SP1‐induced SNHG14 aggravates hypertrophic response in in vitro model of cardiac hypertrophy via up‐regulation of PCDH17

Long, Yadong; Wang, Lin; Li, Zhiqiang

doi:10.1111/jcmm.15073

Cited by 33 publications

(14 citation statements)

References 37 publications

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“…Ang II is the primary mediator of the RAAS system. Using Ang II stimulation in cardiomyocytes as an in vitro experimental model to stimulate TAC- induced cardiac hypertrophy has been reported in our previous study ( Ye et al, 2020 ) and many other researches ( Long et al, 2020 ; Xie et al, 2020 ). In Ang II-challenged rat primary cardiomyocytes, NBP alleviated the expression of MyHC and increased the size of the cells ( Figures 3A–C ).…”

Section: Discussionmentioning

confidence: 88%

DL-3-n-Butylphthalide Attenuates Myocardial Hypertrophy by Targeting Gasdermin D and Inhibiting Gasdermin D Mediated Inflammation

Han

Shi

et al. 2021

Front. Pharmacol.

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Pressure overload leads to a hypertrophic milieu that produces deleterious cardiac dysfunction. Inflammation is a key pathophysiological mechanism underpinning myocardial hypertrophy. DL-3-n-butylphthalide (NBP), a neuroprotective agent, also has potent cardioprotective effects. In this study, the potential of NBP to antagonize myocardial hypertrophy was evaluated in C57BL/6 mice in vivo and in rat primary cardiomyocytes in vitro. In mice, NBP treatment reduced cardiac hypertrophy and dysfunction in a transverse aortic constriction (TAC)-induced pressure overload model. In angiotensin (Ang) II-challenged cardiomyocytes, NBP prevents cell size increases and inhibits gasdermin D (GSDMD)-mediated inflammation. Furthermore, overexpression of GSDMD-N reduced the protective effects of NBP against Ang II-induced changes. Using molecular docking and MD simulation, we found that the GSDMD-N protein may be a target of NBP. Our study shows that NBP attenuates myocardial hypertrophy by targeting GSDMD and inhibiting GSDMD-mediated inflammation.

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Section: Discussionmentioning

confidence: 88%

DL-3-n-Butylphthalide Attenuates Myocardial Hypertrophy by Targeting Gasdermin D and Inhibiting Gasdermin D Mediated Inflammation

Han

Shi

et al. 2021

Front. Pharmacol.

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“…Snhg14 is highly expressed in Parkinson’s disease, and silencing Sngh14 mitigated dopaminergic neuron injury by downregulating a-syn by targeting miR-133b ( Zhang et al, 2019 ). In addition, Sngh14 functions as a ceRNA in Ang II-induced cardiomyocytes to sponge both miR-322-5p and miR-384-5p to elevate PCDH17 levels ( Long et al, 2020 ). The function of m 6 A-modified lncRNAs during skeletal muscle development needs to be further studied.…”

Section: Discussionmentioning

confidence: 99%

Characterization of Long Non-coding RNAs Modified by m6A RNA Methylation in Skeletal Myogenesis

Xie

Tao

Diao

et al. 2021

Front. Cell Dev. Biol.

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Proper development of mammalian skeletal muscle relies on precise gene expression regulation. Our previous studies revealed that muscle development is regulated by both mRNA and long non-coding RNAs (lncRNAs). Accumulating evidence has demonstrated that N6-methyladenosine (m6A) plays important roles in various biological processes, making it essential to profile m6A modification on a transcriptome-wide scale in developing muscle. Patterns of m6A methylation in lncRNAs in developing muscle have not been uncovered. Here, we reveal differentially expressed lncRNAs and report temporal m6A methylation patterns in lncRNAs expressed in mouse myoblasts and myotubes by RNA-seq and methylated RNA immunoprecipitation (MeRIP) sequencing. Many lncRNAs exhibit temporal differential expression, and m6A-lncRNAs harbor the consensus m6A motif “DRACH” along lncRNA transcripts. Interestingly, we found that m6A methylation levels of lncRNAs are positively correlated with the transcript abundance of lncRNAs. Overexpression or knockdown of m6A methyltransferase METTL3 alters the expression levels of these lncRNAs. Furthermore, we highlight that the function of m6A genic lncRNAs might correlate to their nearby mRNAs. Our work reveals a fundamental expression reference of m6A-mediated epitranscriptomic modifications in lncRNAs that are temporally expressed in developing muscle.

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“…Moreover, previous studies reported that SNHG14 and SNRPN are involved in the pathogenesis of cardiac hypertrophy and CHD, respectively. 27 , 28 These results indicated that A-to-I editing events during cardiomyocyte differentiation may also be related to cardiovascular diseases.…”

Section: Resultsmentioning

confidence: 79%

Global RNA editing identification and characterization during human pluripotent-to-cardiomyocyte differentiation

Chen

Liu

Qiao

et al. 2021

Molecular Therapy - Nucleic Acids

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RNA editing is widely involved in stem cell differentiation and development; however, RNA editing events during human cardiomyocyte differentiation have not yet been characterized and elucidated. Here, we identified genome-wide RNA editing sites and systemically characterized their genomic distribution during four stages of human cardiomyocyte differentiation. It was found that the expression level of ADAR1 affected the global number of adenosine to inosine (A-to-I) editing sites but not the editing degree. Next, we identified 43, 163, 544, and 141 RNA editing sites that contribute to changes in amino acid sequences, variation in alternative splicing, alterations in miRNA-target binding, and changes in gene expression, respectively. Generally, RNA editing showed a stage-specific pattern with 211 stage-shared editing sites. Interestingly, cardiac muscle contraction and heart-disease-related pathways were enriched by cardio-specific editing genes, emphasizing the connection between cardiomyocyte differentiation and heart diseases from the perspective of RNA editing. Finally, it was found that these RNA editing sites are also related to several congenital and noncongenital heart diseases. Together, our study provides a new perspective on cardiomyocyte differentiation and offers more opportunities to understand the mechanisms underlying cell fate determination, which can promote the development of cardiac regenerative medicine and therapies for human heart diseases.

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SP1‐induced SNHG14 aggravates hypertrophic response in in vitro model of cardiac hypertrophy via up‐regulation of PCDH17

Cited by 33 publications

References 37 publications

DL-3-n-Butylphthalide Attenuates Myocardial Hypertrophy by Targeting Gasdermin D and Inhibiting Gasdermin D Mediated Inflammation

DL-3-n-Butylphthalide Attenuates Myocardial Hypertrophy by Targeting Gasdermin D and Inhibiting Gasdermin D Mediated Inflammation

Characterization of Long Non-coding RNAs Modified by m6A RNA Methylation in Skeletal Myogenesis

Global RNA editing identification and characterization during human pluripotent-to-cardiomyocyte differentiation

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