ArticleThe American Journal of dermatopathology2017
Activation of PKCα and PI3K Kinases in Hypertrophic and Nodular Port Wine Stain Lesions.
Article in The American Journal of dermatopathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Analysis of Phosphorylated MEK1 Expression Pattern in Cutaneous Dilated Vessels of Capillary Malformations.The Journal of dermatology · 2026Article
- Port-wine stains: molecular drivers, translational models, and emerging theragnostic directions.Lasers in medical science · 2026Review
- In Vitro Models of Sturge-Weber Syndrome: Strengths, Limitations, and Future Goals.International journal of molecular sciences · 2026Review
- Cutaneous laser treatment of port-wine stains and its impact on ocular manifestations in Sturge-Weber syndrome.Frontiers in ophthalmology · 2026Review
- Biomarker development in Sturge-Weber syndrome.Journal of neurodevelopmental disorders · 2025Review
- Carbon dioxide laser ablation as an effective method for treating nodular areas in Port wine stains: a series of two cases.Lasers in medical science · 2025Article
- KRIT1 in vascular biology and beyond.Bioscience reports · 2024Review
- Congenital Vascular and Lymphatic Diseases.Circulation research · 2024Review
- Towards precision medicine in vascular anomalies: Could protein kinase C inhibitors be repurposed for GNAQ/11-related phakomatoses?Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2024Article
- Current clinical evidence is insufficient to support HMME-PDT as the first choice of treatment for young children with port wine birthmarks.Lasers in surgery and medicine · 2024Review
- Perturbations of Glutathione and Sphingosine Metabolites in Port Wine Birthmark Patient-Derived Induced Pluripotent Stem Cells.Metabolites · 2023Article
- Perturbations of glutathione and sphingosine metabolites in Port Wine Birthmark patient-derived induced pluripotent stem cells.bioRxiv : the preprint server for biology · 2023Article
- Pathogenesis of Port-Wine Stains: Directions for Future Therapies.International journal of molecular sciences · 2022Review
- Whole-Genome Sequencing IdentifiedFrontiers in medicine · 2022Article
- GNAQ mutations drive port wine birthmark-associated Sturge-Weber syndrome: A review of pathobiology, therapies, and current models.Frontiers in human neuroscience · 2022Review
- Sturge-Weber syndrome: an update on the relevant issues for neurosurgeons.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2020Review
- The Pathogenesis of Port Wine Stain and Sturge Weber Syndrome: Complex Interactions between Genetic Alterations and Aberrant MAPK and PI3K Activation.International journal of molecular sciences · 2019Review
- Membrane trafficking and exocytosis are upregulated in port wine stain blood vessels.Histology and histopathology · 2019Article
- Ultrastructural characterization of hyperactive endothelial cells, pericytes and fibroblasts in hypertrophic and nodular port-wine stain lesions.The British journal of dermatology · 2017Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Port wine stain (PWS) is a congenital, progressive vascular malformation. Many patients with PWS develop hypertrophy and discrete nodularity during their adult life, but the mechanism(s) remain incompletely understood. In this study, we attempted to investigate activation status of PKCα, PI3K, PDPK1 and PLC-γ and protein levels of PP2A and DAG to explore their potential roles in the formation of hypertrophic and nodular PWS lesions. We found phosphorylated levels of PKCα, PI3K, PDPK1, and PLC-γ and protein levels of PP2A and DAG showed moderate increases in the endothelial cells of hypertrophic PWS as compared to the adjacent normal skin. These increases extended throughout the entire stroma of blood vessels in PWS nodules. Many proliferating cells, such as fibroblasts, also showed strong activation of PKCα, PI3K, PDPK1 and PLC-γ and upregulations of PP2A and DAG in nodular PWS lesions. Our data showed that there is aberrant activation of PKCα, PI3K, PDPK1 and PLC-γ and upregulation of PP2A and DAG mainly in endothelial cells in hypertrophic PWS areas, but presenting in the entire vasculatures and surrounding fibroblasts in PWS nodules. Our data suggest that both PKCα and PI3K signaling pathways contribute to the development of hypertrophy and nodularity in adult PWS.
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