MiR-18a increased the permeability of BTB via RUNX1 mediated down-regulation of ZO-1, occludin and claudin-5

Miao, Yaping; Zhao, Yingyu; Zhao, Liye; Wang, Ping; Liu, Yunhui; Ma, Jun; Xue, Yixue

doi:10.1016/j.cellsig.2014.10.008

Cited by 43 publications

(35 citation statements)

References 43 publications

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“…Simultaneously, overexpression of both USF1 and miR-148b-3p showed the overexpression of USF1 could effectively reverse miR-148b-3p mediated up-regulation on BTB permeability, which pointing out that miR-148b-3p increased BTB permeability by negatively regulating USF1. There were similar studies about miRNA regulating transcription factor to change BTB permeability: miR-18a targeting RUNX1 (Miao et al, 2015) as well as miR-34a targeting PKCε could regulate BTB permeability significantly (Zhao W. et al, 2015). …”

Section: Discussionmentioning

confidence: 89%

“…Above results suggested miR-148b-3p played important roles in the regulation of BTB permeability. Our previous studies unveiled the effects and mechanisms of certain miRNA on BTB permeability, for example, miR-181a targeting KLF6, miR-18a targeting RUNX1, and miR-34c targeting MAZ significantly regulated BTB permeability, respectively (Ma et al, 2014b; Miao et al, 2015; Zhao L. et al, 2015). …”

Section: Discussionmentioning

confidence: 94%

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RETRACTED: The Role of HOTAIR/miR-148b-3p/USF1 on Regulating the Permeability of BTB

Zhao

et al. 2017

Front. Mol. Neurosci.

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Homeobox transcript antisense intergenic RNA (HOTAIR), as a long non-coding RNA (lncRNA), has been considered to play critical roles in the biological properties of various tumors. The purposes of this study were to investigate the role and possible molecular mechanisms of HOTAIR in regulating the permeability of blood tumor barrier (BTB) in vitro. Our present study elucidated that the expressions of HOTAIR and upstream stimulatory factor 1 (USF1) was up-regulated, but miR-148b-3p was down-regulated in glioma microvascular endothelial cells (GECs). Knockdown of HOTAIR could increase the permeability of BTB as well as down-regulated the expressions of tight junction related proteins ZO-1, occludin, claudin-5, but up-regulated miR-148b-3p expressions in GECs. Meanwhile, dual-luciferase reporter assays demonstrated that HOTAIR was a target RNA of miR-148b-3p. Furthermore, overexpression of miR-148b-3p increased the permeability of BTB by down-regulating the expressions of tight junction related proteins and USF1 in GECs, and vice versa. And further result revealed USF1 was a target of miR-148b-3p. Silence of USF1 increased the permeability of BTB duo to their interaction with the promoters of ZO-1, occludin, and claudin-5 in GECs. Taken together, our finding indicated that knockdown of HOTAIR increased BTB permeability via binding to miR-148b-3p, which further reducing tight junction related proteins in GECs by targeting USF1. Thus, HOTAIR will attract more attention since it can serve as a potential target of drug delivery across BTB and may provide novel strategies for glioma treatment.

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Section: Discussionmentioning

confidence: 89%

Section: Discussionmentioning

confidence: 94%

RETRACTED: The Role of HOTAIR/miR-148b-3p/USF1 on Regulating the Permeability of BTB

Zhao

et al. 2017

Front. Mol. Neurosci.

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“…The miRNAs have been shown to play a critical role in regulating the biological function of endothelial cells, and previous research indicated that miRNAs can affect the integrity of the BBB and blood–tumour barrier by decreasing the expression of tight junctions. For example, miR-155, miR-18a and miR-34c were shown to be able to downregulate ZO-1, occludin and claudin-5 expression, thereby, enhancing barrier permeability363738. LncRNAs were also reported to be involved in brain development as well as in some CNS diseases3940.…”

Section: Discussionmentioning

confidence: 99%

Differential transcription profiles of long non-coding RNAs in primary human brain microvascular endothelial cells in response to meningitic Escherichia coli

Yang

Huang²,

et al. 2016

Sci Rep

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Accumulating studies have indicated the influence of long non-coding RNAs (lncRNAs) on various biological processes as well as disease development and progression. However, the lncRNAs involved in bacterial meningitis and their regulatory effects are largely unknown. By RNA-sequencing, the transcriptional profiles of host lncRNAs in primary human brain microvascular endothelial cells (hBMECs) in response to meningitic Escherichia coli were demonstrated. Here, 25,257 lncRNAs were identified, including 24,645 annotated lncRNAs and 612 newly found ones. A total of 895 lncRNAs exhibited significant differences upon infection, among which 382 were upregulated and 513 were downregulated (≥2-fold, p < 0.05). Via bioinformatic analysis, the features of these lncRNAs, their possible functions, and the potential regulatory relationships between lncRNAs and mRNAs were predicted. Moreover, we compared the transcriptional specificity of these differential lncRNAs among hBMECs, human astrocyte cell U251, and human umbilical vein endothelial cells, and demonstrated the novel regulatory effects of proinflammatory cytokines on these differential lncRNAs. To our knowledge, this is the first time the transcriptional profiles of host lncRNAs involved in E. coli-induced meningitis have been reported, which shall provide novel insight into the regulatory mechanisms behind bacterial meningitis involving lncRNAs, and contribute to better prevention and therapy of CNS infection.

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“…Primer sequences, reaction conditions, and optimal cycle numbers of PCR were described previously [35]. The expression level of ZO-1 was analyzed using comparative threshold cycle method (2 −ΔΔCT ) with GAPDH as an internal reference [36]. The expression level of medium without estrogen treatment was set as 1.…”

Section: Methodsmentioning

confidence: 99%

Estrogen decreases tight junction protein ZO-1 expression in human primary gut tissues

Zhou

Zhang

Ding

et al. 2017

Clinical Immunology

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Females have a higher prevalence of most autoimmune diseases; however, the mechanism is unknown. In this study, we examined the expression of tight junction protein zonula occludens 1 (ZO-1) and estrogen receptor (ER)-α/β in human primary gut tissues by immunohistochemistry, immunofluorescence and qPCR. The expression of ZO-1 and ER-β but not ER-α was present in both male and female gut tissues. There was no sex difference in ER-β expression, but ZO-1 expression was decreased in females compared to males. In vitro, estrogen treatment decreased ZO-1 mRNA and protein expression, ZO-1 promoter activity, IL-6 production, and NF-κB activation in human primary gut tissues or the Caco-2 cells, but increased the ER-β expression in Caco-2 cells. Consistently, plasma IL-6 levels in females were reduced relative to males in vivo. Our finding indicates that estrogen may play a role in gut tight junction expression and permeability.

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MiR-18a increased the permeability of BTB via RUNX1 mediated down-regulation of ZO-1, occludin and claudin-5

Cited by 43 publications

References 43 publications

RETRACTED: The Role of HOTAIR/miR-148b-3p/USF1 on Regulating the Permeability of BTB

RETRACTED: The Role of HOTAIR/miR-148b-3p/USF1 on Regulating the Permeability of BTB

Differential transcription profiles of long non-coding RNAs in primary human brain microvascular endothelial cells in response to meningitic Escherichia coli

Estrogen decreases tight junction protein ZO-1 expression in human primary gut tissues

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