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Prenatal treprostinil improves pulmonary arteriolar hypermuscularization in the rabbit model of congenital diaphragmatic hernia

Felix R. De Bie, Yannick Regin, Antoine Dubois, Marianna Scuglia, Tomohiro Arai, Ewout Muylle, David Basurto, Marius Regin, Siska Croubels (UGent) , Marc Cherlet (UGent) , et al.
(2024) BIOMEDICINE & PHARMACOTHERAPY. 170.
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Abstract
Congenital diaphragmatic hernia (CDH) is a congenital malformation characterized by pulmonary hypoplasia, pulmonary hypertension, and cardiac dysfunction. Pulmonary hypertension represents the major cause of neonatal mortality and morbidity. Prenatal diagnosis allows assessment of severity and selection of foetal surgery candidates. We have shown that treprostinil, a prostacyclin analogue with an anti-remodelling effect, attenuates the relative hypermuscularization of the pulmonary vasculature in rats with nitrofen-induced CDH. Here we confirm these observations in a large animal model of surgically-created CDH. In the rabbit model, subcutaneous maternal administration of treprostinil at 150 ng/kg/min consistently reached target foetal concentrations without demonstrable detrimental foetal or maternal adverse effects. In pups with CDH, prenatal treprostinil reduced pulmonary arteriolar proportional medial wall thickness and downregulated inflammation and myogenesis pathways. No effect on alveolar morphometry or lung mechanics was observed. These findings provide further support towards clinical translation of prenatal treprostinil for CDH.
Keywords
LUNG, HYPERTENSION, PHARMACOKINETICS, SILDENAFIL, ABNORMALITIES, HYPOPLASIA, MANAGEMENT, NEWBORNS, GROWTH, Foetal therapy - pulmonary hypertension -, congenital diaphragmatic hernia, treprostinil

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MLA
De Bie, Felix R., et al. “Prenatal Treprostinil Improves Pulmonary Arteriolar Hypermuscularization in the Rabbit Model of Congenital Diaphragmatic Hernia.” BIOMEDICINE & PHARMACOTHERAPY, vol. 170, 2024, doi:10.1016/j.biopha.2023.115996.
APA
De Bie, F. R., Regin, Y., Dubois, A., Scuglia, M., Arai, T., Muylle, E., … Deprest, J. A. (2024). Prenatal treprostinil improves pulmonary arteriolar hypermuscularization in the rabbit model of congenital diaphragmatic hernia. BIOMEDICINE & PHARMACOTHERAPY, 170. https://doi.org/10.1016/j.biopha.2023.115996
Chicago author-date
De Bie, Felix R., Yannick Regin, Antoine Dubois, Marianna Scuglia, Tomohiro Arai, Ewout Muylle, David Basurto, et al. 2024. “Prenatal Treprostinil Improves Pulmonary Arteriolar Hypermuscularization in the Rabbit Model of Congenital Diaphragmatic Hernia.” BIOMEDICINE & PHARMACOTHERAPY 170. https://doi.org/10.1016/j.biopha.2023.115996.
Chicago author-date (all authors)
De Bie, Felix R., Yannick Regin, Antoine Dubois, Marianna Scuglia, Tomohiro Arai, Ewout Muylle, David Basurto, Marius Regin, Siska Croubels, Marc Cherlet, Emily A. Partridge, Karel Allegaert, Francesca M. Russo, and Jan A. Deprest. 2024. “Prenatal Treprostinil Improves Pulmonary Arteriolar Hypermuscularization in the Rabbit Model of Congenital Diaphragmatic Hernia.” BIOMEDICINE & PHARMACOTHERAPY 170. doi:10.1016/j.biopha.2023.115996.
Vancouver
1.
De Bie FR, Regin Y, Dubois A, Scuglia M, Arai T, Muylle E, et al. Prenatal treprostinil improves pulmonary arteriolar hypermuscularization in the rabbit model of congenital diaphragmatic hernia. BIOMEDICINE & PHARMACOTHERAPY. 2024;170.
IEEE
[1]
F. R. De Bie et al., “Prenatal treprostinil improves pulmonary arteriolar hypermuscularization in the rabbit model of congenital diaphragmatic hernia,” BIOMEDICINE & PHARMACOTHERAPY, vol. 170, 2024.
@article{01HNZ725X0FNGNRTWC9N8NNMC9,
  abstract     = {{Congenital diaphragmatic hernia (CDH) is a congenital malformation characterized by pulmonary hypoplasia, pulmonary hypertension, and cardiac dysfunction. Pulmonary hypertension represents the major cause of neonatal mortality and morbidity. Prenatal diagnosis allows assessment of severity and selection of foetal surgery candidates. We have shown that treprostinil, a prostacyclin analogue with an anti-remodelling effect, attenuates the relative hypermuscularization of the pulmonary vasculature in rats with nitrofen-induced CDH. Here we confirm these observations in a large animal model of surgically-created CDH. In the rabbit model, subcutaneous maternal administration of treprostinil at 150 ng/kg/min consistently reached target foetal concentrations without demonstrable detrimental foetal or maternal adverse effects. In pups with CDH, prenatal treprostinil reduced pulmonary arteriolar proportional medial wall thickness and downregulated inflammation and myogenesis pathways. No effect on alveolar morphometry or lung mechanics was observed. These findings provide further support towards clinical translation of prenatal treprostinil for CDH.}},
  articleno    = {{115996}},
  author       = {{De Bie, Felix R. and  Regin, Yannick and  Dubois, Antoine and  Scuglia, Marianna and  Arai, Tomohiro and  Muylle, Ewout and  Basurto, David and  Regin, Marius and Croubels, Siska and Cherlet, Marc and  Partridge, Emily A. and  Allegaert, Karel and  Russo, Francesca M. and  Deprest, Jan A.}},
  issn         = {{0753-3322}},
  journal      = {{BIOMEDICINE & PHARMACOTHERAPY}},
  keywords     = {{LUNG,HYPERTENSION,PHARMACOKINETICS,SILDENAFIL,ABNORMALITIES,HYPOPLASIA,MANAGEMENT,NEWBORNS,GROWTH,Foetal therapy - pulmonary hypertension -,congenital diaphragmatic hernia,treprostinil}},
  language     = {{eng}},
  pages        = {{17}},
  title        = {{Prenatal treprostinil improves pulmonary arteriolar hypermuscularization in the rabbit model of congenital diaphragmatic hernia}},
  url          = {{http://doi.org/10.1016/j.biopha.2023.115996}},
  volume       = {{170}},
  year         = {{2024}},
}
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