Long Non-Coding RNA SNHG8 Plays a Key Role in Myocardial Infarction Through Affecting Hypoxia-Induced Cardiomyocyte Injury

Zhang, Yue; Bian, Yunfei

doi:10.12659/msm.924016

Cited by 12 publications

(10 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A recent study indicated that lncRNA SNHG8 was significantly upregulated in AMI and that it may be correlated with regulation of myocardial cell necrosis and apoptosis ( 12 ). The present study found that, after HI/R induction, SNHG8 exhibited the highest expression among the lncRNAs examined, and it was associated with ischemic myocardial cells, which was consistent with studies by Zhuo et al ( 12 ) and Zhang and Bian ( 38 ). Inhibition of SNHG8 could protect against HI/R-induced myocardial injury by increasing cell viability and proliferation, and by decreasing cell apoptosis.…”

Section: Discussionsupporting

confidence: 93%

Inhibition of lncRNA SNHG8 plays a protective role in hypoxia-ischemia-reoxygenation-induced myocardial injury by regulating miR-335 and RASA1 expression

Liu

Zhou²,

Feng-xiao³

et al. 2021

Mol Med Rep

View full text Add to dashboard Cite

long non-coding (lnc)rnas serve a role in a number of diseases, including different types of cancer and acute myocardial infarction. The aim of the present study was to investigate the protective role of lncrna small nucleolar rna host gene 8 (SNHG8) in hypoxia-ischemia-reoxygenation (Hi/r)-induced myocardial injury and its potential mechanism of action. cell viability, proliferation, creatine kinase myocardial band, cell apoptosis and protein expression levels were determined by cell counting Kit-8 assay, edu assay, ELISA, flow cytometry and western blotting, respectively. The association between SNHG8 and microrna (mir)-335 was confirmed using a dual-luciferase reporter gene assay. The effects of the mir-335 inhibitor transfections had on increasing apoptosis and decreasing H9c2 cell viability were reversed in cells co-transfected with SNHG8 small interfering (si)rna. Furthermore, it was found that mir-335 could regulate raS p21 protein activator 1 (raSa1) expression and that transfection with SNHG8 sirna downregulated raSa1 expression. Silencing of raSa1 protected against Hi/r-induced H9c2 cell injury. However, SNHG8 sirna did not further reduce apoptosis, demonstrating that SNHG8 may act through raSa1, and raSa1 may mediate the protection of SNHG8 sirna in Hi/r myocardial injury. Thus, inhibition of lncrna SNHG8 alleviated Hi/r-induced myocardial damage by regulating mir-335 and raSa1.

show abstract

Section: Discussionsupporting

confidence: 93%

Inhibition of lncRNA SNHG8 plays a protective role in hypoxia-ischemia-reoxygenation-induced myocardial injury by regulating miR-335 and RASA1 expression

Liu

Zhou²,

Feng-xiao³

et al. 2021

Mol Med Rep

View full text Add to dashboard Cite

show abstract

“…Dong et al reported that lncSNHG8 promoted the spread of liver cancer and lung metastasis through sponged with miR-149 [ 25 ]. Several previous studies have confirmed that lncSNHG8 was abnormally expressed in MI, and unstable atherosclerotic plaques are the direct cause of MI [ 12 , 13 ]. In the current study, it was found that the relative expression of lncSNHG8 was upregulated in AS samples.…”

Section: Discussionmentioning

confidence: 88%

“…In a recent study by Zhuo et al, they revealed that lncSNHG8 may be involved in acute myocardial infarction (AMI) through the regulation of SOCS3 expression by sponging miR-411-5p [12]. Zhang et al reported that lncSNHG8 promoted myocardial cell injury and inflammatory response by regulating the NF-kB signaling pathway and participated in the regulation of myocardial infarction (MI) [13]. However, it is unclear whether and how lncSNHG8 participates in AS, which requires further study and analysis.…”

Section: Introductionmentioning

confidence: 99%

Differentiated expression of long non-coding RNA-small nucleolar RNA host gene 8 in atherosclerosis and its molecular mechanism

Wang

Chen

et al. 2021

Bioengineered

View full text Add to dashboard Cite

Atherosclerosis (AS) is one of the most common cardiovascular diseases, and the incidence is increasing year by year. Many studies have shown that long non-coding RNA plays a vital role in the pathogenesis of AS. This study aimed to explore the role and mechanism of lncRNA-small nucleolar RNA host gene 8 (SNHG8) in AS. The expressions of serum lncSNHG8 and miR-224-3p were determined by quantitative real-time polymerase chain reaction (qRT-PCR). The diagnostic meaning of lncSNHG8 in AS was estimated by Receiver operating characteristic (ROC) curve. The correlation between lncSNHG8 and various clinical indicators, as well as miR-244-3p was evaluated by Pearson correlation coefficient analysis. Cell proliferation and migration were estimated by cell counting kit-8 (CCK-8) and Transwell assay. The interaction between lncSNHG8 and miR-224-3p was proved by luciferase reporter gene assay. The expression level of lncSNHG8 was increased in AS patients, while miR-224-3p expression was decreased. The ROC curve indicated that lncSNHG8 with high serum expression had the ability to distinguish AS. Pearson correlation coefficient exhibited that the level of miR-224-3p was negatively correlated with the level of lncSNHG8. The results of cell experiments indicated that inhibition of the expression of lncSNHG8 significantly inhibited the proliferation and migration of vascular smooth muscle cells (VSMCs). Luciferase reporter gene experiments confirmed that there was a target relationship between lncSNHG8 and miR-224-3p. In conclusion, lncSNHG8 had high diagnostic value for AS. It promoted the proliferation and migration of VSMCs by adsorption and inhibition of miR-224-3p.

show abstract

“…In non-tumor diseases, upregulated SNHG8 serves as a competitive endogenous RNA by sponging miR-425-5p, and inhibits the SIRT1/NF-κB signaling pathway to attenuate the ischemia-induced microglial in ammatory response (21). However, SNHG8 also affects myocardial infarction by promoting activity in the NF-κB pathway (22). This opposite phenomenon re ects the high tissue or cell speci city of lncRNAs and their diverse mechanisms of action, including transcriptional regulation in cis or trans, organization of nuclear domains, and regulation of proteins or RNAs (19,20).…”

Section: Discussionmentioning

confidence: 99%

“…The lncRNA SNHG8 inhibits the sirtuin1mediated NF-κB pathway by sponging miR-425-5p in brain microvascular endothelial cells (21). Also, SNHG8 is upregulated in H9c2 rat cardiomyocytes under hypoxia and activates the NF-κB pathway (22). However, the expression pattern of SNHG8 and its effect on the NF-κB pathway during OTM are unclear.…”

Section: Introductionmentioning

confidence: 99%

A reduced level of the long non-coding RNA SNHG8 activates the NF-kappaB pathway by releasing functional HIF-1alpha in a hypoxic inflammatory microenvironment

Wang

Yang

Han

et al. 2021

Preprint

View full text Add to dashboard Cite

Background A series of biochemical responses, including hypoxia and aseptic inflammation, occur in periodontal ligament cells (PDLCs) during periodontal tissue remodeling of orthodontic tooth movement (OTM). However, the role of long non-coding RNA (lncRNA) in these responses is still largely unknown. We investigated the role of the lncRNA SNHG8 in hypoxic and inflammatory responses during OTM, and explored the underlying mechanisms. Methods The expression pattern of SNHG8, and hypoxic and inflammatory responses under compressive force, were analyzed by qRT-PCR, immunohistochemistry, and western blotting, in vivo and in vitro. The effect of overexpression or knockdown of SNHG8 on the nuclear factor-kappaB (NF-κB) pathway was evaluated. RNA sequencing was performed for mechanistic analysis. The interaction between SNHG8 and hypoxia-inducible factor (HIF)-1α was studied using catRAPID, RNA immunoprecipitation, and RNA pulldown assays. The effect of the SNHG8–HIF-1α interaction on the NF-κB pathway was determined by western blotting. Results The NF-κB pathway was activated, and HIF-1α release was stabilized, in PDLCs under compressive force as well as in OTM model rats. The SNHG8 level markedly decreased both in vivo and in vitro. Overexpression of SNHG8 decreased the expression levels of inflammatory cytokines, the phosphorylation of p65, and the degradation of IκBα in PDLCs, whereas knockdown of SNHG8 reversed these effects. Mechanically, RNA sequencing showed that differentially expressed genes were enriched in cellular response to hypoxia after SNHG8 overexpression. SNHG8 binds to HIF-1α, thus preventing HIF-1 from activating downstream genes, including those related to the NF-κB pathway. Conclusion SNHG8 binds to HIF-1α. During OTM, the expression of SNHG8 dramatically decreased, releasing free functional HIF-1α and activating the downstream NF-κB pathway. These data suggest a novel lncRNA-regulated mechanism during periodontal tissue remodeling in OTM.

show abstract

Long Non-Coding RNA SNHG8 Plays a Key Role in Myocardial Infarction Through Affecting Hypoxia-Induced Cardiomyocyte Injury

Cited by 12 publications

References 28 publications

Inhibition of lncRNA SNHG8 plays a protective role in hypoxia-ischemia-reoxygenation-induced myocardial injury by regulating miR-335 and RASA1 expression

Inhibition of lncRNA SNHG8 plays a protective role in hypoxia-ischemia-reoxygenation-induced myocardial injury by regulating miR-335 and RASA1 expression

Differentiated expression of long non-coding RNA-small nucleolar RNA host gene 8 in atherosclerosis and its molecular mechanism

A reduced level of the long non-coding RNA SNHG8 activates the NF-kappaB pathway by releasing functional HIF-1alpha in a hypoxic inflammatory microenvironment

Contact Info

Product

Resources

About