system
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: BACKGROUND, METHODS, RESULTS. Meshes: Animals, Atrophy, CD4-Positive T-Lymphocytes, Fibrosis, Galectin 3, Graft Survival, Histocompatibility, Histocompatibility Antigens Class II, Interleukin-4, Kidney Diseases, Kidney Transplantation, Kidney Tubules, Macrophage Activation, Macrophages, Mice, Mice, Inbred C57BL, Mice, Knockout, Time Factors, Transplantation, Isogeneic.
user
Is tubular atrophy and interstitial fibrosis after renal transplantation dependent on galectin-3? Context: Chronic allograft injury (CAI), characterized by interstitial fibrosis and tubular atrophy, leads to a progressive decline in graft function, resulting in the loss of 5% of renal transplants per annum, and eludes specific therapies. Galectin-3 (gal-3) is a β-galactoside-binding lectin expressed in diverse fibrotic tissue, and mice deficient in gal-3 have reduced fibrosis in kidney, liver, and lung models. The role of gal-3 in CAI is examined in this study. We adopted a murine model of CAI, characterized by a single class II mismatch between BM12 donor and C57BL/6 recipient strains. Syngeneic transplants served as controls (C57BL/6). Transplants were then performed between BM12 donors and gal-3 null recipients on a C57BL/6 background. Transplantation of BM12 kidneys into C57BL6 mice was associated with interstitial fibrosis (P<0.0001), tubular atrophy (P<0.0001), and upregulation in gal-3 expression (P=0.002), compared with syngeneic controls. Transplanting BM12 kidneys into gal-3 null mice resulted in significant preservation of tubules (P=0.008) and reduced interstitial fibrosis (P=0.01), with decreased myofibroblast activation (P=0.01) and collagen I expression (P=0.04), compared with wild type controls. The number of infiltrating leukocytes was unaltered by abrogation of gal-3, but reduced expression of YM1 (P=0.0001), a marker of alternative macrophage activation, along with a reduction in the number of circulating CD4-positive T cells (P=0.01), and reduced expression of interleukin-4 (P=0.02) in gal-3 null mice suggest possible mechanisms by which gal-3 may promote renal transplant fibrosis.
assistant
Our results suggest a potential role for gal-3 in CAI, and this represents a potentially exciting therapeutic target. Final Decision: yes