Ultrastructural podocyte morphometry to assess glomerular damage in Alport disease and the effects of TUDCA on Alport disease
OA Version
Citation
Abstract
The Henderson lab, in collaboration with Dr. Richard Miller's lab at UTSW, aimed to investigate the function of apoptosis in podocyte damage in renal disease. The primary focus was on the effects of a supplementary chemical called tauroursodeoxycholic acid (TUDCA), which has anti-apoptotic activity, on podocyte injury and its potential to repair the shape and structure of the foot process. TUDCA may function as a possible anti-apoptotic molecule, hence preventing renal harm. Using a mouse model of Alport syndrome, the course of renal damage and the degree of kidney injury were investigated using renal section histological and ultrastructural examination. To gain a better understanding of the function of apoptosis in kidney damage and foot process effacement, we evaluated renal structure, including kidney histology, glomerular capillary and podocyte structure at the ultrastructural level. The goal of this study was to determine if this protective effect applied to podocyte injury brought on by modifications to the podocyte's structural surroundings, such as basement membrane disruption in the Alport model. Kidneys from TUDCA-treated and untreated Alport mice at 4 and 7 months from the Miller lab were assessed for glomerular and podocyte structure using electron microscopy. In the untreated Alport mice, there were clear indications of injury to the kidney cortex, mainly affecting the glomerulus; ultrastructurally, the podocyte foot processes displayed effacement. TUDCA-treated mice exhibited improved tubule-interstitium and glomerulus. In conclusion, TUDCA has shown to ameliorate the effacement of foot processes in the Alport mouse model, restoring the morphology of podocytes and reducing the impact of the disease to the kidney cortex to some extent.
Description
2024
License
Attribution 4.0 International