miR-143 inhibits interleukin-13-induced inflammatory cytokine and mucus production in nasal epithelial cells from allergic rhinitis patients by targeting IL13Rα1

Teng, Yaoshu; Zhang, Ruxin; Liu, Chunhui; Zhou, Lingling; Wang, Hong; Zhuang, Wenjie; Huang, Yu; Hong, Zhicong

doi:10.1016/j.bbrc.2014.12.058

Cited by 71 publications

(62 citation statements)

References 28 publications

(34 reference statements)

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“…MI patients exhibited an upregulation of miR-143 and -145, involved in macrophage differentiation and activation, from peripheral blood monocytes [220, 221]. Interestingly, miR-143 has been shown to have anti-inflammatory effects during allergic rhinitis by inhibiting IL-13 secretion, suggesting a similar role in cardiac monocytes or macrophages [177]. Monocyte-derived miRNAs also influence neighboring cells, as the expression of miR-126 in circulating monocytes is highly linked to angiogenesis and vascular inflammation [76].…”

Section: Inflammatory Responses Post-mi and Ncrnas Derived From Immunmentioning

confidence: 99%

Inflammatory cells and their non-coding RNAs as targets for treating myocardial infarction

2018

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Myocardial infarction triggers infiltration of several types of immune cells that coordinate both innate and adaptive immune responses. These play a dual role in post-infarction cardiac remodeling by initiating and resolving inflammatory processes, which needs to occur in a timely and well-orchestrated way to ensure a reestablishment of normalized cardiac functions. Thus, therapeutic modulation of immune responses might have benefits for infarct patients. While such strategies have shown great potential in treating cancer, applications in the post-infarction context have been disappointing. One challenge has been the complexity and plasticity of immune cells and their functions in cardiac regulation and healing. The types appear in patterns that are temporally and spatially distinct, while influencing each other and the surrounding tissue. A comprehensive understanding of the immune cell repertoire and their regulatory functions following infarction is sorely needed. Processes of cardiac remodeling trigger additional genetic changes that may also play critical roles in the aftermath of cardiovascular disease. Some of these changes involve non-coding RNAs that play crucial roles in the regulation of immune cells and may, therefore, be of therapeutic interest. This review summarizes what is currently known about the functions of immune cells and non-coding RNAs during post-infarction wound healing. We address some of the challenges that remain and describe novel therapeutic approaches under development that are based on regulating immune responses through non-coding RNAs in the aftermath of the disease.

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Section: Inflammatory Responses Post-mi and Ncrnas Derived From Immunmentioning

confidence: 99%

Inflammatory cells and their non-coding RNAs as targets for treating myocardial infarction

2018

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“…After exposure of cells to zero, 100, 400 or 800 μg/ml of PM 2.5 for 24 hours, the mRNA levels of GM-CSF, TNF-α, IL-13, eotaxin, IL-6 and IL-8 were measured by real-time qRT-PCR as previously described (Teng et al 2015). Briefly, total RNA of RPMI 2650 cells was extracted using Trizol reagent (Invitrogen, Shanghai, China), and reverse transcribed into cDNA using SuperScript III Reverse Transcriptase (Invitrogen).…”

Section: Real-time Quantitative Reverse Transcription Pcr (Qrt-pcr)mentioning

confidence: 99%

Airborne Fine Particulate Matter Induces Oxidative Stress and Inflammation in Human Nasal Epithelial Cells

Hong

Guo

Zhang

et al. 2016

Tohoku J. Exp. Med.

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125

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Airborne fine particulate matter with an aerodynamic diameter equal to or smaller than 2.5 μ m is abbreviated as PM 2.5 , which is one of the main components in air pollution. Exposure to PM 2.5 is associated with increased risk of many human diseases, including chronic and allergic rhinitis, but the underlying molecular mechanism for its toxicity has not been fully elucidated. We have hypothesized that PM 2.5 may cause oxidative stress and enhance inflammatory responses in nasal epithelial cells. Accordingly, we used human RPMI 2650 cells, derived from squamous cell carcinoma of the nasal septum, as a model of nasal epithelial cells, and exposed them to PM 2.5 that was collected at Fudan University (31.3°N, 121.5°E) in Shanghai, China. PM 2.5 exposure decreased the viability of RPMI 2650 cells, suggesting that PM 2.5 may impair the barrier function of nasal epithelial cells. Moreover, PM 2.5 increased the levels of intracellular reactive oxygen species (ROS) and the nuclear translocation of NF-E2-related factor-2 (Nrf2). Importantly, PM 2.5 also decreased the activities of superoxide dismutase, catalase and glutathione peroxidase. Pretreatment with N-Acetyl-L-cysteine (an anti-oxidant) reduced the degree of the PM 2.5 -induced oxidative stress in RPMI 2650 cells. In addition, PM 2.5 increased the production of granulocyte-macrophage colonystimulating factor, tumor necrosis factor-α, interleukin-13 and eotaxin (C-C motif chemokine ligand 11), each of which initiates and/or augments local inflammation. These results suggest that PM 2.5 may induce oxidative stress and inflammatory responses in human nasal epithelial cells, thereby leading to nasal inflammatory diseases. The present study provides insights into cellular injury induced by PM 2.5 .

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“…Using a miRNA microarray assay, Yu et al (2011) showed that the miRNA expression profile was altered in the nasal mucosa of AR patients. And also, miR-143 was found to inhibit interleukin-13-induced inflammatory cytokine and mucus production in nasal epithelial cells from AR patients by targeting IL13Rα1 (Teng et al 2015). These studies have suggested that the non-coding RNAs are involved in the regulation of AR-related gene expression and the pathological process of AR.…”

Section: Discussionmentioning

confidence: 93%

Identification and Functional Profiling of Differentially Expressed Long Non-Coding RNAs in Nasal Mucosa with Allergic Rhinitis

Teng

Liu

et al. 2017

Tohoku J. Exp. Med.

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Long non-coding RNAs (lncRNAs) have been proved to play important roles in a variety of human immune diseases. However, their pathological effects on the development of allergic rhinitis (AR) have not been clearly understood. The aim of this study was to determine the expression profile of lncRNAs in nasal mucosa of AR patients by lncRNA microarray and to predict potential roles of specific lncRNAs in the pathogenic mechanisms of AR by analysis of lncRNA-mRNA co-expression network, Gene Ontology (GO) and pathway. The lncRNA microarray analysis showed that a total of 2,259 lncRNAs (1,033 up-regulated and 1,226 down-regulated) and 704 mRNAs (157 up-regulated and 547 down-regulated) were significantly differentially expressed in the nasal mucosa samples from 4 AR patients as compared to those from 4 non-allergic subjects (fold change > 2; P < 0.05). In addition, the lncRNA-mRNA co-expression network contained 143 network nodes including 76 lncRNAs and 67 mRNAs, in which 117 significant correlation pairs presented as positive, and 108 pairs presented as negative. The results from GO and pathway analysis indicated that the lncRNAs-coexpressed mRNAs were enriched in several biological processes and cellular signaling pathways related to AR development, such as positive regulation of interleukin-13 secretion, Fc epsilon RI signaling pathway and NF-kappa B signaling pathway. To summary, our study provides important information on the molecular mechanisms and biological functions of these AR-related lncRNAs, which could be utilized for developing novel therapeutic strategies for AR.

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miR-143 inhibits interleukin-13-induced inflammatory cytokine and mucus production in nasal epithelial cells from allergic rhinitis patients by targeting IL13Rα1

Cited by 71 publications

References 28 publications

Inflammatory cells and their non-coding RNAs as targets for treating myocardial infarction

Inflammatory cells and their non-coding RNAs as targets for treating myocardial infarction

Airborne Fine Particulate Matter Induces Oxidative Stress and Inflammation in Human Nasal Epithelial Cells

Identification and Functional Profiling of Differentially Expressed Long Non-Coding RNAs in Nasal Mucosa with Allergic Rhinitis

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