Dataset Information

LncRNA ANRIL knockdown relieves myocardial cell apoptosis in acute myocardial infarction by regulating IL-33/ST2.

ABSTRACT: Objective: To investigate the role of lncRNA ANRIL in the modulation of myocardial cell apoptosis in acute myocardial infarction (AMI).Methods: AMI mice model was established, and lncRNA ANRIL, IL-33 and ST2 expressions were detected by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot. The apoptosis of myocardial cells was detected by TUNEL assay. RNA pull-down and RNA immunoprecipitation (RIP) assays were used to confirm the interaction between lncRNA ANRIL and USP17.Results: Compared with sham group, lncRNA ANRIL and ST2 expression levels were up-regulated, and the apoptosis of myocardial cells was increased in heart tissues of AMI group. Compared with normoxia group, the apoptosis of mouse myocardial cell HL-1 and primary murine myocardial cells was increased, and lncRNA ANRIL and ST2 expression levels were up-regulated in hypoxia group. We also found up-regulation of IL-33 in AMI group and hypoxia group. Besides, lncRNA ANRIL affected deubiquitinase USP17-mediated degradation of IL-33. Interfering lncRNA ANRIL reduced the apoptosis of myocardial cells through IL-33/ST2 pathway. In vivo experiments found that interfering lncRNA ANRIL relieved myocardial cell apoptosis and improved heart function in AMI mice.Conclusion: LncRNA ANRIL regulated myocardial cell apoptosis through IL-33/ST2 pathway.

SUBMITTER: Yang J

PROVIDER: S-EPMC6927712 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

LncRNA ANRIL knockdown relieves myocardial cell apoptosis in acute myocardial infarction by regulating IL-33/ST2.

Yang Jinhua J Huang Xianwei X Hu Fudong F Fu Xin X Jiang Zhengming Z Chen Kui K

Cell cycle (Georgetown, Tex.) 20191101 23

<b>Objective</b>: To investigate the role of lncRNA ANRIL in the modulation of myocardial cell apoptosis in acute myocardial infarction (AMI).<b>Methods</b>: AMI mice model was established, and lncRNA ANRIL, IL-33 and ST2 expressions were detected by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot. The apoptosis of myocardial cells was detected by TUNEL assay. RNA pull-down and RNA immunoprecipitation (RIP) assays were used to confirm the interaction between lncRNA ANR ...[more]

PMID: 31674275

Similar Datasets

Project description:Objective: Previous studies have demonstrated the protective effects of renal denervation (RDN) in pre-existing heart failure, but the effects of immediate RDN after acute myocardial infarction (AMI) on subsequent cardiac remodeling have not been reported. This study aimed to investigate the cardioprotective effects of immediate RDN after AMI and its underlying mechanism. Methods: AMI was induced by intracoronary gelatin sponge embolization in 14 Shanghai white pigs that were randomized to undergo either renal angiography (AMI+sham group) or RDN (AMI+RDN group) after 1 h of hemodynamic monitoring. Cardiac function of the two groups was measured at baseline, 1 h post-AMI and at the 1 month follow-up (1M-FU) by transthoracic echocardiography (TTE). Plasma NT-proBNP, soluble ST2 (sST2), norepinephrine (NE), and renin-angiotensin-aldosterone system activity were detected simultaneously. The renal cortex was harvested for NE measurement after the 1M-FU, and the renal arteries were stained with tyrosine hydroxylase for the evaluation of sympathetic activity. Heart tissues in the non-ischemic areas were collected to assess histological and molecular left ventricular (LV) remodeling by pathological staining, RT-PCR, and western blotting. Results: There was no difference in the hemodynamic stability or cardiac function between the two groups at baseline and 1 h post-AMI. Six pigs from each of the two groups completed the 1M-FU. TTE analysis revealed the improved cardiac function of immediate RDN in the AMI+RDN group and circulating NT-proBNP levels were lower than those in the AMI+sham group. Further analysis showed significantly less interstitial fibrosis in the remote non-ischemic myocardium after immediate RDN, together with decreased cardiomyocyte hypertrophy and inflammatory cell infiltration. sST2 levels in circulating and myocardial tissues of animals in the AMI+RDN group were significantly higher than those in the AMI+sham group, accompanied by corresponding alterations in IL-33/ST2 and downstream signaling. Conclusions: Immediate RDN can improve cardiac function and myocardial remodeling after AMI via modulation of IL-33/ST2 and downstream signaling.

Project description:Interleukin 33 (IL-33) is highly expressed in barrier sites, acting via the suppression of tumorigenicity 2 receptor (ST2). IL-33/ST2 axis has long been known to play a pivotal role in immunity and cell homeostasis by promoting wound healing and tissue repair. However, it is also involved in the loss of balance between extensive inflammation and tissue regeneration lead to remodeling, the hallmark of fibrosis. The aim of the current review is to critically evaluate the available evidence regarding the role of the IL-33/ST2 axis in organ fibrosis. The role of the axis in tissue remodeling is better understood considering its crucial role reported in organ development and regeneration. Generally, the IL-33/ST2 signaling pathway has mainly anti-inflammatory/anti-proliferative effects; however, chronic tissue injury is responsible for pro-fibrogenetic responses. Regarding pulmonary fibrosis mature IL-33 enhances pro-fibrogenic type 2 cytokine production in an ST2- and macrophage-dependent manner, while full-length IL-33 is also implicated in the pulmonary fibrotic process in an ST2-independent, Th2-independent fashion. In liver fibrosis, evidence indicate that when acute and massive liver damage occurs, the release of IL-33 might act as an activator of tissue-protective mechanisms, while in cases of chronic injury IL-33 plays the role of a hepatic fibrotic factor. IL-33 signaling has also been involved in the pathogenesis of acute and chronic pancreatitis. Moreover, IL-33 could be used as an early marker for ulcer-associated activated fibroblasts and myofibroblast trans-differentiation; thus one cannot rule out its potential role in inflammatory bowel disease-associated fibrosis. Similarly, the upregulation of the IL-33/ST2 axismay contribute to tubular cell injury and fibrosis via epithelial to mesenchymal transition (EMT) of various cell types in the kidneys. Of note, IL-33 exerts a cardioprotective role via ST2 signaling, while soluble ST2 has been demonstrated as a marker of myocardial fibrosis. Finally, IL-33 is a crucial cytokine in skin pathology responsible for abnormal fibroblast proliferation, leukocyte infiltration and morphologic differentiation of human endothelial cells. Overall, emerging data support a novel contribution of the IL-33/ST2 pathway in tissue fibrosis and highlight the significant role of the Th2 pattern of immune response in the pathophysiology of organ fibrosis.

Dataset Information

LncRNA ANRIL knockdown relieves myocardial cell apoptosis in acute myocardial infarction by regulating IL-33/ST2.

Publications

LncRNA ANRIL knockdown relieves myocardial cell apoptosis in acute myocardial infarction by regulating IL-33/ST2.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets