Dysregulation of lncRNA SNHG1/miR‑145 axis affects the biological function of human carotid artery smooth muscle cells as a mechanism of carotid artery restenosis

Ma, Huanhuan; Dong, Aisheng

doi:10.3892/etm.2021.9867

Cited by 7 publications

(5 citation statements)

References 35 publications

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“…SNHG1 was initially identified as a cancer-related lncRNA by several studies [ 8 , 9 ]. Recently, Ma et al [ 24 ] reported that SNHG1 was significantly upregulated in serum samples of patients with restenosis,inhibition of SNHG1 served a protective role against restenosis by suppressing HA-VSMCs proliferation and migration. However, the effects of SNHG1 on the pathologic changes of blood vessels may be dependent on the different pathological states.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA SNHG1 alleviates high glucose-induced vascular smooth muscle cells calcification/senescence by post-transcriptionally regulating Bhlhe40 and autophagy via Atg10

et al. 2022

J Physiol Biochem

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Long noncoding RNAs (lncRNAs) are emerging regulators of vascular diseases, yet their role in diabetic vascular calcification/aging remains poorly understood. In this study, we identified a down-expressed lncRNA SNHG1 in high glucose (HG)-induced vascular smooth muscle cells (HA-VSMCs), which induced excessive autophagy and promoted HA-VSMCs calcification/senescence. Overexpression of SNHG1 alleviated HG-induced HA-VSMCs calcification/senescence. The molecular mechanisms of SNHG1 in HA-VSMCs calcification/senescence were explored by RNA pull-down, RNA immunoprecipitation, RNA stability assay, luciferase reporter assay, immunoprecipitation and Western blot assays. In one mechanism, SNHG1 directly interacted with Bhlhe40 mRNA 3′-untranslated region and increased Bhlhe40 mRNA stability and expression. In another mechanism, SNHG1 enhanced Bhlhe40 protein SUMOylation by serving as a scaffold to facilitate the binding of SUMO E3 ligase PIAS3 and Bhlhe40 protein, resulting in increased nuclear translocation of Bhlhe40 protein. Moreover, Bhlhe40 suppressed the expression of Atg10, which is involved in the process of autophagosome formation. Collectively, the protective effect of SNHG1 on HG-induced HA-VSMCs calcification/senescence is accomplished by stabilizing Bhlhe40 mRNA and promoting the nuclear translocation of Bhlhe40 protein. Our study could provide a novel approach for diabetic vascular calcification/aging.

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Section: Discussionmentioning

confidence: 99%

Long noncoding RNA SNHG1 alleviates high glucose-induced vascular smooth muscle cells calcification/senescence by post-transcriptionally regulating Bhlhe40 and autophagy via Atg10

et al. 2022

J Physiol Biochem

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“…31 Serum SNHG1 and miR-145 are highly expressed and lowly expressed, respectively, in CAS patients with restenosis. 32 It is worthy to mention that RMST is linked to regulating cerebral ischemia. A publication shows that declined RMST expression plays an important protective role in cerebral ischemia by protecting nerves and inhibiting infarcted brain size, which provides a novel target for ischemic stroke.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA RMST serves as a diagnostic biomarker in patients with carotid artery stenosis and predicts the occurrence of cerebral ischemic event: A retrospective study

Wang

Zhao

et al. 2022

Vascular

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Objectives The purpose of this retrospective study is to explore the diagnostic and prognostic roles of serum RMST in carotid artery stenosis (CAS). Methods Serum levels of RMST were detected in CAS patients, and the relationship between degree of carotid stenosis and RMST levels was analyzed. The ROC curve was drawn to evaluate RMST value in predicting the risk of CAS. Then, all CAS patients received a 5-year follow-up. K-M curve was used to analyze the significance of RMST on prognosis of CAS patients. Multi-factor cox logistic regression analysis was conducted to evaluate independent factors for outcome of CAS patients. Results An increased RMST expression was certified in CAS patients when compared with healthy controls. The increase of serum RMST expression was related to high degree of carotid stenosis. In addition, serum RMST was a possible diagnosis and an independent influencing factor of prognosis in patients with CAS. Conclusions Raised serum RMST level was found in patients with CAS. Detecting RMST expression levels was of high value for predicting the occurrence and outcomes in CAS.

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“…For instance, a clinical trait revealed that circulating miR-106b-5p could differentiate asymptomatic CAS from healthy individuals, and it also was able to predict the occurrence of the cerebral ischemic event [Jiang 2020]. LncRNA SNHG1 was demonstrated to indicate the risk of restenosis of CAS patients and regulate the biological processes of HVMSCs [Ma 2021]. miR-222-3p was identified as a dysregulated miRNA in CAS, which implies its potential in serving as a biomarker of CAS.…”

Section: Discussionmentioning

confidence: 99%

The Clinical Significance of Lncrna GAS5 And Mir-222-3p in Carotid Artery Stenosis

Li¹,

Zhang²,

He³

et al. 2022

HSF

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Background: Carotid artery stenosis (CAS) is the major pathogen of cerebral infarction and brain death. Early detection and risk prediction could help the diagnosis and improve the outcome of patients. The clinical significance of lncRNA GAS5 (GAS5) and miR-222-3p in the diagnosis and prognosis of CAS was evaluated in this study to explore novel effective biomarkers of CAS. Methods: A total of 72 CAS patients and 63 healthy individuals (control) were enrolled in this study. The expression levels of GAS5 and miR-222-3p in study subjects were detected using PCR. The ROC, Kaplan-Meier, and Cox regression analyses were carried out to estimate the diagnostic and prognostic value of GAS5 and miR-222-3p in CAS. The interaction between GAS5 and miR-222-3p was disclosed by the dual-luciferase reporter. Results: The reduced expression of GAS5 and elevated expression of miR-222-3p were observed in CAS patients compared with the healthy controls, and a significant correlation between their expression levels in CAS was revealed. GAS5 and miR-222-3p could discriminate CAS patients from the healthy controls with high sensitivity and specificity. The GAS5 downregulation and miR-222-3p upregulation could predict the poor prognosis of CAS patients and may be associated with the severe development of patients. In human vascular smooth muscle cells, miR-222-3p could negatively regulate the luciferase activity of GAS5. Conclusion: Both GAS5 and miR-222-3p served as the diagnostic and prognostic biomarkers of CAS. The function of GAS5 might result from the regulation of miR-222-3p, which needs further validation.

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Dysregulation of lncRNA SNHG1/miR‑145 axis affects the biological function of human carotid artery smooth muscle cells as a mechanism of carotid artery restenosis

Cited by 7 publications

References 35 publications

Long noncoding RNA SNHG1 alleviates high glucose-induced vascular smooth muscle cells calcification/senescence by post-transcriptionally regulating Bhlhe40 and autophagy via Atg10

Long noncoding RNA SNHG1 alleviates high glucose-induced vascular smooth muscle cells calcification/senescence by post-transcriptionally regulating Bhlhe40 and autophagy via Atg10

Long non-coding RNA RMST serves as a diagnostic biomarker in patients with carotid artery stenosis and predicts the occurrence of cerebral ischemic event: A retrospective study

The Clinical Significance of Lncrna GAS5 And Mir-222-3p in Carotid Artery Stenosis

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