Up-regulation of microRNA-210 induces immune dysfunction via targeting FOXP3 in CD4+ T cells of psoriasis vulgaris

Zhao, Ming; Wang, Litao; Liang, Gongping; Zhang, Peng; Deng, Xin-jie; Tang, Qian; Zhai, Hanyue; Chang, Christopher; Y, Su; Lu, Qianjin

doi:10.1016/j.clim.2013.10.009

Cited by 131 publications

(117 citation statements)

References 40 publications

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“…Guinea-Viniefar et al demonstrated that the inhibition of miR-21 ameliorated disease pathology in patient-derived psoriatic skin xenotransplants in mice and in a psoriasis-like mouse model [34]. Zhao et al reported that the down-regulation of miR-210 improves immune dysfunction in CD4 + T cells of psoriasis patients [35]. In our study, we detected the effect of miR-138 overexpression in CD4 + T cells from psoriasis patients.…”

Section: Discussionsupporting

confidence: 59%

MicroRNA-138 regulates the balance of Th1/Th2 via targeting RUNX3 in psoriasis

et al. 2015

Immunology Letters

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Section: Discussionsupporting

confidence: 59%

MicroRNA-138 regulates the balance of Th1/Th2 via targeting RUNX3 in psoriasis

et al. 2015

Immunology Letters

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“…miR-194 has been suggested as a tumour suppressor that inhibits cell proliferation through targeting various target genes in numerous cancers [17, 18-20]. The expression of miR-194 was decreased in gastric cancer [21], laryngeal squamous cell carcinoma [22] and neuroblastoma [23], and the overexpression of miR-194 could inhibit tumour growth and enhance the sensitivity of tumours to radiotherapy and chemotherapy. In the past decades, an increasing number of studies concerning the relationship between miR-194 and osteosarcoma have been published.…”

Section: Discussionmentioning

confidence: 99%

miR-194 Suppresses Proliferation and Migration and Promotes Apoptosis of Osteosarcoma Cells by Targeting CDH2

Miao

Wang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Studies have shown that miR-194 functions as a tumour suppressor and is associated with tumour growth and metastasis. This study intends to uncover the mechanism of tumour suppression by miR-194. The expression of miR-194 in osteosarcoma cell lines and tissues were monitored by real-time PCR. Methods: The proliferation ability was examined by MTT assay. Migration and apoptosis of cells were monitored by migration assay and flow cytometry, respectively. The regulation of miR-194 on CDH2 was determined by luciferase assays and western blot assays. Results: The results showed that miR-194 was significantly reduced in osteosarcoma compared with that in normal bone tissue. Overexpression of miR-194 significantly attenuated the proliferation and migration and induced the apoptosis of osteosarcoma cells. Furthermore, we demonstrated that miR-194 has inhibited the malignant behaviour of osteosarcoma by downregulating CDH2 expression. Conclusions: These findings suggested that miR-194 may act as a tumour suppressor in osteosarcoma. miR-194/CDH2 may be a novel therapeutic target in the treatment of osteosarcoma.

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“…In acute kidney tissue injury, circulating levels of miR-210 are significantly up-regulated and correlated with patient mortality suggesting, a pro-inflammatory role for this miRNA 38 . MiR-210 was also shown to have a pro-inflammatory role by promoting inflammatory cytokine expression in CD-4 + T cells from psoriasis vulgaris patients 39 . Together, our results from the intestine and intestinal epithelial cells compared to results from other organs (stomach or skin) and different cells (macrophages or T-cells) indicate that regulation of miR-210 expression is tissue- and cell type-specific and it differs during acute or chronic inflammation.…”

Section: Discussionmentioning

confidence: 98%

Neurotensin Promotes the Development of Colitis and Intestinal Angiogenesis via Hif-1α–miR-210 Signaling

Bakirtzi

Law

Xue

et al. 2016

The Journal of Immunology

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Neurotensin (NT) via its receptor 1 (NTR1) modulates development of colitis, decreases HIF-1α/PHD2 interaction, stabilizes and increases HIF-1α transcriptional activity and promotes intestinal angiogenesis. HIF-1α induces miR-210 expression while miR-210 is strongly up-regulated in response to NT in NCM460 human colonic epithelial cells overexpressing NTR1 (NCM460-NTR1). Here we examined whether NT activates a NTR1-HIF-1α-miR-210 cascade using in vitro (NCM460-NTR1 cells) and in vivo [transgenic mice overexpressing (HIF-1α-OE) or lacking HIF-1α (HIF-1α-KO) in intestinal epithelial cells and mice lacking NTR1 (NTR1-KO)] models. Pre-treatment of NCM460-NTR1 cells with the HIF-1α inhibitor PX-478 or silencing of HIF-1α (si-HIF-1α) attenuated miR-210 expression in response to NT. Intracolonic 2,4,6-trinitrobenzenesulfonic acid (TNBS) administration (2-day model) increased colonic miR-210 expression that was significantly reduced in NTR1-KO, HIF-1α-KO mice, and in wild-type (WT) mice pre-treated intracolonicaly with locked nucleic acid anti-miR-210 (LNA-anti-miR-210). In contrast, HIF-1α-OE mice showed increased miR-210 expression at baseline that was further increased following TNBS administration. HIF-1α-OE mice had also exacerbated TNBS-induced neovascularization compared to TNBS-exposed WT mice. TNBS-induced neovascularization was attenuated in HIF-1α-KO mice, or mice pre-treated intracolonicaly with anti-miR-210. Intracolonic anti-miR-210 also reduced colitis in response to TNBS (2 days). Importantly, miR-210 expression was increased in tissue samples from ulcerative colitis patients (UC). We conclude that NT exerts its proinflammatory and proangiogenic effects during acute colitis via an NTR1-PHD2/HIF-1α-miR-210 signaling pathway. Our results also demonstrate that miR-210 plays a proinflammatory role in the development of colitis.

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Up-regulation of microRNA-210 induces immune dysfunction via targeting FOXP3 in CD4+ T cells of psoriasis vulgaris

Cited by 131 publications

References 40 publications

MicroRNA-138 regulates the balance of Th1/Th2 via targeting RUNX3 in psoriasis

MicroRNA-138 regulates the balance of Th1/Th2 via targeting RUNX3 in psoriasis

miR-194 Suppresses Proliferation and Migration and Promotes Apoptosis of Osteosarcoma Cells by Targeting CDH2

Neurotensin Promotes the Development of Colitis and Intestinal Angiogenesis via Hif-1α–miR-210 Signaling

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