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- W4207084242 abstract "Abstract The Multi-gene claudin ( CLDN ) family of tight junction proteins have isoform-specific roles in blood-tissue barrier regulation. Although CLDN17 , a putative anion pore-forming CLDN , is assumed to regulate anion balance across the blood-tissue barriers, our knowledge about CLDN17 is limited. The current study investigated how Cldn17 deficiency in mice affects blood-tissue barrier integrity and vascular permeability. Cldn17 −/− mice revealed no breeding abnormalities, but the newborn pups exhibited delayed growth until they turned 8-weeks. Adult Cldn17 −/− mice displayed electrolyte imbalance, oxidative stress, increased vascular leakage, increased bone density, and organ injury. In addition, these mice demonstrated increased leukocytosis. A xenograft model to study pathological neovascularization showed higher vascular density in tumors developed in Cldn17 −/− mice compared to wild-type controls. RNA-sequencing revealed hyperactivation of signaling pathways associated with inflammation and reactive oxygen species generation, demonstrating the importance of Cldn17 in blood-tissue barrier maintenance." @default.
- W4207084242 created "2022-01-26" @default.
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- W4207084242 date "2022-01-24" @default.
- W4207084242 modified "2023-09-24" @default.
- W4207084242 title "Claudin17 deficient mice display leaky vasculature and organ injury accompanied by oxidative stress and inflammation" @default.
- W4207084242 doi "https://doi.org/10.21203/rs.3.rs-1270153/v1" @default.
- W4207084242 hasPublicationYear "2022" @default.
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