Mutations of protocadherin 19 in female epilepsy (PCDH19-FE) lead to allopregnanolone deficiency

Hum Mol Genet. 2015 Sep 15;24(18):5250-9. doi: 10.1093/hmg/ddv245. Epub 2015 Jun 29.

Abstract

Protocadherin 19 (PCDH19) female limited epilepsy (PCDH19-FE; also known as epilepsy and mental retardation limited to females, EFMR; MIM300088) is an infantile onset epilepsy syndrome with or without intellectual disability (ID) and autism. We investigated transcriptomes of PCDH19-FE female and control primary skin fibroblasts, which are endowed to metabolize neurosteroid hormones. We identified a set of 94 significantly dysregulated genes in PCDH19-FE females. Intriguingly, 43 of the 94 genes (45.7%) showed gender-biased expression; enrichment of such genes was highly significant (P = 2.51E-47, two-tailed Fisher exact test). We further investigated the AKR1C1-3 genes, which encode crucial steroid hormone-metabolizing enzymes whose key products include allopregnanolone and estradiol. Both mRNA and protein levels of AKR1C3 were significantly decreased in PCDH19-FE patients. In agreement with this, the blood levels of allopregnanolone were also (P < 0.01) reduced. In conclusion, we show that the deficiency of neurosteroid allopregnanolone, one of the most potent GABA receptor modulators, may contribute to PCDH19-FE. Overall our findings provide evidence for a role of neurosteroids in epilepsy, ID and autism and create realistic opportunities for targeted therapeutic interventions.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3-Hydroxysteroid Dehydrogenases / genetics
  • 3-Hydroxysteroid Dehydrogenases / metabolism
  • Adolescent
  • Adult
  • Age of Onset
  • Aldo-Keto Reductase Family 1 Member C3
  • Cadherins / genetics*
  • Child
  • Child, Preschool
  • Cluster Analysis
  • Epilepsy / blood*
  • Epilepsy / diagnosis
  • Epilepsy / genetics*
  • Female
  • Fibroblasts / metabolism
  • Gene Expression Profiling
  • Gene Expression Regulation
  • Gene Regulatory Networks
  • Humans
  • Hydroxyprostaglandin Dehydrogenases / genetics
  • Hydroxyprostaglandin Dehydrogenases / metabolism
  • Infant
  • Infant, Newborn
  • Intellectual Disability / genetics
  • Middle Aged
  • Mutation*
  • Phenotype
  • Pregnanolone / blood
  • Pregnanolone / deficiency*
  • Protocadherins
  • Reproducibility of Results
  • Signal Transduction
  • Young Adult

Substances

  • Cadherins
  • PCDH19 protein, human
  • Protocadherins
  • Pregnanolone
  • 3-Hydroxysteroid Dehydrogenases
  • Hydroxyprostaglandin Dehydrogenases
  • AKR1C3 protein, human
  • Aldo-Keto Reductase Family 1 Member C3