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

Autor: Adil MS; Clinical and Experimental Therapeutics, College of Pharmacy, University of Georgia, Augusta, GA 30912, USA.; Research Division, Charlie Norwood VA Medical Center, Augusta, GA 30912, USA., Parvathagiri V; Clinical and Experimental Therapeutics, College of Pharmacy, University of Georgia, Augusta, GA 30912, USA.; Research Division, Charlie Norwood VA Medical Center, Augusta, GA 30912, USA., Verma A; Clinical and Experimental Therapeutics, College of Pharmacy, University of Georgia, Augusta, GA 30912, USA.; Research Division, Charlie Norwood VA Medical Center, Augusta, GA 30912, USA., Liu F; Clinical and Experimental Therapeutics, College of Pharmacy, University of Georgia, Augusta, GA 30912, USA.; Research Division, Charlie Norwood VA Medical Center, Augusta, GA 30912, USA., Rudraraju M; Clinical and Experimental Therapeutics, College of Pharmacy, University of Georgia, Augusta, GA 30912, USA.; Research Division, Charlie Norwood VA Medical Center, Augusta, GA 30912, USA., Narayanan SP; Clinical and Experimental Therapeutics, College of Pharmacy, University of Georgia, Augusta, GA 30912, USA.; Research Division, Charlie Norwood VA Medical Center, Augusta, GA 30912, USA., Somanath PR; Clinical and Experimental Therapeutics, College of Pharmacy, University of Georgia, Augusta, GA 30912, USA.; Research Division, Charlie Norwood VA Medical Center, Augusta, GA 30912, USA.
Jazyk: angličtina
Zdroj: Cells [Cells] 2022 May 29; Vol. 11 (11). Date of Electronic Publication: 2022 May 29.
DOI: 10.3390/cells11111782
Abstrakt: 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 hyperactivation of signaling pathways and downregulation of SOD1 expression in kidneys associated with inflammation and reactive oxygen species generation, demonstrating the importance of Cldn17 in the maintenance of electrolytes and reactive oxygen species across the blood-tissue barrier.
Databáze: MEDLINE
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