SOCS1 gene promoter methylation status is associated with in-stent restenosis after percutaneous coronary intervention.

Abstract

BACKGROUND:

Inflammation is involved in the development of In-stent restenosis (ISR) after percutaneous coronary intervention. We aimed to investigate the association between of suppressor of cytokine signaling-1 (SOCS1), a major negative regulator for inflammation, and the occurrence of ISR in Chinese patients.

METHODS:

We enrolled patients with coronary artery disease who underwent PCI with stenting. PCI procedures were performed successfully and a follow-up angiography was repeated 1 year later to determine ISR presence. Real-time quantitative reverse transcription polymerase chain reaction and methylation-specific polymerase chain reaction (MSP) was used for SOCS1 methylation status determination.

RESULTS:

There are a total of 187 patients had SOCS1 methylation while there are 275 had no methylated SOCS1. Patients with SOCS1 methylation have a higher inflammatory status. Of note, patients with SOCS1 methylation had a significantly lower SOCS1 mRNA levels compared to those without. Patients with ISR tend to have a significantly higher percentage of SOCS1 gene methylation (P<0.001). We next conducted the Binary logistic regression analyses to determine the correlation of SOCS1 with ISR, using demographic and clinical characteristics. Our data show that SOCS1 methylation is the only factors which are closely associated with ISR incidence. Patients with SOCS1 methylation are 5 times more likely to have ISR after successful PCI as opposed to those without SOCS1 methylation (P<0.001).

CONCLUSION:

Our data suggest that blood SOCS1 gene promoter methylation status is closely associated with ISR occurrence, thus may be used as a marker to predict ISR.

• Authors: Liang Zhou, Ningfu Wang, Hong Li, Guoxin Tong, Jianmin Yang, Lei Lai, Hao Pan, Xianhua Ye, Jinyu Huang
• Journal: Oncotarget (Oncotarget) Vol. 8 Issue 34 Pg. 56959-56967 (Aug 22 2017) ISSN: 1949-2553 [Electronic] United States
• PMID: 28915645 (Publication Type: Journal Article)