Hypolipidaemia among patients with PMM2-CDG is associated with low circulating PCSK9 levels: a case report followed by observational and experimental studies

J Med Genet. 2020 Jan;57(1):11-17. doi: 10.1136/jmedgenet-2019-106102. Epub 2019 Aug 7.

Abstract

Background: Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors are novel therapeutics for reducing low-density lipoprotein cholesterol (LDLc). While serious side-effects have not been observed in short-term clinical trials, there remain concerns that long-term PCSK9 inhibition may cause neurocognitive side-effects.

Methods and results: An adult male with childhood-onset global developmental delay, cerebellar atrophy and severe hypolipidaemia underwent extensive biochemical and genetic investigations. Initial testing revealed low circulating PCSK9 levels and a common loss-of-function PCSK9 polymorphism, but these findings did not fully account for severe hypolipidaemia. Whole-exome sequencing was subsequently performed and identified two pathogenic phosphomannose mutase 2 (PMM2) variants (p.Arg141His and p.Pro69Ser) known to cause PMM2-associated congenital disorder of glycosylation (PMM2-CDG). A diagnosis of PMM2-CDG was consistent with the proband's neurological symptoms and severe hypolipidaemia. Given that PMM2-CDG is characterised by defective protein N-glycosylation and that PCSK9 is a negative regulator of LDLc, we postulated that loss of PCSK9 N-glycosylation mediates hypolipidaemia among patients with PMM2-CDG. First, in an independent cohort of patients with PMM2-CDG (N=8), we verified that circulating PCSK9 levels were significantly lower in patients than controls (p=0.0006). Second, we conducted in vitro experiments in hepatocyte-derived cells to evaluate the effects of PCSK9 N-glycosylation loss on LDL receptor (LDLR) activity. Experimental results suggest that defective PCSK9 N-glycosylation reduces the ability of circulating PCSK9 to degrade LDLR.

Conclusion: Life-long exposure to genetically lower PCSK9 per se is unlikely to cause neurocognitive impairment. Both observational and experimental findings suggest that hypolipidaemia in PMM2-CDG may be partially mediated by loss of PCSK9 N-glycosylation and/or its regulators.

Keywords: LDL cholesterol; PCSK9; PMM2; congenital disorder of glycosylation; neurocognitive side-effects.

Publication types

  • Case Reports
  • Observational Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Cohort Studies
  • Congenital Disorders of Glycosylation / complications
  • Congenital Disorders of Glycosylation / genetics*
  • Congenital Disorders of Glycosylation / metabolism
  • DNA Mutational Analysis
  • Dyslipidemias / etiology
  • Dyslipidemias / metabolism*
  • Exome Sequencing
  • Gene Expression Regulation
  • Glycosylation
  • Hep G2 Cells
  • Humans
  • Loss of Function Mutation
  • Male
  • Pedigree
  • Phosphotransferases (Phosphomutases) / deficiency*
  • Phosphotransferases (Phosphomutases) / genetics
  • Phosphotransferases (Phosphomutases) / metabolism
  • Polymorphism, Genetic
  • Proprotein Convertase 9 / blood*
  • Proprotein Convertase 9 / genetics
  • Proprotein Convertase 9 / metabolism
  • Protein Processing, Post-Translational
  • Proteolysis
  • Receptors, LDL / genetics
  • Receptors, LDL / metabolism*

Substances

  • LDLR protein, human
  • Receptors, LDL
  • PCSK9 protein, human
  • Proprotein Convertase 9
  • Phosphotransferases (Phosphomutases)
  • phosphomannomutase 2, human

Supplementary concepts

  • Congenital disorder of glycosylation type 1A

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