colloid osmotic pressure of the blood, regulating the vascular tone, and rapidly changing the intercellular connection, and maintaining normal physiological function. Tight junction has been discovered as an important structural basis of intercellular connection and may play a key role in intercellular connection injuries or vascular diseases and selenium (Se) deficiency symptoms. Hence, we replicated the Se-deficient broilers model and detected the specific microRNA in response to Se-deficient vein by using quantitative real time-PCR (qRT-PCR) analysis. Also, we selected miR-128-1-5p based on differential expression in vein tissue and confirmed its target gene cell adhesion molecule 1 (CADM1) by the dual luciferase reporter assay and qRT-PCR in VECs. We made the ectopic miR-128-1-5p expression for the purpose of validating its function on tight junction. The result showed that miR-128-1-5p and CADM1 were involved in the ZO-1-mediated tight junction, increased paracellular permeability, and arrested cell cycle. We presumed that miR-128-1-5p and Se deficiency might trigger tight junction. Interestingly, miR-128-1-5p inhibitor and fasudil in part hinder the destruction of the intercellular structure caused by Se deficiency. The miR-128-1-5p/CADM1/tight junction axis provides a new avenue toward understanding the mechanism of Se deficiency, revealing a novel regulation model of tight junction injury in vascular diseases.

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MicroRNA-107 prevents amyloid-beta induced blood-brain barrier disruption and endothelial cell dysfunction by targeting Endophilin-1

Cited by 47 publications

References 42 publications

The role of LINC00094/miR‐224‐5p (miR‐497‐5p)/Endophilin‐1 axis in Memantine mediated protective effects on blood‐brain barrier in AD microenvironment

The role of LINC00094/miR‐224‐5p (miR‐497‐5p)/Endophilin‐1 axis in Memantine mediated protective effects on blood‐brain barrier in AD microenvironment

MicroRNA Regulation of Endothelial Junction Proteins and Clinical Consequence

MiR‐128‐1‐5p regulates tight junction induced by selenium deficiency via targeting cell adhesion molecule 1 in broilers vein endothelial cells

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