miR-153-3p Targets βII Spectrin to Regulate Formaldehyde-Induced Cardiomyocyte Apoptosis

Yang, Po; Yang, Yanyan; He, Xiangqin; Sun, Peng; Zhang, Ying; Song, Xiaoxia; Tian, Yu; Zong, Tingyu; Ma, Jianmin; Chen, Xiaofei; Lv, Qifeng; Yu, Tao; Jiang, Zhirong

doi:10.3389/fcvm.2021.764831

Cited by 11 publications

(5 citation statements)

References 64 publications

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“…Specifically, in cardiac diseases, it has been found that miR-153-3p contributes to mitochondrial fragmentation in cardiac hypertrophy [ 9 ]. The regulatory influence of miR-153-3p on cardiomyocyte apoptosis by directly targeting β II spectrin has also been uncovered [ 14 ]. Recent evidence has also pointed out that miR-153-3p is able to affect cardiomyocyte apoptosis induced by formaldehyde [ 14 ].…”

Section: Introductionmentioning

confidence: 99%

“…The regulatory influence of miR-153-3p on cardiomyocyte apoptosis by directly targeting β II spectrin has also been uncovered [ 14 ]. Recent evidence has also pointed out that miR-153-3p is able to affect cardiomyocyte apoptosis induced by formaldehyde [ 14 ]. Herein, we aim to figure out whether miR-153-3p is a participant of the Gm15834-centered ceRNA regulatory axis.…”

Section: Introductionmentioning

confidence: 99%

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LncRNA Gm43843 Promotes Cardiac Hypertrophy via miR-153-3p/Cacna1c Axis

Cai

2022

Evidence-Based Complementary and Alternative Medicine

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Long noncoding RNAs (lncRNAs) have been reported to engage in many human diseases, including cardiac hypertrophy. Cardiac hypertrophy was mainly caused by excessive pressure load, which can eventually lead to a decline in myocardial contractility. Gm43843, a novel lncRNA, has not been well explored in cardiac hypertrophy so far. Herein, we are going to search the function and the underlying molecular mechanism of Gm43843 in cardiac hypertrophy. Gm43843 levels were measured via qRT-PCR in mouse myocardial cells when they are treated with angiogenin II (Ang II) or transfected with different plasmids. Western blot assay was implemented to detect the cardiac hypertrophy-related protein markers, while the cell was analyzed via immunofluorescence (IF) assay to evaluate the hypertrophy. Meanwhile, the binding of Gm43843 and the putative targets was examined based on mechanistic assay results. We found that Gm43843 expression was increased with the elevated concentration of Ang II. Inhibited Gm43843 was detected to reduce the hypertrophy of mouse myocardial cells. Meanwhile, Gm43843/miR-153-3p/Cacna1c axis was found to modulate cardiac hypertrophy. In short, Gm43843 promotes cardiac hypertrophy via miR-153-3p/Cacna1c axis.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

LncRNA Gm43843 Promotes Cardiac Hypertrophy via miR-153-3p/Cacna1c Axis

Cai

2022

Evidence-Based Complementary and Alternative Medicine

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“…Correspondingly, the TUNEL‐positive cells we quantified corroborated the significant increase during MRLC RNAi knockdown (Figure 5B ). We quantified the expression levels of caspase‐2 , 48 caspase‐7 , 49 the pro‐apoptotic gene bak 50 and antiapoptotic gene Bcl‐2 , 51 which are reported to be involved in apoptosis. qPCR quantification showed their upregulation in MRLC RNAi animals ( n = 30 animals; Figure 5C ).…”

Section: Resultsmentioning

confidence: 99%

MRLC controls apoptotic cell death and functions to regulate epidermal development during planarian regeneration and homeostasis

et al. 2023

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Adult stem cells (ASCs) are pluripotent cells with the capacity to self‐renew and constantly replace lost cells due to physiological turnover or injury. Understanding the molecular mechanisms of the precise coordination of stem cell proliferation and proper cell fate decision is important to regeneration and organismal homeostasis. The planarian epidermis provides a highly tractable model to study ASC complex dynamic due to the distinct spatiotemporal differentiation stages during lineage development. Here, we identified the myosin regulatory light chain (MRLC) homologue in the Dugesia japonica transcriptome. We found high expression levels of MRLC in wound region during regeneration and also expressed in late epidermal progenitors as an essential regulator of the lineage from neoblasts to mature epidermal cells. We investigated the function of MRLC using in situ hybridization, real‐time polymerase chain reaction and double fluorescent and uncovered the potential mechanism. Knockdown of MRLC leads to a remarkable increase in cell death, causes severe abnormalities during regeneration and homeostasis and eventually leads to animal death. The global decrease in epidermal cell in MRLC RNAi animals induces accelerated epidermal proliferation and differentiation. Additionally, we find that MRLC is co‐expressed with cdc42 and acts cooperatively to control the epidermal lineage development by affecting cell death. Our results uncover an important role of MRLC, as an inhibitor of apoptosis, involves in epidermal development.

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“…The cells stained with TUNEL (TdT-mediated dUTP nick-end labeling) were considered apoptotic. The total number of apoptotic cells was calculated using DAPI (2-(4-amidinophenyl)-6-indolecarbamidine dihydrochloride) staining [ 19 ].…”

Section: Methodsmentioning

confidence: 99%

The Long Noncoding RNA Gm9866/Nuclear Factor-κB Axis Promotes Macrophage Polarization

Liao

Ruan

Chen

et al. 2023

Mediators of Inflammation

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Macrophages are a type of immune cells with high levels of plasticity and heterogeneity. They can polarize into M1 or M2 functional phenotypes. These two phenotypes exhibit a dynamic balance during polarization-related diseases and play opposing roles. Long noncoding RNAs (lncRNAs) play an important role in biological processes such as cell proliferation, death, and differentiation; however, how long noncoding RNAs affect the cellular functionality of macrophages remains to be studied. Long noncoding RNA Gm9866 was found to be closely related to macrophage polarization through bioinformatics analysis. In this study, by conducting real-time polymerase chain reaction analysis, it was observed that long noncoding RNA Gm9866 expression significantly increased after treatment with interleukin-4 but significantly decreased after treatment with lipopolysaccharide. Fluorescence in situ hybridization revealed that long noncoding RNA Gm9866 was expressed mainly in the nucleus. Real-time polymerase chain reaction analysis showed that overexpression of long noncoding RNA Gm9866 in RAW264.7 cells further promoted the expression of M2 markers MRC1 (macrophage mannose receptor 1) and MRC2 (macrophage mannose receptor 2). Western blotting analysis demonstrated inhibition of nuclear factor-κB (NF-κB) expression. EdU (5-ethynyl-2 ′ -deoxyuridine) and TUNEL (TdT-mediated dUTP nick-end labeling) staining assays revealed that overexpression of long noncoding RNA Gm9866 promoted cell proliferation and inhibited apoptosis. These findings thus indicated that long noncoding RNA Gm9866 promoted macrophage polarization and inhibited the nuclear factor-κB signaling pathway. Thus, long noncoding RNA Gm9866 may serve as a potential diagnostic and therapeutic target for polarization-related diseases such as infectious diseases, inflammatory diseases, liver fibrosis, and tumors.

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miR-153-3p Targets βII Spectrin to Regulate Formaldehyde-Induced Cardiomyocyte Apoptosis

Cited by 11 publications

References 64 publications

LncRNA Gm43843 Promotes Cardiac Hypertrophy via miR-153-3p/Cacna1c Axis

LncRNA Gm43843 Promotes Cardiac Hypertrophy via miR-153-3p/Cacna1c Axis

MRLC controls apoptotic cell death and functions to regulate epidermal development during planarian regeneration and homeostasis

The Long Noncoding RNA Gm9866/Nuclear Factor-κB Axis Promotes Macrophage Polarization

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