Analysis of circulating miRNAs in patients with familial hypercholesterolaemia treated by LDL/Lp(a) apheresis

Atheroscler Suppl. 2017 Nov:30:128-134. doi: 10.1016/j.atherosclerosissup.2017.05.037. Epub 2017 Jun 1.

Abstract

Background: LDL/Lp(a) apheresis therapy is a well-established method of aggressively lowering LDL and Lp(a). Recently, miRNAs have been discussed as markers of vascular status including atherosclerosis. MiRNAs inhibit post-transcriptional processes through RNA duplex formation resulting in gene silencing or regulation of gene expression.

Materials and methods: We measured a profile of 175 plasma-circulating miRNAs using pre-defined Serum/Plasma Focus Human microRNA PCR Panels in pooled samples of 11 subjects with familial hypercholesterolaemia under long-term apheresis treatment. Subsequently we analysed expressions of ten pre-selected miRNAs potentially involved in lipid homeostasis in the same group of subjects. We compared plasma-circulating miRNA levels isolated from peripheral blood collected immediately before and after apheresis.

Results: The greatest differences in plasma levels were found in miR-451a, miR-16, miR-19a/b, miR-223 and miR-185. In subsequent individual miRNA assay we detected a significant increase in miR-33b levels after apheresis (P < 0.05). Additionally, correlations between plasma lipids and miR-33a (P < 0.04) and miR-122 (P < 0.01) have been determined. Moreover, miR-122 levels in LDLR homozygotes were higher compared to heterozygotes after, but not before, apheresis treatment (P < 0.04).

Conclusions: LDL/Lp(a) apheresis has an impact on miRNAs associated with lipid homeostasis and vascular status.

Keywords: Apheresis; Familial hypercholesterolaemia; miRNA.

Publication types

  • Comparative Study

MeSH terms

  • Adult
  • Aged
  • Biomarkers / blood
  • Blood Component Removal / adverse effects
  • Blood Component Removal / methods*
  • Cholesterol, LDL / blood*
  • Circulating MicroRNA / blood*
  • Circulating MicroRNA / genetics
  • Female
  • Genetic Predisposition to Disease
  • Heterozygote
  • Homozygote
  • Humans
  • Hyperlipoproteinemia Type II / blood
  • Hyperlipoproteinemia Type II / diagnosis
  • Hyperlipoproteinemia Type II / genetics
  • Hyperlipoproteinemia Type II / therapy*
  • Lipoprotein(a) / blood*
  • Male
  • Middle Aged
  • Phenotype
  • Time Factors
  • Transcriptome
  • Treatment Outcome

Substances

  • Biomarkers
  • Cholesterol, LDL
  • Circulating MicroRNA
  • Lipoprotein(a)