Silencing of long non-coding RNA NEAT1 improves Treg/Th17 imbalance in preeclampsia via the miR-485-5p/AIM2 axis

Chen, Jiying; Zhang, Yonggang; Tan, Wenqing; Gao, Hanchao; Xiao, Shuixiu; Gao, Jinhua; Zhu, Zhiying

doi:10.1080/21655979.2021.1982306

Cited by 18 publications

(11 citation statements)

References 37 publications

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“…Studies have uncovered that lncRNAs are important regulators in occurrence and development of diverse diseases including UC, suggesting lncRNAs are potentially biomarkers and therapeutic targets for treatment of UC. LncRNA NEAT1 is frequently regulated in various human diseases [ 9 , 18 ]. Moreover, particular lncRNAs have been reported to be associated with intestinal epithelial barrier functions [ 19 , 20 ].…”

Section: Discussionmentioning

confidence: 99%

“…Recent study revealed that long non-coding RNA SNHG5 was upregulated in intestinal mucosa tissues of UC patients to regulate ulcerative colitis via microRNA-375/Janus kinase-2 axis [ 8 ], suggesting lncRNAs are crucial regulators and biomarkers in UC. LncRNA-NEAT1 (long non-coding RNA nuclear paraspeckle assembly transcript 1) is frequently dysregulated in diverse human diseases [ 9 ]. However, the precise roles and molecular mechanisms of NEAT1 in IECs dysfunction during UC remain unclear.…”

Section: Introductionmentioning

confidence: 99%

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Inhibition of LncRNA-NEAT1 alleviates intestinal epithelial cells (IECs) dysfunction in ulcerative colitis by maintaining the homeostasis of the glucose metabolism through the miR-410-3p-LDHA axis

Liu

Jihong

et al. 2022

Bioengineered

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Dysfunction of intestinal epithelial cells (IECs) leads to intestinal epithelial barrier damage and critically involves in the pathogenesis and development of ulcerative colitis (UC). Accumulating studies revealed essential functions of non-coding RNAs in UC. LncRNA NEAT1 (long non-coding RNA nuclear paraspeckle assembly transcript 1) is frequently dysregulated in diverse human diseases. Currently, the precise roles of NEAT1 in the dysfunction of IECs during UC remain unclear. We report NEAT1 was significantly upregulated in IECs from UC patients. In addition, microRNA-410-3p was remarkedly suppressed in IECs from UC patients. Silencing NEAT1 effectively ameliorates the LPS-induced IECs dysfunction. Bioinformatical analysis, RNA pull-down and luciferase assays illustrated that NEAT1 sponged miR-410-3p to downregulate its expression in IECs. Interestingly, the glucose metabolism was obviously elevated in IECs from UC compared with normal colon tissues. Furthermore, NEAT1 promoted and miR-410-3p suppressed glucose metabolism of IECs. We identified lactate dehydrogenase A (LDHA), a glucose metabolism key enzyme, was a direct target of miR-410-3p in IECs. Rescue experiments verified that restoration of miR-410-3p in NEAT1-overexpressing IECs successfully overcame the NEAT1-promoted cell death under LPS treatment by targeting LDHA. In summary, these results unveiled new roles and molecular mechanisms for the NEAT1-mediated IECs dysfunction during the ulcerative colitis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Inhibition of LncRNA-NEAT1 alleviates intestinal epithelial cells (IECs) dysfunction in ulcerative colitis by maintaining the homeostasis of the glucose metabolism through the miR-410-3p-LDHA axis

Liu

Jihong

et al. 2022

Bioengineered

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“…Additionally, a study reported that miR-146a-5p can regulate Th17 cell differentiation and thus influence the Treg/Th17 balance [ 21 ]. miR-485-5p increased CD4+ Treg cells differentiation and promoted the Treg/Th17 imbalance induced by the knockdown of NEAT1 expression [ 37 ]. Data show that Tregs in the TME play a key role in maintaining immune tolerance.…”

Section: Discussionmentioning

confidence: 99%

microRNA-128-3p inhibits CD4+ regulatory T cells enrichment by targeting interleukin 16 in gastric cancer

et al. 2021

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Previous studies have confirmed that microRNA (miR)-128-3p is expressed at low levels in gastric cancer (GC), and low miR-128-3p expression promotes the growth of GC cells. However, whether the dysregulation of miR-128-3p expression affects tumor-infiltrating lymphocytes (TILs) and leads to immune escape remains unclear. In the present study, predictive bioinformatics approaches showed that miR-128-3p expression was inversely correlated with tumor-infiltrating lymphocyte enrichment. When CD4 + T cells and regulatory T cells (Tregs) were enriched, lower miR-128-3p expression was associated with worse overall survival. However, when numbers of CD8 + T cells were decreased, the upregulation of miR-128-3p expression had a favorable effect on GC prognosis. Dual-luciferase reporter assays and cell biology experiments revealed that interleukin 16 (IL16) was the target of miR-128-3p and was negatively regulated by miR-128-3p. In addition, GC cells were cocultured with T lymphocytes, and the subsequent flow cytometric analysis showed that overexpression of miR-128-3p in tumor cells decreased the percentages of CD4+ CD25+ Foxp3+ Tregs by downregulating IL16 expression in GC, whereas miR-128-3p inhibition had the opposite effect. Moreover, the recombinant IL16 reversed the effects of miR-128-3p overexpression, and a competitive antibody against the IL16 receptor CD4 also reversed the effects of miR-128-3p knockdown. These studies identified the mechanism by which the miR-128-3p/IL16 axis promotes the infiltration of CD4+ Tregs in GC, and this mechanism will be a promising therapeutic target in GC immunotherapy.

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“…Chen et al. demonstrated that miR-485-5p inhibition suppressed Treg cells and the Treg/Th17 balance, but elevated Th17 cells, by targeting Absent in melanoma 2 ( 175 ).…”

Section: Mirnas In the Teff/treg Balancementioning

confidence: 99%

The role of miRNAs in T helper cell development, activation, fate decisions and tumor immunity

Xu,

Chen,

Chang

et al. 2024

Front. Immunol.

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T helper (Th) cells are central members of adaptive immunity and comprise the last line of defense against pathogen infection and malignant cell invasion by secreting specific cytokines. These cytokines then attract or induce the activation and differentiation of other immune cells, including antibody-producing B cells and cytotoxic CD8+ T cells. Therefore, the bidirectional communication between Th cells and tumor cells and their positioning within the tumor microenvironment (TME), especially the tumor immune microenvironment (TIME), sculpt the tumor immune landscape, which affects disease initiation and progression. The type, number, and condition of Th cells in the TME and TIME strongly affect tumor immunity, which is precisely regulated by key effectors, such as granzymes, perforins, cytokines, and chemokines. Moreover, microRNAs (miRNAs) have emerged as important regulators of Th cells. In this review, we discuss the role of miRNAs in regulating Th cell mediated adaptive immunity, focusing on the development, activation, fate decisions, and tumor immunity.

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Silencing of long non-coding RNA NEAT1 improves Treg/Th17 imbalance in preeclampsia via the miR-485-5p/AIM2 axis

Cited by 18 publications

References 37 publications

Inhibition of LncRNA-NEAT1 alleviates intestinal epithelial cells (IECs) dysfunction in ulcerative colitis by maintaining the homeostasis of the glucose metabolism through the miR-410-3p-LDHA axis

Inhibition of LncRNA-NEAT1 alleviates intestinal epithelial cells (IECs) dysfunction in ulcerative colitis by maintaining the homeostasis of the glucose metabolism through the miR-410-3p-LDHA axis

microRNA-128-3p inhibits CD4+ regulatory T cells enrichment by targeting interleukin 16 in gastric cancer

The role of miRNAs in T helper cell development, activation, fate decisions and tumor immunity

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