Identifying Involvement of H19-miR-675-3p-IGF1R and H19-miR-200a-PDCD4 in Treating Pulmonary Hypertension with Melatonin

Wang, Ran; Zhou, Sijing; Wu, Peipei; Li, Min; Ding, Xing; Lee, Sun; Xu, Xuan; Zhou, Xuexin; Zhou, Luqian; Cao, Chao; Fei, Guanghe

doi:10.1016/j.omtn.2018.08.015

Cited by 55 publications

(35 citation statements)

References 62 publications

(73 reference statements)

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“…The total RNA content in each plasma sample collected from the mice models was isolated by using a Trizol kit assay kit (Invitrogen, Carlsbad, CA, USA) following the standard protocol provided by the kit manufacturer. 35 , 36 In the next step, the isolated RNA was subjected to real-time PCR to determine the relative expression of miR-10a, miR-26a, miR-30a, miR-34c, miR-99b, miR-122a, miR-123-prec, miR-124a-prec b , miR-125a-prec b , miR-140 s b , miR-145-prec, miR-146-prec b , miR-191-prec, miR-192, miR-219-prec, miR-222-prec, miR-223-prec, miR-122, and IL-17a mRNA by the calculation provided by the 2 −ΔΔCt method. The qPCR data for miRNAs were normalized to RNU48, while the qPCR data for IL-17a mRNA was normalized to GAPDH.…”

Section: Methodsmentioning

confidence: 99%

Microbiota Imbalance Contributes to COPD Deterioration by Enhancing IL-17a Production via miR-122 and miR-30a

Zhu

Zhou

Xu³

et al. 2020

Molecular Therapy - Nucleic Acids

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The changes of microbiota in lungs could change interleukin-17a (IL-17a) expression by altering microRNAs (miRNAs) profile, thus contributing to the pathogenesis of chronic obstructive pulmonary disease (COPD). In this study, we aimed to study molecular mechanisms’ underlying effect of microbiota imbalance on COPD deterioration. Real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA) were performed to analyze expression of miRNAs and IL-17a mRNA. ELISA was used to evaluate abundance of IL-17a in plasma, peripheral blood monocyte, and sputum of COPD mice and patients. Luciferase assay was performed to explore underlying molecular mechanisms. The expression of miR-122, miR-30a, and miR-99b were remarkably decreased in COPD mice, while the expression of IL-17a was notably increased in plasma, peripheral blood monocytes, and lung tissues of COPD mice. The levels of Lactobacillus/Moraxella and IL-17a expression were significantly enhanced in sputum of exacerbated COPD patients, along with notably decreased expression of miR-122 and miR-30a. Luciferase assay confirmed that miR-122 and miR-30a played an inhibitory role in IL-17a expression. We identified miR-122 and miR-30a as differentially expressed miRNAs in sputum and plasma of COPD patients in exacerbation-month12 group. Furthermore, downregulated miR-122 and miR-30a expression associated with microbiota imbalance may contribute to COPD deterioration by enhancing IL-17a production.

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Section: Methodsmentioning

confidence: 99%

Microbiota Imbalance Contributes to COPD Deterioration by Enhancing IL-17a Production via miR-122 and miR-30a

Zhu

Zhou

Xu³

et al. 2020

Molecular Therapy - Nucleic Acids

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“…Melatonin also diminishes bleomycin-induced lung fibrosis in mice by inhibiting transforming growth factor β 1 (TGF-β1) [ 200 , 201 ] and it is protective in radiation-induced lung injury by suppressing the NOD-like receptor protein 3 (NLRP3) inflammasome [ 70 , 202 ]. Through its antioxidant and anti-inflammatory effects, melatonin is beneficial in pulmonary hypertension [ 203 , 204 , 205 ], enhances the NO-independent acetylcholine’s vasodilatory effect, decreases the systolic pressure of the right ventricle, and prevents right ventricular hypertrophy [ 206 ]. By diminishing TGF-β1 activity, apoptosis, and endoplasmic reticulum stress via Sirtuin-1 upregulation in animal studies, melatonin could be protective in chronic obstructive pulmonary disease (COPD) [ 72 , 207 ].…”

Section: Melatonin As An Adjuvant In Respiratory Distress Caused Bmentioning

confidence: 99%

Melatonin’s Impact on Antioxidative and Anti-Inflammatory Reprogramming in Homeostasis and Disease

et al. 2020

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There is a growing consensus that the antioxidant and anti-inflammatory properties of melatonin are of great importance in preserving the body functions and homeostasis, with great impact in the peripartum period and adult life. Melatonin promotes adaptation through allostasis and stands out as an endogenous, dietary, and therapeutic molecule with important health benefits. The anti-inflammatory and antioxidant effects of melatonin are intertwined and are exerted throughout pregnancy and later during development and aging. Melatonin supplementation during pregnancy can reduce ischemia-induced oxidative damage in the fetal brain, increase offspring survival in inflammatory states, and reduce blood pressure in the adult offspring. In adulthood, disturbances in melatonin production negatively impact the progression of cardiovascular risk factors and promote cardiovascular and neurodegenerative diseases. The most studied cardiovascular effects of melatonin are linked to hypertension and myocardial ischemia/reperfusion injury, while the most promising ones are linked to regaining control of metabolic syndrome components. In addition, there might be an emerging role for melatonin as an adjuvant in treating coronavirus disease 2019 (COVID 19). The present review summarizes and comments on important data regarding the roles exerted by melatonin in homeostasis and oxidative stress and inflammation related pathologies.

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“…Meanwhile, H19 has been proven to be the primary transcript for microRNA‐675 (Dykes & Emanueli, 2017; Luo et al, 2019; Park, Mitra, Rahat, Kim, & Pfeifer, 2017). H19/miR‐675 were found to be associated with different types of diseases (Fan, Peng, Liang, Yang, & Zhang, 2019; Luo et al, 2019; Muller et al, 2019; Wang et al, 2018). Besides, H19 also acts as a competing endogenous RNA for other microRNAs (Dykes & Emanueli, 2017).…”

Section: Discussionmentioning

confidence: 99%

LncRNA H19 is involved in myocardial ischemic preconditioning via increasing the stability of nucleolin protein

Chen

Liu

Tang

et al. 2020

Journal Cellular Physiology

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Myocardial ischemic preconditioning (IP) is defined as a brief period of myocardial ischemia/reperfusion (I/R) that significantly reduces injury during the subsequent exposure to long-term I/R. However, the underlying mechanisms of myocardial IP are yet to be elucidated. This study investigated the expression and roles of long noncoding RNA (lncRNA) H19 in myocardial IP in vitro and in vivo. LncRNA H19 expression levels were analyzed by quantitative reverse-transcription polymerase chain reaction, cell viability was determined by the Cell Counting Kit-8 assay, apoptosis was evaluated based on the caspase 3 activity, and RNA immunoprecipitation was performed to examine the interaction between lncRNA H19 and nucleolin. The results of this study showed that lncRNA H19 expression was significantly upregulated in mouse hearts subjected to myocardial IP, in rat H9C2 cells exposed to H 2 O 2 preconditioning (H 2 O 2 -PC), and in neonatal rat cardiomyocytes subjected to hypoxia preconditioning. H19 knockdown abrogated the H 2 O 2 -PC-mediated protection in cardiomyocytes evidenced by the decreased cell viability and increased caspase-3 activity. Conversely, H19 overexpression enhanced the protective role of H 2 O 2 -PC in cardiomyocytes. In addition, H19 overexpression increased the expression of nucleolin, whereas H19 ablation abrogated H 2 O 2 -PC-induced upregulation of nucleolin in cardiomyocytes. Furthermore, H19 overexpression increased the stabilization of nucleolin; an interaction between H19 and nucleolin was identified using the RNA-protein interaction studies. Furthermore, nucleolin small interfering RNA relieved the protective role of lncRNA H19. These findings demonstrated that the lncRNA H19 is involved in myocardial IP via increasing the stability of nucleolin protein and lncRNA H19 may represent a potential therapeutic target for the treatment of the myocardial injury.

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Identifying Involvement of H19-miR-675-3p-IGF1R and H19-miR-200a-PDCD4 in Treating Pulmonary Hypertension with Melatonin

Cited by 55 publications

References 62 publications

Microbiota Imbalance Contributes to COPD Deterioration by Enhancing IL-17a Production via miR-122 and miR-30a

Microbiota Imbalance Contributes to COPD Deterioration by Enhancing IL-17a Production via miR-122 and miR-30a

Melatonin’s Impact on Antioxidative and Anti-Inflammatory Reprogramming in Homeostasis and Disease

LncRNA H19 is involved in myocardial ischemic preconditioning via increasing the stability of nucleolin protein

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