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Dysregulation of apoptosis: a possible mechanism leading to chronic progressive renal histological changes in lupus nephritis 被引量:2

Dysregulation of apoptosis: a possible mechanism leading to chronic progressive renal histological changes in lupus nephritis
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摘要 To evaluate apoptosis in lupus nephritis and the relationship between the existence of apoptotic cells in renal tissue and histopathological or clinical changes Methods Apoptosis was detected by in situ nick end labeling techniques (TUNEL) in renal biopsies from 25 patients with type Ⅳ lupus nephritis (LN), 12 patients with IgA nephropathy IgAN, 4 patients with idiopathic mesangioproliferative glomerulonephritis (MsPGN) and 3 patients with acute poststreptococcal glomerulonephritis (APGN) Normal renal tissue obtained at nephrectomy for hypernephroma in 4 adults was used as control Proliferating cells were identified by proliferating cell nuclear antigen (PCNA) in these patients Results Compared to other proliferative glomerulo^nephritis and controls, the patients with lupus nephritis had less apoptotic cells, a higher ratio of PCNA+ cells/TdT+ cells (P/T) in renal tissues; and their P/T ratio in glomeruli and tubulointerstitium correlated with the chronicity index, r =0 4983 ( P =0 0132), r =0 8399 ( P <0 001), r =0 6614 ( P =0 0033), respectively P/T ratios in the glomerulus and tubule had a positive correlation with 24 hour urinary protein, r =0 8554 ( P <0 001) and r =0 7134 ( P =0 001); and a negative correlation with creatinine clearance (Ccr), r =-0 4880 ( P =0 0133) and r =-0 7229 ( P =0 001), which in tubules positively correlated with serum creatinine (Scr), r =0 4107 ( P =0 0414) Conclusions Apoptosis is reduced in proliferative lupus nephritis Intense proliferation without a commensurate increase in apoptosis is a possible mechanism that leads to chronic progressive renal histopathological changes To evaluate apoptosis in lupus nephritis and the relationship between the existence of apoptotic cells in renal tissue and histopathological or clinical changes Methods Apoptosis was detected by in situ nick end labeling techniques (TUNEL) in renal biopsies from 25 patients with type Ⅳ lupus nephritis (LN), 12 patients with IgA nephropathy IgAN, 4 patients with idiopathic mesangioproliferative glomerulonephritis (MsPGN) and 3 patients with acute poststreptococcal glomerulonephritis (APGN) Normal renal tissue obtained at nephrectomy for hypernephroma in 4 adults was used as control Proliferating cells were identified by proliferating cell nuclear antigen (PCNA) in these patients Results Compared to other proliferative glomerulo^nephritis and controls, the patients with lupus nephritis had less apoptotic cells, a higher ratio of PCNA+ cells/TdT+ cells (P/T) in renal tissues; and their P/T ratio in glomeruli and tubulointerstitium correlated with the chronicity index, r =0 4983 ( P =0 0132), r =0 8399 ( P <0 001), r =0 6614 ( P =0 0033), respectively P/T ratios in the glomerulus and tubule had a positive correlation with 24 hour urinary protein, r =0 8554 ( P <0 001) and r =0 7134 ( P =0 001); and a negative correlation with creatinine clearance (Ccr), r =-0 4880 ( P =0 0133) and r =-0 7229 ( P =0 001), which in tubules positively correlated with serum creatinine (Scr), r =0 4107 ( P =0 0414) Conclusions Apoptosis is reduced in proliferative lupus nephritis Intense proliferation without a commensurate increase in apoptosis is a possible mechanism that leads to chronic progressive renal histopathological changes
出处 《Chinese Medical Journal》 SCIE CAS CSCD 2000年第12期26-30,共5页 中华医学杂志(英文版)
基金 This work was supported by a grant from Shanghai Scientific Technologi cal Committee(No 954119005).
关键词 lupus nephritis APOPTOSIS proliferating cell nuclear antigen lupus nephritis apoptosis proliferating cell nuclear antige?
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  • 1Shimizu A,Kitamura H,Masuda Y,et al.Apoptosis in the repair process of experimental proliferative glomerulonephritis. Kidney International . 1995
  • 2Cheng J,Zhou T,Liu C,et al.Protection from Fas-mediated apoptosis by a soluble form of the Fas molecule. Science . 1994
  • 3Tax WJ,Kramers C,van Bruggen MC,et al.Apoptosis,nucleosomes, and nephritis in systemic lupus erythematosus. Kidney International . 1995
  • 4Shimizu A,Kitamura H,Masuda Y,et al.Rare glomerular capillary regeneration and subsequent capillary regression with endothelial cell apoptosis in progressive glomerulonephritis. American Journal of Pathology . 1997
  • 5Harrison DJ.Cell death in the diseased glomerulus. Histopathology . 1988
  • 6Barker AJ,Mooney A,Hughes J,et al.Mesangial cell apoptosis: the major mechanism for resolution of glomerular hypercellularity in experimental mesangial proliferative nephritis. The Journal of Clinical Investigation . 1994
  • 7Sugiyama H,Kashihara N,Makino H,et al.Reactive oxygen species induce apoptosis in cultured human mesangial cells. Journal of the American Society of Nephrology . 1996
  • 8Takemura T,Murakami K,Miyazato H,et al.Expression of Fas antigen and Bcl-2 in human glomerulonephritis. Kidney International . 1995
  • 9Soto H,Mosquera J,Rodriguez-Iturbe B,et al.Apoptosis in proliferative glomerulonephritis: decreased apoptosis expression in lupus nephritis. Nephrology Dialysis Transplantation . 1997
  • 10Hockenberg D.Defining apoptosis. American Journal of Pathology . 1995

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