|Efficacy of galectins in the amelioration of nephrotoxic serum nephritis in Wistar Kyoto rats|
|Tsuchiyama, Y; Wada, J; Zhang, H; Morita, Y; Hiragushi, K; Hida, K; Shikata, K; Yamamura, M; Kanwar, YS; Makino, H|
|关键词||dexamethasone crescentic glomerulonephritis apoptosis CD8(+) cells macrophages immune response|
|WOS标题词||Science & Technology|
|类目[WOS]||Urology & Nephrology|
|研究领域[WOS]||Urology & Nephrology|
|关键词[WOS]||GALACTOSIDE-BINDING-PROTEIN ; CELL-GROWTH ; CRESCENTIC GLOMERULONEPHRITIS ; WKY RATS ; EXPRESSION ; LECTIN ; ADHESION ; IDENTIFICATION ; APOPTOSIS ; CARCINOMA|
Background. Galectins are characterized by specific affinity for beta -galactoside sugars, and they play a role in diverse biological processes, including cell adhesion, cell proliferation, and apoptosis. Galectin-1, -3, and -9 have been implicated in modulating the immune response.
Methods. Nephrotoxic serum nephritis, which is characterized by crescent formation and glomerular influx of CD8(+) cells into glomerular capillaries, was induced in Wistar Kyoto (WKY) rats by injecting rabbit antiglomerular basement membrane serum. Following induction, the rats were treated either with phosphate-buffered saline or dexamethasone, galectin-1, galectin-3, or galectin-9 on alternate days and were sacrificed at day 14. At day 8, splenic lymphocytes were isolated and employed for terminal deoxytransferase-mediated uridine triphosphate nick end-labeling (TUNEL) assay to assess the degree of apoptosis, and the kidneys were utilized to determine the extent of influx of CD4(+) and CD8(+) cells and glomerular damage.
Results. Dexamethasone induced a marked apoptosis of splenic CD4(+) and CD8(+) cells, and it inhibited the production of anti-rabbit IgG and the influx of CD8(+) cells and macrophages into the renal glomeruli. Crescent formation and excretion of urinary proteins were also reduced. Galectin-9 failed to induce apoptosis in the CD4(+) cells; however, it induced apoptosis in the CD8(+) cells and inhibited the infiltration of CD8(+) cells. Although galectin-1 and -3 did not induce the apoptosis in the T cells, they inhibited the accumulation of macrophages in the renal glomeruli. Like dexamethasone, the galectins also reduced the crescentic formation, proliferation of glomerular cells, and excretion of urinary proteins.
Conclusions. Galectin-9 selectively induces apoptosis of the activated CD8(+) cells, while the macrophage influx into the kidney is modulated by all three galectins. This finding raises an interesting possibility for the utility of galectins in the modulation of macrophages that are involved in immune-mediated glomerular diseases.
|作者单位||1.Okayama Univ, Sch Med, Dept Med 3, Okayama 7008558, Japan|
2.Beijing Med Univ, Teaching Hosp 1, Dept Nephrol, Beijing 100083, Peoples R China
3.Northwestern Univ, Sch Med, Dept Pathol, Chicago, IL 60611 USA
|Tsuchiyama, Y,Wada, J,Zhang, H,et al. Efficacy of galectins in the amelioration of nephrotoxic serum nephritis in Wistar Kyoto rats[J]. KIDNEY INTERNATIONAL,2000,58(5):1941-1952.|
|APA||Tsuchiyama, Y.,Wada, J.,Zhang, H.,Morita, Y.,Hiragushi, K.,...&Makino, H.(2000).Efficacy of galectins in the amelioration of nephrotoxic serum nephritis in Wistar Kyoto rats.KIDNEY INTERNATIONAL,58(5),1941-1952.|
|MLA||Tsuchiyama, Y,et al."Efficacy of galectins in the amelioration of nephrotoxic serum nephritis in Wistar Kyoto rats".KIDNEY INTERNATIONAL 58.5(2000):1941-1952.|