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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Adaptor Proteins, Signal Transducing, Animals, Blotting, Western, Collagen Type IV, Cytoskeletal Proteins, Glomerular Basement Membrane, Glomerulonephritis, Integrin alpha3beta1, Kidney Glomerulus, Laminin, Membrane Proteins, Mice, Mice, Inbred C57BL, Mice, Inbred DBA, Mice, Inbred ICR, Mice, Knockout, Microscopy, Electron, Transmission, Microscopy, Fluorescence, Nephrotic Syndrome, Phosphoprotein Phosphatases, Podocytes, Proteinuria, Species Specificity, Tensins.
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Do tenc1-deficient mice develop glomerular disease in a strain-specific manner? Context: Tenc1 (also known as tensin2) is an integrin-associated focal adhesion molecule that is broadly expressed in mouse tissues including the liver, muscle, heart and kidney. A mouse strain carrying mutated Tenc1, the ICR-derived glomerulonephritis (ICGN) strain, develops severe nephrotic syndrome. To elucidate the function of Tenc1 in the kidney, Tenc1(ICGN) was introduced into 2 genetic backgrounds, i.e. DBA/2J (D2) and C57BL/6J (B6), strains that are respectively susceptible and resistant to chronic kidney disease. Biochemical and histological analysis revealed that homozygous Tenc1(ICGN) mice develop nephrotic syndrome on the D2 background (D2GN) but not on the B6 background (B6GN). Initially, abnormal assembly and maturation of glomerular basement membrane (GBM) were observed, and subsequently effacement of podocyte foot processes was noted in the kidneys of D2GN but not B6GN mice. These defects are likely to be involved in the integrin signaling pathway.
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This study suggests that Tenc1 contributes to the maintenance of GBM structures and that the genetic background influences the severity of nephrotic syndrome. Final Decision: yes