The potential function of SP1 and CPPED1 in restenosis after percutaneous coronary intervention

Wang, Zhiyong; Liang, Shumin; Cai, Xinyong; Zhou, Yuxuan; Hong, Lang; Li, Sanjun

doi:10.1111/jocs.17218

Cited by 2 publications

(2 citation statements)

References 31 publications

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“… 76 Moreover, it has been reported that Sp1 is lowly expressed in the model rats with carotid balloon injury, and Sp1 overexpression reduces injury-induced neointimal formation and restenosis rate. 77 Therefore, findings from the study and previous studies clearly infer a functional role for TGFβ1/Sp1/SNHG18 signal axis in controlling and sustaining VSMC contractile phenotype as well as in preventing injury-induced adverse arterial remodelling.…”

Section: Discussionsupporting

confidence: 55%

Small nucleolar RNA host gene 18 controls vascular smooth muscle cell contractile phenotype and neointimal hyperplasia

Niu,

Zhang,

Yang

et al. 2024

Cardiovascular Research

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Aims Long non-coding RNA (LncRNA) small nucleolar RNA host gene 18 (SNHG18) has been widely implicated in cancers. However, little is known about its functional involvement in vascular diseases. Herein, we attempted to explore a role for SNHG18 in modulating vascular smooth muscle cell (VSMC) contractile phenotype and injury-induced neointima formation. Methods and Results Analysis of single cell RNA sequencing and transcriptomic datasets showed decreased levels of SNHG18 in injured and atherosclerotic murine and human arteries, which is positively associated with VSMC contractile genes. SNHG18 was upregulated in VSMCs by TGFβ1 through transcription factors Sp1 and SMAD3. SNHG18 gene gain/loss-of-function studies revealed that VSMC contractile phenotype was positively regulated by SNHG18. Mechanistic studies showed that SNHG18 promotes a contractile VSMC phenotype by up-regulating miR-22-3p. SNHG18 up-regulates miR-22 biogenesis and miR-22-3p production by competitive binding with the A-to-I RNA editing enzyme, adenosine deaminase acting on RNA-2 (ADAR2). Surprisingly, we observed that ADAR2 inhibited miR-22 biogenesis not through increasing A-to-I editing within primary miR-22, but by interfering the binding of microprocessor complex subunit DGCR8 to primary miR-22. Importantly, perivascular SNHG18 overexpression in the injured vessels dramatically up-regulated the expression levels of miR-22-3p and VSMC contractile genes, and prevented injury-induced neointimal hyperplasia. Such modulatory effects were reverted by miR-22-3p inhibition in the injured arteries. Finally, we observed a similar regulator role for SNHG18 in human VSMCs, and a decreased expression level of both SNHG18 and miR-22-3p in diseased human arteries; and we found that the expression level of SNHG18 was positively associated with that of miR-22-3p in both healthy and diseased human arteries. Conclusion We demonstrate that SNHG18 is a novel regulator in governing VSMC contractile phenotype and preventing injury-induced neointimal hyperplasia. Our findings have important implications for therapeutic targeting snhg18/miR-22-3p signalling in vascular diseases.

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Section: Discussionsupporting

confidence: 55%

Small nucleolar RNA host gene 18 controls vascular smooth muscle cell contractile phenotype and neointimal hyperplasia

Niu,

Zhang,

Yang

et al. 2024

Cardiovascular Research

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“…Multiple factors have been implicated in the science and mechanism of coronary artery restenosis after PCI such as endothelial progenitor cells (EPCs), Specificity Protein 1 (SP1), Calcineurin-Like Phosphodiesterase Domain containing 1 (CPPED1), medication non-compliance (Statins, and renin-angiotensin-aldosterone system blockers reduce in-stent restenosis), high levels of HB-EGF, interleukin-10 and interleukin-18, and sedentary lifestyle [1,[6][7][8][9][10]. A study also argued there may be an association between the occurrence of ISR and anemia thus recommending that anemia should be assessed at the follow up clinic visits [9].…”

Section: Introductionmentioning

confidence: 99%

Untitled

2024

IJCMCR

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Coronary artery disease remains one of the leading causes of cardiovascular mortality worldwide. With advancement of medical therapy, percutaneous coronary intervention with stenting has become a cornerstone in the management of acute coronary syndrome. However, complications such as restenosis of stent has become a bane in the treatment of coronary artery disease. Factors such as sedentary lifestyle, nonadherence to medication, mechanical factors such as stent expansion, stent trauma, stent allergy, genetic factors have been implicated in the occurrence of in-stent restenosis. Patients often present in overt symptomatic acute coronary syndrome. Coronary angiography remains the mainstay of diagnosis. Treatments such as placement of drug-eluting stents, drug coated balloons, vascular brachytherapy and balloon angioplasty have been employed in the management.

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The potential function of SP1 and CPPED1 in restenosis after percutaneous coronary intervention

Cited by 2 publications

References 31 publications

Small nucleolar RNA host gene 18 controls vascular smooth muscle cell contractile phenotype and neointimal hyperplasia

Small nucleolar RNA host gene 18 controls vascular smooth muscle cell contractile phenotype and neointimal hyperplasia

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