Claudin-17 Deficiency in Mice Results in Kidney Injury Due to Electrolyte Imbalance and Oxidative Stress.

ABSTRACT: The multi-gene claudin (CLDN) family of tight junction proteins have isoform-specific roles in blood-tissue barrier regulation. CLDN17, a putative anion pore-forming CLDN based on its structural characterization, is assumed to regulate anion balance across the blood-tissue barriers. However, our knowledge about CLDN17 in physiology and pathology is limited. The current study investigated how Cldn17 deficiency in mice affects blood electrolytes and kidney structure. Cldn17^-/- mice revealed no breeding abnormalities, but the newborn pups exhibited delayed growth. Adult Cldn17^-/- mice displayed electrolyte imbalance, oxidative stress, and injury to the kidneys. Ingenuity pathway analysis followed by RNA-sequencing revealed

SUBMITTER: Adil MS 

PROVIDER: S-EPMC9180152 | biostudies-literature | 2022 May

REPOSITORIES: biostudies-literature