LncRNA H19 suppresses pyroptosis of cardiomyocytes to attenuate myocardial infarction in a PBX3/CYP1B1-dependent manner

Han, Yong; Dong, Bo; Chen, Meijuan; Yao, Chanjiao

doi:10.1007/s11010-020-03998-y

Cited by 26 publications

(13 citation statements)

References 35 publications

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“…Moreover, downregulation of lncRNA-H19 reduced the cerebral infarct volume and inflammatory response and facilitated hippocampal neurogenesis and repairing process [8,38]. Importantly, the latest studies revealed that lncRNA-H19 was involved in microglia and cardiomyocyte pyroptosis, respectively, following retinal and myocardial ischemia injury [10][11][12]. However, the expression and action of lncRNA-H19 in NSC pyroptosis following OGD exposure remain unclear.…”

Section: Discussionmentioning

confidence: 99%

“…Abundant studies revealed that lncRNA-H19, an imprinted gene seated at chromosome 11, exerted important roles on the onset and development of ischemic stroke, involving neuronal apoptosis and autophagy, microglial polarization, and inflammatory response [7][8][9]. Notably, the latest researches have provided much evidence that lncRNA-H19 is involved in microglia pyroptosis induced by retinal ischemia injury and cardiomyocyte pyroptosis triggered by myocardial ischemia infarction [10][11][12]. To the best of our knowledge, whether and how lncRNA-H19 contributes to NSC pyroptosis and affects neurogenesis following OGD has never been investigated.…”

Section: Introductionmentioning

confidence: 99%

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HBO Alleviates Neural Stem Cell Pyroptosis via lncRNA-H19/miR-423-5p/NLRP3 Axis and Improves Neurogenesis after Oxygen Glucose Deprivation

Feng

Tian

et al. 2022

Oxidative Medicine and Cellular Longevity

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Due to the limited neurogenesis capacity, there has been a big challenge in better recovery from neurological dysfunction caused by stroke for a long time. Neural stem cell (NSC) programmed death is one of the unfavorable factors for neural regeneration after stroke. The types of death such as apoptosis and necroptosis have been deeply investigated while the pyroptosis of NSCs is not quite understood. Although it is well accepted that hyperbaric oxygen (HBO) alleviates the oxygen-glucose deprivation (OGD) injury after stroke and reduces programmed death of NSCs, whether NSC pyroptosis is involved in this process is still unknown. Therefore, this study is aimed at studying the potential effect of HBO treatment on NSC pyroptosis following OGD exposure, as well as its influence on NSC proliferation and differentiation in vitro. The results revealed that OGD increased NOD-like receptor protein 3 (NLRP3) expression to induce the pyroptotic death of NSCs, which was rescued by HBO treatment. And the upregulated lncRNA-H19 functioned as a molecular sponge of miR-423-5p to target NLRP3 for NSC pyroptosis following OGD. Most importantly, it was confirmed that HBO exerted protection of NSCs against pyroptosis by inhibiting lncRNA-H19/miR-423-5p/NLRP3 axis. Moreover, HBO restraint of lncRNA-H19-associated pyroptosis benefited the proliferation and neuronal differentiation of NSCs. It was concluded that HBO attenuated NSC pyroptosis via lncRNA-H19/miR-423-5p/NLRP3 axis and enhanced neurogenesis following OGD. The findings provide new insight into NSC programmed death and enlighten therapeutic strategy after stroke.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

HBO Alleviates Neural Stem Cell Pyroptosis via lncRNA-H19/miR-423-5p/NLRP3 Axis and Improves Neurogenesis after Oxygen Glucose Deprivation

Feng

Tian

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…Pyroptosis is a new type of programmed inflammatory death, discovered after apoptosis and necrosis. 87 Similar to in apoptosis, pyroptotic cells undergo nuclear condensation and chromatin DNA fragmentation and become TUNEL-stain positive. Compared with necrosis, in the process of pyroptosis, the formation of pores disrupts the balance of ion gradients on both sides of the cell membrane, leading to water intake, cell swelling, cell membrane rupture, and release of proinflammatory mediators, including IL-1β, IL-18, ATP, and HMGB1.…”

Section: The Role Of Lncrnas In Pyroptosismentioning

confidence: 96%

The Crosstalk Between Long Non-Coding RNAs and Various Types of Death in Cancer Cells

Tang

Zhu

Liang

et al. 2021

Technol Cancer Res Treat

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With the increasing aging population, cancer has become one of the leading causes of death worldwide, and the number of cancer cases and deaths is only anticipated to grow further. Long non-coding RNAs (lncRNAs), which are closely associated with the expression level of downstream genes and various types of bioactivity, are regarded as one of the key regulators of cancer cell proliferation and death. Cell death, including apoptosis, necrosis, autophagy, pyroptosis, and ferroptosis, plays a vital role in the progression of cancer. A better understanding of the regulatory relationships between lncRNAs and these various types of cancer cell death is therefore urgently required. The occurrence and development of tumors can be controlled by increasing or decreasing the expression of lncRNAs, a method which confers broad prospects for cancer treatment. Therefore, it is urgent for us to understand the influence of lncRNAs on the development of different modes of tumor death, and to evaluate whether lncRNAs have the potential to be used as biological targets for inducing cell death and predicting prognosis and recurrence of chemotherapy. The purpose of this review is to provide an overview of the various forms of cancer cell death, including apoptosis, necrosis, autophagy, pyroptosis, and ferroptosis, and to describe the mechanisms of different types of cancer cell death that are regulated by lncRNAs in order to explore potential targets for cancer therapy.

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“…103 A recent study revealed that H19 can suppress cardiomyocyte pyroptosis to alleviate myocardial infarction progression and improve survival mainly through regulating pre-B cell leukemia homeobox 3 (PBX3) and its target gene cytochrome P450 1B1 (CYP1B1). 104 Mao et al 105 reported that lncRNA KLF3-AS1 in exosomes secreted from human MSCs acts as a ceRNA to upregulate SIRT1 expression by directly sponging miR-138-5p, thus decreasing cardiomyocyte pyroptosis and attenuating myocardial infarction progression. Similarly, transfection of a miR-138-5p inhibitor reduced pyroptosis and infarct size with KLF3-AS1 exosome incubation both in vitro and in vivo, whereas knockdown of SIRT1 upregulated NLRP3, ASC, cleaved caspase-1, IL-1b, and IL-18 expressions and reversed the protective effect of exosomal KLF3-AS1 in hypoxic cardiomyocytes.…”

Section: Myocardial I/r Injury and Myocardial Infarctionmentioning

confidence: 99%

Regulation of pyroptosis in cardiovascular pathologies: Role of noncoding RNAs

Gao

Chen

Wei

et al. 2021

Molecular Therapy - Nucleic Acids

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Cardiovascular disease (CVD) is one of the most important diseases endangering human life. The pathogenesis of CVDs is complex. Pyroptosis, which differs from traditional apoptosis and necrosis, is characterized by cell swelling until membrane rupture, resulting in the release of cell contents and activation of a strong inflammatory response. Recent studies have revealed that inflammation and pyroptosis play important roles in the progression of CVDs. Noncoding RNAs (ncRNAs) are considered promising biomarkers and potential therapeutic targets for the diagnosis and treatment of various diseases, including CVDs. Growing evidence has revealed that ncRNAs can mediate the transcriptional or posttranscriptional regulation of pyroptosis-related genes by participating in the pyroptosis regulatory network. The role and molecular mechanism of pyroptosis-regulating ncRNAs in cardiovascular pathologies are attracting increasing attention. Here, we summarize research progress on pyroptosis and the role of ncRNAs, particularly microRNAs (miRNAs), long ncRNAs (lncRNAs), and circular RNAs (circRNAs), in the regulation of pyroptosis in CVD pathologies. Identifying these disease-related ncRNAs is important for understanding the pathogenesis of CVDs and providing new targets and ideas for their prevention and treatment.Noncoding RNAs (ncRNAs) account for up to 98%-99% of the human genome and participate in regulating the expression of protein-coding genes. 10,11 The interaction between ncRNAs and protein-coding genes forms a highly complex RNA regulatory network. Abnormalities in ncRNAs are closely related to numerous diseases. Recent efforts to identify the molecular mechanisms underlying the pathogenesis of CVDs have revealed a significant regulatory role of ncRNAs in the occurrence and development of major CVDs, such as myocardial infarction, coronary heart disease, atrial fibrillation, atherosclerosis, cardiomyopathy, and heart failure. [12][13][14] The main classes of ncRNAs are microRNAs (miRNAs), long ncRNAs

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LncRNA H19 suppresses pyroptosis of cardiomyocytes to attenuate myocardial infarction in a PBX3/CYP1B1-dependent manner

Cited by 26 publications

References 35 publications

HBO Alleviates Neural Stem Cell Pyroptosis via lncRNA-H19/miR-423-5p/NLRP3 Axis and Improves Neurogenesis after Oxygen Glucose Deprivation

HBO Alleviates Neural Stem Cell Pyroptosis via lncRNA-H19/miR-423-5p/NLRP3 Axis and Improves Neurogenesis after Oxygen Glucose Deprivation

The Crosstalk Between Long Non-Coding RNAs and Various Types of Death in Cancer Cells

Regulation of pyroptosis in cardiovascular pathologies: Role of noncoding RNAs

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