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• W2058289451 abstract "Pathways of caspase-mediated apoptosis in autosomal-dominant polycystic kidney disease (ADPKD).BackgroundWe have recently demonstrated an increase in apoptosis in Han:SPRD rat kidneys with autosomal-dominant polycystic kidney disease (ADPKD). Caspase-3 and caspase-7 are major mediators of apoptosis. There are two pathways of caspase-3 and caspase-7–mediated apoptosis: (1) the “extrinsic” pathway involving the death receptor Fas, Fas ligand (FasL), and caspase-8 and (2) the “mitochondrial” or “intrinsic” pathway involving Bcl-2 proteins, caspase-2, cytochrome c release, and caspase-9. The aim of the present study was to investigate the pathways of apoptosis in 3-week-old Han:SPRD rats with ADPKD.MethodsFluorescent substrates were used to measure caspase activity. mRNA and protein was determined by ribonuclease protection assays and immunoblotting, respectively. The effect of caspase inhibitors on caspase activity in polycystic kidneys was determined.ResultsCaspase-3 and caspase-7 activity was more than 100% increased in homozygous (Cy/Cy) compared to heterozygous (Cy/+) and normal littermate control (+/+) kidneys. Ribonuclease protection assays demonstrated no difference in caspase-3 mRNA. On immunoblotting, there was an increase in the proform of caspase-3 and caspase-7 in Cy/Cy compared to +/+ and Cy/+ kidneys. Caspase-8 and caspase-9 activity was more than 100% increased in Cy/Cy compared to Cy/+ and +/+ kidneys. On immunoblotting, there was an increase of the proform of both caspase-8 and caspase-9 in Cy/Cy kidneys. There was also an increase in cytochrome c release into the cytosol and an increase in caspase-2 protein and activity in Cy/Cy kidneys. On ribonuclease protection assay there was no difference in FasL mRNA between +/+, Cy/+, and Cy/Cy kidneys. Short-term treatment of Cy/Cy rats with the caspase inhibitor IDN-8050 resulted in inhibition of caspase-3 and caspase-7 activity in the kidney.ConclusionIn Cy/Cy kidneys with ADPKD, there was an increase of the proform of caspase-9, an increase in cytochrome c release into the cytosol, and an increase in caspase-2 protein and activity demonstrating involvement of the intrinsic pathway. There was an increase in the proform of caspase-8 demonstrating involvement of the extrinsic pathway. No differences in FasL mRNA were seen suggesting that the extrinsic pathway is independent of the death receptor ligand, FasL. Pathways of caspase-mediated apoptosis in autosomal-dominant polycystic kidney disease (ADPKD). We have recently demonstrated an increase in apoptosis in Han:SPRD rat kidneys with autosomal-dominant polycystic kidney disease (ADPKD). Caspase-3 and caspase-7 are major mediators of apoptosis. There are two pathways of caspase-3 and caspase-7–mediated apoptosis: (1) the “extrinsic” pathway involving the death receptor Fas, Fas ligand (FasL), and caspase-8 and (2) the “mitochondrial” or “intrinsic” pathway involving Bcl-2 proteins, caspase-2, cytochrome c release, and caspase-9. The aim of the present study was to investigate the pathways of apoptosis in 3-week-old Han:SPRD rats with ADPKD. Fluorescent substrates were used to measure caspase activity. mRNA and protein was determined by ribonuclease protection assays and immunoblotting, respectively. The effect of caspase inhibitors on caspase activity in polycystic kidneys was determined. Caspase-3 and caspase-7 activity was more than 100% increased in homozygous (Cy/Cy) compared to heterozygous (Cy/+) and normal littermate control (+/+) kidneys. Ribonuclease protection assays demonstrated no difference in caspase-3 mRNA. On immunoblotting, there was an increase in the proform of caspase-3 and caspase-7 in Cy/Cy compared to +/+ and Cy/+ kidneys. Caspase-8 and caspase-9 activity was more than 100% increased in Cy/Cy compared to Cy/+ and +/+ kidneys. On immunoblotting, there was an increase of the proform of both caspase-8 and caspase-9 in Cy/Cy kidneys. There was also an increase in cytochrome c release into the cytosol and an increase in caspase-2 protein and activity in Cy/Cy kidneys. On ribonuclease protection assay there was no difference in FasL mRNA between +/+, Cy/+, and Cy/Cy kidneys. Short-term treatment of Cy/Cy rats with the caspase inhibitor IDN-8050 resulted in inhibition of caspase-3 and caspase-7 activity in the kidney. In Cy/Cy kidneys with ADPKD, there was an increase of the proform of caspase-9, an increase in cytochrome c release into the cytosol, and an increase in caspase-2 protein and activity demonstrating involvement of the intrinsic pathway. There was an increase in the proform of caspase-8 demonstrating involvement of the extrinsic pathway. No differences in FasL mRNA were seen suggesting that the extrinsic pathway is independent of the death receptor ligand, FasL." @default.
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• W2058289451 date "2005-03-01" @default.
• W2058289451 modified "2023-09-27" @default.
• W2058289451 title "Pathways of caspase-mediated apoptosis in autosomal-dominant polycystic kidney disease (ADPKD)" @default.
• W2058289451 cites W1436936464 @default.
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• W2058289451 cites W1965597819 @default.
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• W2058289451 cites W2039232401 @default.
• W2058289451 cites W2041466047 @default.
• W2058289451 cites W2047825570 @default.
• W2058289451 cites W2062853648 @default.
• W2058289451 cites W2070702585 @default.
• W2058289451 cites W2072894284 @default.
• W2058289451 cites W2073561578 @default.
• W2058289451 cites W2081145901 @default.
• W2058289451 cites W2087100422 @default.
• W2058289451 cites W2088406835 @default.
• W2058289451 cites W2091418555 @default.
• W2058289451 cites W2093401766 @default.
• W2058289451 cites W2102471726 @default.
• W2058289451 cites W2113621700 @default.
• W2058289451 cites W2139098448 @default.
• W2058289451 cites W2141869612 @default.
• W2058289451 cites W2149967205 @default.
• W2058289451 cites W2156179144 @default.
• W2058289451 cites W2157999078 @default.
• W2058289451 cites W2158056147 @default.
• W2058289451 cites W2163408738 @default.
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• W2058289451 cites W2324111799 @default.
• W2058289451 cites W2333074204 @default.
• W2058289451 cites W4255535345 @default.
• W2058289451 doi "https://doi.org/10.1111/j.1523-1755.2005.00155.x" @default.
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