LncRNA H19 Inhibits the Progression of Sepsis-Induced Myocardial Injury via Regulation of the miR-93-5p/SORBS2 Axis

Shu, Bin; Li, Jiayan; Liu, Ya-Jiang; Tang, Xiaowu Shirley; Zhou, Zheng; Luo, Liang-Xian

doi:10.1007/s10753-020-01340-8

Cited by 24 publications

(19 citation statements)

References 49 publications

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“…The expression of cytochrome c in mitochondria was upregulated, while that in cytoplasm was downregulated. This result indicated that the overexpression of H19 alleviated inflammation and mitochondrial apoptosis in LPS-induced cardiomyocytes ( 100 ). Studies have also pointed out that knocking down SOX2OT can significantly enhance cardiac function, inhibit the decline in ΔΨm, and reduce the production of mitochondrial ROS in mice with septic cardiomyopathy, while upregulating SOX2OT can reverse all of these effects.…”

Section: Effects Of Lncrna Regulation On Mitochondrial Dysfunction In Septic Cardiomyopathymentioning

confidence: 92%

Roles of LncRNAs in Regulating Mitochondrial Dysfunction in Septic Cardiomyopathy

Liu

Wang

2021

Front. Immunol.

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Sepsis is an abnormal systemic inflammatory response of the host immune system to infection and can lead to fatal multiorgan dysfunction syndrome. Epidemiological studies have shown that approximately 10-70% of sepsis cases can lead to septic cardiomyopathy. Since the pathogenesis of septic cardiomyopathy is not clear, it is difficult for medical doctors to treat the disease. Therefore, finding effective interventions to prevent and reduce myocardial damage in septic cardiomyopathy is clinically significant. Epigenetics is the study of stable genetic phenotype inheritance that does not involve changing gene sequences. Epigenetic inheritance is affected by both gene and environmental regulation. Epigenetic studies focus on the modification and influence of chromatin structure, mainly including chromatin remodelling, DNA methylation, histone modification and noncoding RNA (ncRNA)-related mechanisms. Recently, long ncRNA (lncRNA)-related mechanisms have been the focus of epigenetic studies. LncRNAs are expected to become important targets to prevent, diagnose and treat human diseases. As the energy metabolism centre of cells, mitochondria are important targets in septic cardiomyopathy. Intervention measures to prevent and treat mitochondrial damage are of great significance for improving the prognosis of septic cardiomyopathy. LncRNAs play important roles in life activities. Recently, studies have focused on the involvement of lncRNAs in regulating mitochondrial dysfunction. However, few studies have revealed the involvement of lncRNAs in regulating mitochondrial dysfunction in septic cardiomyopathy. In this article, we briefly review recent research in this area.

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Section: Effects Of Lncrna Regulation On Mitochondrial Dysfunction In Septic Cardiomyopathymentioning

confidence: 92%

Roles of LncRNAs in Regulating Mitochondrial Dysfunction in Septic Cardiomyopathy

Liu

Wang

2021

Front. Immunol.

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“…The myocardial tissues of rats were pretreated according to the instructions of TUNEL staining kits, subjected to antigen retrieval, blocked, labeled, stained in dark, dehydrated, and mounted with neutral balsam, followed by microscopic examination. The cells stained yellowish brown in the field of view were apoptotic, and the ratio of number of TUNEL-positive cells to that of total cells indicated the apoptosis rate [ 10 ].…”

Section: Methodsmentioning

confidence: 99%

Protective role of emodin in rats with post-myocardial infarction heart failure and influence on extracellular signal-regulated kinase pathway

Liu¹,

Liang²

2021

Bioengineered

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We aimed to explore the effects of emodin on the energy metabolism of myocardial cells in rats with post-myocardial infarction (MI) heart failure (HF) and the extracellular signal-regulated kinase (ERK) pathway. The model of MI was established by ligation of the left anterior descending branch. After 4 weeks, the rats with left ventricular ejection fraction (LVEF) of ≤45% were used aspost-MI HF model animals and randomly divided into model, low-dose, middle-dose, high-dose and control groups (n=10). Low-, middle- and high-dose groups were gavaged with 20 mg/kg, 40 mg/kg and 60 mg/kg emodin daily, respectively. After administration for 14 d, the changes in LVEF, left ventricular end-systolic diameter (LVESD), left ventricular end-diastolic diameter (LVEDD) and interventricular septum thickness (IVS) were analyzed. The apoptosis rate of myocardial cells was detected by TUNEL staining. The levels of serum cardiac troponin I (cTnI) and peroxisome proliferator-activated receptor-γ coactivator-1 (PGC-1) were determined using ELISA, and the expressions of mitochondrial respiratory chain complex I protein and phosphorylated-ERK (p-ERK) in myocardial tissues were determined by Western blotting. Compared with model group, LVEDD, LVESD, apoptosis rate of myocardial cells, levels of serum cTnI and PGC-1, and expressions of complex I and p-ERK in myocardial tissues significantly decreased, while LVEF and IVS increased in low-dose, middle-dose, high-dose and control groups (P<0.05). The changes in the above indices were significantly dependent on the dose of emodin (P<0.05).Emodin can significantly relieve post-MI HF, reduce the apoptosis rate of myocardial tissues, and ameliorate the cardiac function of rats.

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“…Once total RNA was extracted from lung tissues and cells using a TRIzol kit (Invitrogen) [41], it was first necessary to detect RNA concentration and purity using a UV spectrophotometer (UV-1800, Shimadzu, Kyoto, Japan) and measure RNA quantity and integrity using a NanoDrop spectrophotometer (Thermo Fisher Scientific) and an Agilent Bioanalyzer RNA 6000 Nano kit (Agilent Technologies, Beijing, China) [42]. The expression pattern of H19 was tested using the One Step SYBR ® PrimeScript ® PLUS RT-RNA PCR kit (Takara, Dalian, China).…”

Section: Reverse Transcription-quantitative Polymerase Chain Reaction...mentioning

confidence: 99%

“…The membranes were added with primary antibodies against Bax (ab0261, 1:2000, Beyotime), Bcl-2 (ab182858, 1:800, Abcam, Cambridge, MA, USA) and TGFBR3 (ab166705, 1:800, Abcam) for overnight incubation at 4 °C. The membranes were washed and then incubated with HRP-labeled goat anti-rabbit secondary antibody IgG (ab48386, 1:2000, Abcam) at room temperature for 1-h [42], visualized with enhanced chemiluminescence working solution (EMD Millipore, Billerica, MA, USA), and images were captured. The protein band density was detected using Image J software 1.48 (NIH, Bethesda, MD, USA) with β-actin as an internal control.…”

Section: Western Blotmentioning

confidence: 99%

LncRNA H19 alleviates sepsis-induced acute lung injury by regulating the miR-107/TGFBR3 axis

Hao

Wei

2022

BMC Pulm Med

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Objective Acute lung injury (ALI) increases sepsis morbidity and mortality. LncRNA H19 plays a critical role in sepsis. miR-107 is highly-expressed and TGFβ type III receptor (TGFBR3) is poorly-expressed in sepsis, yet their roles in sepsis development require further investigation. This study aimed to investigate the mechanism of H19 in alleviating sepsis-induced ALI through the miR-107/TGFBR3 axis. Methods Mice were intravenously injected with Ad-H19 adenovirus vector or control vector one week before establishing the mouse model of cecal ligation and puncture (CLP). Pulmonary microvascular endothelial cells (PMVECs) were transfected with oe-H19 or oe-NC plasmids and then stimulated by lipopolysaccharide (LPS). Lung injury was assessed via hematoxylin–eosin staining, measurement of wet-to-dry (W/D) ratio, and TUNEL staining. Levels of H19, miR-107, and TGFBR3 were determined by RT-qPCR. Apoptosis of PMVECs was evaluated by flow cytometry. Levels of Bax and Bcl-2 in lung tissues and PMVECs were measured using Western blot. Total protein concentration and the number of total cells, neutrophils, and macrophages in bronchoalveolar lavage fluid (BALF) were quantified. Levels of TNF-α, IL-1β, IL-6, and IL-10 in BALF, lung tissues, and PMVECs were measured by ELISA. Cross-linking relationships among H19, miR-107 and TGFBR3 were verified by dual-luciferase and RIP assays. Results H19 was poorly-expressed in CLP-operated mice. H19 overexpression attenuated sepsis-induced ALI, which was manifested with complete alveolar structure, decreased lung injury score and lung W/D ratio, and inhibited apoptosis in CLP-operated mice, which was manifested with decreased number of TUNEL-positive cells and Bax level and increased Bcl-2 level. CLP-operated mice had increased concentration of total protein and number of total cells, neutrophils, and macrophages in BALF, which was nullified by H19 overexpression. H19 overexpression declined levels of TNF-α, IL-1β, and IL-6 and elevated IL-10 levels. H19 inhibited LPS-induced PMVEC apoptosis and pro-inflammatory cytokine production. H19 targeted TGFBR3 as the ceRNA of miR-107. miR-107 overexpression or silencing TGFBR3 partially averted the inhibition of H19 overexpression on LPS-induced PMVEC apoptosis and pro-inflammatory cytokine production. Conclusion LncRNA H19 inhibited LPS-induced PMVEC apoptosis and pro-inflammatory cytokine production and attenuated sepsis-induced ALI by targeting TGFBR3 as the ceRNA of miR-107.

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LncRNA H19 Inhibits the Progression of Sepsis-Induced Myocardial Injury via Regulation of the miR-93-5p/SORBS2 Axis

Cited by 24 publications

References 49 publications

Roles of LncRNAs in Regulating Mitochondrial Dysfunction in Septic Cardiomyopathy

Roles of LncRNAs in Regulating Mitochondrial Dysfunction in Septic Cardiomyopathy

Protective role of emodin in rats with post-myocardial infarction heart failure and influence on extracellular signal-regulated kinase pathway

LncRNA H19 alleviates sepsis-induced acute lung injury by regulating the miR-107/TGFBR3 axis

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