Tight junction composition is altered in the epithelium of polycystic kidneys

• Published in: The Journal of pathology Vol. 216; no. 1; pp. 120 - 128
• Main Authors: Yu, ASL, Kanzawa, SA, Usorov, A, Lantinga-van Leeuwen, IS, Peters, DJM
• Format: Journal Article
• Language: English
• Published: Chichester, UK John Wiley & Sons, Ltd 01.09.2008; Wiley
• Subjects: Animals; autosomal dominant polycystic kidney disease; Biological and medical sciences; claudins; Epithelial Cells - metabolism; Humans; Investigative techniques, diagnostic techniques (general aspects); Kidney - metabolism; Kidneys; Malformations of the urinary system; Medical sciences; Membrane Proteins - genetics; Membrane Proteins - metabolism; Mice; Nephrology. Urinary tract diseases; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques; Polycystic Kidney, Autosomal Dominant - genetics; Polycystic Kidney, Autosomal Dominant - metabolism; renal cysts; tight junctions; Tight Junctions - genetics; Tight Junctions - metabolism; Tumor Cells, Cultured; Kidney disease; Composition; Membrane protein; Urinary system disease; Polycystic kidney; Kidney cyst; Cell junction; Autosome; autosomal dominant polycystic kidney disease; Epithelium; Genetic disease; renal cysts; Anatomic pathology; Nephropathy; Tight junction; Benign neoplasm; tight junctions; claudins

Kidney cysts in autosomal dominant polycystic kidney disease (ADPKD) undergo progressive enlargement together with luminal fluid secretion. This involves active, uphill transcellular Cl⁻ transport which drives passive Na⁺ and water secretion. Implicit in this mechanism is the assumption that the par...