PUBLICATION

Somatic loss-of-function PIK3R1 and activating non-hotspot PIK3CA mutations associated with Capillary Malformation with Dilated Veins (CMDV)

Authors
De Bortoli, M., Queisser, A., Pham, V.C., Dompmartin, A., Helaers, R., Boutry, S., Claus, C., De Roo, A.K., Hammer, F., Brouillard, P., Abdelilah-Seyfried, S., Boon, L.M., Vikkula, M.
ID
ZDB-PUB-240304-6
Date
2024
Source
The Journal of investigative dermatology   144(9): 2066-2077.e6 (Journal)
Registered Authors
Abdelilah-Seyfried, Salim
Keywords
NGS, PI3K signaling, endothelial, somatic, zebrafish
MeSH Terms
  • Aged
  • Class I Phosphatidylinositol 3-Kinases*/genetics
  • Child
  • Signal Transduction/genetics
  • Middle Aged
  • Adult
  • Female
  • Capillaries*/abnormalities
  • Capillaries*/pathology
  • Loss of Function Mutation
  • Male
  • Vascular Malformations*/genetics
  • Vascular Malformations*/pathology
  • Humans
  • High-Throughput Nucleotide Sequencing
  • Zebrafish*/genetics
  • Animals
  • Veins/abnormalities
  • Veins/pathology
  • Endothelial Cells/metabolism
  • Endothelial Cells/pathology
  • Class Ia Phosphatidylinositol 3-Kinase*/genetics
  • Adolescent
PubMed
38431221 Full text @ J. Invest. Dermatol.
Abstract
Common capillary malformations (CMs) are red vascular skin lesions, most commonly associated with somatic activating GNAQ or GNA11 mutations. We focused on CMs lacking such a mutation to identify novel genetic causes. We used targeted next-generation-sequencing on 82 lesions. Bioinformatic analysis allowed the identification of 9 somatic pathogenic variants in PIK3R1 and PIK3CA, encoding for the regulatory and catalytic subunits of the PI3K kinase, respectively. Re-characterization of these lesions unraveled a common phenotype: a pale Capillary Malformation associated with visible Dilated Veins (CMDV). Primary-endothelial cells from two PIK3R1-mutated lesions were isolated and PI3K-AKT-mTOR and RAS-RAF-MAPK signaling were assessed by western-blot. This unveiled an abnormal increase in AKT phosphorylation, effectively reduced by PI3K pathway inhibitors, such as mTOR, AKT and PIK3CA-inhibitors. The effects of mutant PIK3R1 were further studied using zebrafish embryos. Endothelium-specific expression of PIK3R1 mutants resulted in abnormal development of the posterior capillary-venous plexus. In summary, CMDV emerges as a clinical entity associated with somatic pathogenic variants in PIK3R1 or PIK3CA (non-hotspot). Our findings suggest that the activated AKT signaling can be effectively reversed by PI3K-pathway inhibitors. Additionally, the proposed zebrafish model, holds promise as a valuable tool for future drug screening aimed at developing patient-tailored treatments.
Genes / Markers
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Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping