The Roles of H19 in Regulating Inflammation and Aging

Wang, Bin; Suen, Chun-wai; Ma, Hongwei; Wang, Yan; Kong, Ling; Qin, Dajiang; Lee, Wayne; Li, Gang

doi:10.3389/fimmu.2020.579687

Cited by 45 publications

(29 citation statements)

References 115 publications

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“…The increased cell death rate and reduced cell viability were induced by the ISO, whereas, downregulation of H19 changed these trends, which disclosed that H19 was associated with the ISO-caused damage. Moreover, researches on the influence of H19 in inflammation have been found recently [37]. The abnormal levels of TNF-α, IL-6, and IL-1β were induced by the ISO and reversed by the inhibited H19 expression, indicating H19 exerted expansionary impacts in inflammation.…”

Section: Discussionmentioning

confidence: 99%

Effects of Long Noncoding RNA H19 on Isoflurane-Induced Cognitive Dysregulation by Promoting Neuroinflammation

Lin

Cui

et al. 2021

Neuroimmunomodulation

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Introduction: Isoflurane (ISO) may cause neuronal apoptosis and synaptic disorder during development, and damage long-term learning and memory function. This observation aimed to study the function of H19 in vitro and in vivo tests and the further mechanism was identified. Methods: ISO cell models and rat models were established and reactive oxygen species (ROS) identified. The viability and apoptosis of HT22 cells were detected by the MTT and flow cytometer. Morris water maze test was conducted to analyze the neurotoxicity of ISO on spatial learning and memory ability. Quantitative PCR was the method to verify the expression of H19. The concentration of inflammatory indicators was identified by enzyme-linked immunosorbent assay. Results: 1.5% and 2% ISO led to the neurotoxicity of HT22 cells and increased expression of H19. Silenced H19 meliorated these adverse impacts of ISO. Interference of H19 exerted neuroprotective roles by repressing modified neurological severity score, inhibiting escape latency, elevating distance and time of target area, and controlling ROS and inflammation. MiR-17-5p might be a promising competing endogenous RNA of H19. The expression of miR-17-5p was reduced in the ISO group and reversed by the absence of H19. Conclusion: Our results of in vitro and in vivo assay indicated that the absence of HT22 is a neuroprotective regulator of cognition and inflammation by accumulating miR-17-5p.

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Section: Discussionmentioning

confidence: 99%

Effects of Long Noncoding RNA H19 on Isoflurane-Induced Cognitive Dysregulation by Promoting Neuroinflammation

Lin

Cui

et al. 2021

Neuroimmunomodulation

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“…H19 also plays a pivotal role in diverse in ammations. In rheumatoid arthritis, H19 promoted the in ammation by degradation of miR-103a [50]; in ankylosing spondylitis, H19 interacts with miR-675-5p and miR-22-5p to increase IL-17A/IL-23 release [51]; H19 also regulates ageing and age-related diseases by interplay with in ammation [52]. H19 also contributes to the genesis and metastasis of different type of cancers by reexpression in cancer tissues, e. g., hepatocellular carcinoma [53], thyroid cancer cells [54], non-small cell lung cancer [55], etc.…”

Section: Discussionmentioning

confidence: 99%

Role of LncRNA H19/miR-93-5p/Orai1 axis in the regulation of human bronchial smooth muscle cell functions and airway remodeling in murine models of asthma

Xiang¹,

Wan²,

Wang³

et al. 2021

Preprint

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Background Type 2 cytokine Interleukin (IL)-13 regulates airway remodeling in asthma by acting on store-operated Ca2+ entry (SOCE) in airway smooth muscle cells. The underlying mechanisms of this regulating effect of IL-13 are not fully understood. Methods Bioinformatic analysis identified interactions of microRNA 93-5p with Orai1, the pore-forming molecule of SOCE, and long non-coding RNA H19 respectively. We investigated the role of H19/miR-93-5p/Orai1 axis in the regulation of proliferation and migration of in vitro cultured human bronchial smooth muscle cells (hBSMCs) induced by IL-13. Functional relevance of H19 in airway inflammation and airway remodeling was investigated in acute and chronic murine models of asthma. Results IL-13 dose-dependently increased the expression of H19 and Orai1 and decreased the expression of miR-93-5p in hBSMCs; H19 siRNA reversed IL-13-induced miR-93-5p and Orai1 expression, and the proliferation and migration of hBSMCs. IL-13-promoted expression of H19 and Orai1 was reduced by miR-93-5p mimic and enhanced by miR-93-5p inhibitor. IL-13-promoted hBSMCs proliferation was enhanced by miR-93-5p inhibitor but not changed by miR-93-5p mimic; whereas IL-13-promoted hBSMCs migration was enhanced by miR-93-5p inhibitor and reduced by miR-93-5p mimic. MiR-93-5p mimic enhanced the inhibiting effect of H19 siRNA on IL-13-induced Orai1 mRNA expression, whereas miR-93-5p inhibitor reversed the inhibiting effects of H19 siRNA on IL-13-induced H19 and Orai1 mRNA and protein expression. The inhibiting effect of H19 siRNA on IL-13-induced hBSMCs proliferation and migration was reversed by miR-93-5p inhibitor but not changed by miR-935p mimic. In the lungs of both asthma mice models, the expression of H19 and Orai1 was higher than in control mice. In acute asthma mice, H19 siRNA reduced Orai1 expression, inflammatory cell infiltration and goblet cell hyperplasia in the lungs, and IL-13 levels in the bronchoalveolar lavage fluid. In chronic asthma mice, H19 siRNA reduced Orai1 expression, inflammatory cell infiltration, goblet cell hyperplasia, collagen deposition and smooth muscle mass in the lungs, as well as IL-13 levels in the BALF. Conclusion IL-13 increases the proliferation and migration of airway smooth muscle cells by acting on H19/miR-93-5p/Orai1 axis, which also regulates airway inflammation and airway remodeling in murine models of asthma.

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“…Its expression reaches its highest level in the human embryo and decreases with aging [22]. Previous studies have found that lncRNAH19 plays a role in physiological and pathological processes such as inflammation, aging, and tumorigenesis [23,24]. In recent years, an increasing number of studies have reported that it can regulate the intestinal mucosal mechanical barrier through various mechanisms and indirectly participate in the progression of intestinal diseases.…”

Section: Regulatory Effects Of Different Lncrnas Onmentioning

confidence: 99%

The Role of lncRNAs in Regulating the Intestinal Mucosal Mechanical Barrier

Chen

Zhang

et al. 2021

BioMed Research International

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lncRNA is a transcript that is more than 200 bp in length. Currently, evidence has shown that lncRNA is of great significance in cell activity, involved in epigenetics, gene transcription, chromatin regulation, etc. The existence of an intestinal mucosal mechanical barrier hinders the invasion of pathogenic bacteria and toxins, maintaining the stability of the intestinal environment. Serious destruction or dysfunction of the mechanical barrier often leads to intestinal diseases. This review first summarizes the ability of lncRNAs to regulate the intestinal mucosal mechanical barrier. We then discussed how lncRNAs participate in various intestinal diseases by regulating the intestinal mucosal mechanical barrier. Finally, we envision its potential as a new marker for diagnosing and treating intestinal inflammatory diseases.

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The Roles of H19 in Regulating Inflammation and Aging

Cited by 45 publications

References 115 publications

Effects of Long Noncoding RNA H19 on Isoflurane-Induced Cognitive Dysregulation by Promoting Neuroinflammation

Effects of Long Noncoding RNA H19 on Isoflurane-Induced Cognitive Dysregulation by Promoting Neuroinflammation

Role of LncRNA H19/miR-93-5p/Orai1 axis in the regulation of human bronchial smooth muscle cell functions and airway remodeling in murine models of asthma

The Role of lncRNAs in Regulating the Intestinal Mucosal Mechanical Barrier

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