Placenta · 2025
Aquaporin-1 and aquaporin-4 in human placental angiogenesis: insights into the critical interaction with caveolin-1.
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Reppetti Julieta, Germán Gornalusse, Tomás Etcheverry, Mariana Farina, Alicia Damiano, Nora Martínez
Аннотация
UNLABELLED: The authors regret that the abstract was not included in the online and PubMed versions of the article. The correct abstract is provided below:
INTRODUCTION:: Angiogenesis is fundamental to normal placental development. Placenta vasculature is formed by two types of endothelial cells: microvascular and macrovascular endothelial cell that differ in morphology, gene expression and function. Caveolae are lipid rafts coated with caveolin-1 (Cav-1). Aquaporins (AQPs) are transmembrane water channels that move water in response to osmotic gradients. Recently, it has been suggested that AQPs and Cav-1 are also crucial for efficient cell migration and tubulogenesis. We investigated the role of caveolae/Cav-1 in placental vasculature development and its interaction with AQP1 and AQP4.
METHODS:: Human placental microvascular endothelial cells (hPMEC) and EA. hy926 cells were used as models for microvasculature and macrovasculature, respectively. Gene, protein expression and co-localization of Cav-1, AQP1, and AQP4 ware analyzed by RT-qPCR, western blotting and immunofluorescence. Physical interactions between Cav-1 and AQP1/AQP4 were examined by immunoprecipitation. Cells were treated with methyl-β-cyclodextrin (MβCD) to disrupt caveolae, tetraethylammonium chloride (TEA) to block AQP1 and AQP4, specific siRNAs for Cav-1 and AQP1, and the AQP4 inhibitor TGN-020, then cell migration and tubulogenesis were evaluated.
RESULTS:: Cav-1 co-localized with AQP1 and AQP4 in placental endothelial cells. Disruption of caveolae or inhibition of AQP1, AQP4, or Cav-1 significantly impaired cell migration. Silencing Cav-1 or AQP1, or blocking AQP4, reduced tubulogenesis in both endothelial cell types.
CONCLUSIONS:: Angiogenesis of placental endothelial cells requires appropriate expression and function of AQP1 and AQP4, as well as an intact caveolar structure for proper cell migration and tubulogenesis. Any perturbations might result in aberrant angiogenesis leading to serious pregnancy disorders such as preeclampsia or fetal growth restriction. The authors would like to apologise for any inconvenience caused.
INTRODUCTION:: Angiogenesis is fundamental to normal placental development. Placenta vasculature is formed by two types of endothelial cells: microvascular and macrovascular endothelial cell that differ in morphology, gene expression and function. Caveolae are lipid rafts coated with caveolin-1 (Cav-1). Aquaporins (AQPs) are transmembrane water channels that move water in response to osmotic gradients. Recently, it has been suggested that AQPs and Cav-1 are also crucial for efficient cell migration and tubulogenesis. We investigated the role of caveolae/Cav-1 in placental vasculature development and its interaction with AQP1 and AQP4.
METHODS:: Human placental microvascular endothelial cells (hPMEC) and EA. hy926 cells were used as models for microvasculature and macrovasculature, respectively. Gene, protein expression and co-localization of Cav-1, AQP1, and AQP4 ware analyzed by RT-qPCR, western blotting and immunofluorescence. Physical interactions between Cav-1 and AQP1/AQP4 were examined by immunoprecipitation. Cells were treated with methyl-β-cyclodextrin (MβCD) to disrupt caveolae, tetraethylammonium chloride (TEA) to block AQP1 and AQP4, specific siRNAs for Cav-1 and AQP1, and the AQP4 inhibitor TGN-020, then cell migration and tubulogenesis were evaluated.
RESULTS:: Cav-1 co-localized with AQP1 and AQP4 in placental endothelial cells. Disruption of caveolae or inhibition of AQP1, AQP4, or Cav-1 significantly impaired cell migration. Silencing Cav-1 or AQP1, or blocking AQP4, reduced tubulogenesis in both endothelial cell types.
CONCLUSIONS:: Angiogenesis of placental endothelial cells requires appropriate expression and function of AQP1 and AQP4, as well as an intact caveolar structure for proper cell migration and tubulogenesis. Any perturbations might result in aberrant angiogenesis leading to serious pregnancy disorders such as preeclampsia or fetal growth restriction. The authors would like to apologise for any inconvenience caused.