Role of apoptosis in the progression of secondary hyperparathyroidism
In many tissues, cell proliferation is counterbalanced by apoptosis. Hyperparathyroidism is one of the most important complications in long term dialysis patients and is characterized by remarkable cell proliferation of parathyroid cells. Therefore, alteration in the regulation and clearance of exce...
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| Published in | Nihon Jinzo Gakkai shi Vol. 38; no. 8; pp. 323 - 328 |
|---|---|
| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | Japanese |
| Published |
Japan
Japanese Society of Nephrology
1996
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0385-2385 1884-0728 |
| DOI | 10.14842/jpnjnephrol1959.38.323 |
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| Abstract | In many tissues, cell proliferation is counterbalanced by apoptosis. Hyperparathyroidism is one of the most important complications in long term dialysis patients and is characterized by remarkable cell proliferation of parathyroid cells. Therefore, alteration in the regulation and clearance of excess cells by apoptosis may occur in hyperparathyroidism. In the present study, we evaluated the expression of Ki-67 (proliferative cell associated protein) and Bcl-2 (apoptosis-preventing molecules), and the number of apoptotic cells in the nodular lesion of parathyroid glands with secondary hyperpara thyroidism (2°HPT), as compared with primary hyperparathyroidism(1°HPT) for clarification of the role of apoptosis in the development of 2° HPT. The number of Ki-67+ cells was remarkably increased in 2°HPT (12.02 ± 10.87, mean ± SD) compared to in 1° HPT (0.81 ± 0.53) (p<0.01). However, the number of apoptotic cells was significantly decreased in 2° HPT(0.10+0.06) compared to in 1° HPT(0.31±0.19)(p<0.05). To the contrary, Bcl-2+ cells were increased in 2°HPT(0.35+ 0.23) compared to in 1° HPT(0.10 ± 0.13) (plt;0.05). These results suggest that the mechanisms of parathyroid cell proliferation are different in each nodular lesion of 1° HPT and 2° HPT. Furthermore, the remarkable proliferation of parathyroid glands may have been due to the reduction of the apoptotic process via Bcl-2 expression in 2°HPT. |
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| AbstractList | In many tissues, cell proliferation is counterbalanced by apoptosis. Hyperparathyroidism is one of the most important complications in long term dialysis patients and is characterized by remarkable cell proliferation of parathyroid cells. Therefore, alteration in the regulation and clearance of excess cells by apoptosis may occur in hyperparathyroidism. In the present study, we evaluated the expression of Ki-67 (proliferative cell associated protein) and Bcl-2(apoptosis-preventing molecules), and the number of apoptotic cells in the nodular lesion of parathyroid glands with secondary hyperparathyroidism(2 degrees HPT), as compared with primary hyperparathyroidism(1 degree HPT) for clarification of the role of apoptosis in the development of 2 degrees HPT. The number of Ki-67+ cells was remarkably increased in 2 degrees HPT(12.02 +/- 10.87, mean +/- SD) compared to in 1 degree HPT(0.81 +/- 0.53) (p < 0.01). However, the number of apoptotic cells was significantly decreased in 2 degrees HPT(0.10 +/- 0.06) compared to in 1 degree HPT(0.31 +/- 0.19) (p < 0.05). To the contrary, Bcl-2+ cells were increased in 2 degrees HPT(0.35 +/- 0.23) compared to in 1 degree HPT(0.10 +/- 0.13) (p < 0.05). These results suggest that the mechanisms of parathyroid cell proliferation are different in each nodular lesion of 1 degree HPT and 2 degrees HPT. Furthermore, the remarkable proliferation of parathyroid glands may have been due to the reduction of the apoptotic process via Bcl-2 expression in 2 degrees HPT.In many tissues, cell proliferation is counterbalanced by apoptosis. Hyperparathyroidism is one of the most important complications in long term dialysis patients and is characterized by remarkable cell proliferation of parathyroid cells. Therefore, alteration in the regulation and clearance of excess cells by apoptosis may occur in hyperparathyroidism. In the present study, we evaluated the expression of Ki-67 (proliferative cell associated protein) and Bcl-2(apoptosis-preventing molecules), and the number of apoptotic cells in the nodular lesion of parathyroid glands with secondary hyperparathyroidism(2 degrees HPT), as compared with primary hyperparathyroidism(1 degree HPT) for clarification of the role of apoptosis in the development of 2 degrees HPT. The number of Ki-67+ cells was remarkably increased in 2 degrees HPT(12.02 +/- 10.87, mean +/- SD) compared to in 1 degree HPT(0.81 +/- 0.53) (p < 0.01). However, the number of apoptotic cells was significantly decreased in 2 degrees HPT(0.10 +/- 0.06) compared to in 1 degree HPT(0.31 +/- 0.19) (p < 0.05). To the contrary, Bcl-2+ cells were increased in 2 degrees HPT(0.35 +/- 0.23) compared to in 1 degree HPT(0.10 +/- 0.13) (p < 0.05). These results suggest that the mechanisms of parathyroid cell proliferation are different in each nodular lesion of 1 degree HPT and 2 degrees HPT. Furthermore, the remarkable proliferation of parathyroid glands may have been due to the reduction of the apoptotic process via Bcl-2 expression in 2 degrees HPT. In many tissues, cell proliferation is counterbalanced by apoptosis. Hyperparathyroidism is one of the most important complications in long term dialysis patients and is characterized by remarkable cell proliferation of parathyroid cells. Therefore, alteration in the regulation and clearance of excess cells by apoptosis may occur in hyperparathyroidism. In the present study, we evaluated the expression of Ki-67 (proliferative cell associated protein) and Bcl-2 (apoptosis-preventing molecules), and the number of apoptotic cells in the nodular lesion of parathyroid glands with secondary hyperpara thyroidism (2°HPT), as compared with primary hyperparathyroidism(1°HPT) for clarification of the role of apoptosis in the development of 2° HPT. The number of Ki-67+ cells was remarkably increased in 2°HPT (12.02 ± 10.87, mean ± SD) compared to in 1° HPT (0.81 ± 0.53) (p<0.01). However, the number of apoptotic cells was significantly decreased in 2° HPT(0.10+0.06) compared to in 1° HPT(0.31±0.19)(p<0.05). To the contrary, Bcl-2+ cells were increased in 2°HPT(0.35+ 0.23) compared to in 1° HPT(0.10 ± 0.13) (plt;0.05). These results suggest that the mechanisms of parathyroid cell proliferation are different in each nodular lesion of 1° HPT and 2° HPT. Furthermore, the remarkable proliferation of parathyroid glands may have been due to the reduction of the apoptotic process via Bcl-2 expression in 2°HPT. In many tissues, cell proliferation is counterbalanced by apoptosis. Hyperparathyroidism is one of the most important complications in long term dialysis patients and is characterized by remarkable cell proliferation of parathyroid cells. Therefore, alteration in the regulation and clearance of excess cells by apoptosis may occur in hyperparathyroidism. In the present study, we evaluated the expression of Ki-67 (proliferative cell associated protein) and Bcl-2(apoptosis-preventing molecules), and the number of apoptotic cells in the nodular lesion of parathyroid glands with secondary hyperparathyroidism(2 degrees HPT), as compared with primary hyperparathyroidism(1 degree HPT) for clarification of the role of apoptosis in the development of 2 degrees HPT. The number of Ki-67+ cells was remarkably increased in 2 degrees HPT(12.02 +/- 10.87, mean +/- SD) compared to in 1 degree HPT(0.81 +/- 0.53) (p < 0.01). However, the number of apoptotic cells was significantly decreased in 2 degrees HPT(0.10 +/- 0.06) compared to in 1 degree HPT(0.31 +/- 0.19) (p < 0.05). To the contrary, Bcl-2+ cells were increased in 2 degrees HPT(0.35 +/- 0.23) compared to in 1 degree HPT(0.10 +/- 0.13) (p < 0.05). These results suggest that the mechanisms of parathyroid cell proliferation are different in each nodular lesion of 1 degree HPT and 2 degrees HPT. Furthermore, the remarkable proliferation of parathyroid glands may have been due to the reduction of the apoptotic process via Bcl-2 expression in 2 degrees HPT. |
| Author | YOSHIMURA, Ashio IWASAKI, Shigeki SUGENOYA, Youichi IDEURA, Terukuni INUI, Kiyoko UDA, Susumu TAIRA, Takayasu |
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| References | 2. Wyllie AH, Kerr JFR, Currie AR: Cell death: the significance of apoptosis. Int Rev Cytol 68: 251-306, 1980 4. Tsujimoto Y, Cossman J, Jaffe E, Croce CM: Involvement of the bcl-2 gene in follicular lymphoma. Science 228: 1440-1443, 1985 19. Yin XM, Oltvai ZN, Korsmeyer SJ: BH 1 and BH2 domeins of Bcl - 2 are required for inhibition of apoptosis and heterodimerization with Bax. Nature 369: 321-323, 1994 23. Bissonnette RP, Echeverri F, Mahboubi A, Green DR: Apoptotic cell death induced by c-myc is inhibited by bcl-2. Nature 359: 552-554, 1992 24. Fanidi A, Harrington EA, Evan G1: Cooperative interaction between c-myc and bcl - 2 proto-oncogenes. Nature 359: 554-556, 1992 14. Falchetti A, Bale AE, Amorosi A, Bordi C, Cicci P, Bandini S, Marx SJ, Brandi ML: Progression of uremic hyperparathyroidism involves allelic loss on chromosome 11. J Clin Endocrinol Metab 76: 139-144, 1993 3. Raff MC: Social controls on cell survival and cell death. Nature 356: 397-400, 1992 5. Vaux DL, Cory S, Adams JM: Bcl-2 gene promotes haemopoietic cell survival and cooperates with c-myc to immortalize pre-B cells. Nature 335: 440-442, 1988 7. Yoshimura A, Taira T, Ideura T: Expression of apoptosis-related molecules in acute renal injury. Exp Nephrol 4: 15-18, 1996 16. Motokura T, Bloom T, Kim HG, Juppner H, Ruderman JV, Kronenberg HM, Arnold A: A novel cyclin encoded by a bcl 1-linked candidate oncogene. Nature 350: 512-515, 1991 6. Borzillo GV, Endo K, Tsujimoto Y: Bcl-2 confers growth and survival advantage to interleukin 7-dependent early pre-B cells which become factor independent by a multiple process in culture. Oncogene 7: 869-876, 1992 8. Uda S, Yoshimura A, Inui K, Sugenoya Y, Nabeshima K, Taira T, Ideura T: Glomerular expression of apoptosis-related molecules in rats with mesangial proliferative nephritis (abstract). J Am Soc Nephrol 5: 797, 1994 20. Fukagawa M, Yi H, Kurokawa K: Calcitriol induces apoptosis of hyperplastic parathyroid cells in uremic rats. (abstract) J Am Soc Nephrol 2: 635, 1991 12. Szabo A, Merke J, Beier E, Mall G, Ritz E: 1, 25(OH)2 vitamin D3 inhibits parathyroid cell proliferation in experimental uremia. Kidney Int 35: 1049-1956, 1989 1. Kerr,JFR,Wyilie AH,Currie AR:Apoptosis:A basic biological phenomenon with wide-ranging implications in tissue kinetics.Br J Cancer 26:239-257,1972 18. Oltvai ZN, Milliman CL, Korsmeyer SJ: Bcl - 2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programed cell death. Cell 74: 609-619, 1993 15. Arnold A, Brown MF, Urena P, Gaz RD, Sarfati E, Drüeke TB: Monoclonality of parathyroid tumors in chronic renal failure and in primary parathyroid hyperplasia. J Clin Invest 95: 2047-2053, 1995 21. Evan Gl: Induction of apoptosis in fibroblasts by cmyc protein. Cell 69: 119-128, 1992 13. Duh QY, Gum ET, Sancho JJ, Levin KE, Raper SE, Clark OH: Epidermal growth factor receptors in parathyroid tumors. J Surg Res 40: 569-573, 1986 11. Gavrieli Y, Sherman Y, Ben-Sasson SA: Identification of programmed cell death in situ via specific labeling of nuclear DNA fragmentation. J Cell Biol 119: 493-501, 1992 22. Shi Y, Glynn JM, Guilbert LJ, Cotter TG, Bissonnette RP, Green DR: Role for c-myc in activation-induced apoptotic cell death in Tcell hybridomas. Science 257: 212-214, 1992 9. Yoshimura A, Sugenoya Y, Uda S, Inui K, Iwasaki S, Taira T, Ideura T: Expression of apoptosis-preventing Bcl-2 protein and -inducing Fas antigen in glomeruli of IgA nephropathy. Contrib Nephrol 118: 48-53, 1996 17. Majino G, Joris I: Apoptosis, oncosis and necrosis An overview of cell death. Am J Pathol 146: 3-15, 1995 10. Thiele J, Fischer R: Bone marrow tissue and proliferation markers: results and general problems. Virchows Archiv A Pathol Anat 423: 409-416, 1993 |
| References_xml | – reference: 1. Kerr,JFR,Wyilie AH,Currie AR:Apoptosis:A basic biological phenomenon with wide-ranging implications in tissue kinetics.Br J Cancer 26:239-257,1972 – reference: 21. Evan Gl: Induction of apoptosis in fibroblasts by cmyc protein. Cell 69: 119-128, 1992 – reference: 15. Arnold A, Brown MF, Urena P, Gaz RD, Sarfati E, Drüeke TB: Monoclonality of parathyroid tumors in chronic renal failure and in primary parathyroid hyperplasia. J Clin Invest 95: 2047-2053, 1995 – reference: 17. Majino G, Joris I: Apoptosis, oncosis and necrosis An overview of cell death. Am J Pathol 146: 3-15, 1995 – reference: 7. Yoshimura A, Taira T, Ideura T: Expression of apoptosis-related molecules in acute renal injury. Exp Nephrol 4: 15-18, 1996 – reference: 11. Gavrieli Y, Sherman Y, Ben-Sasson SA: Identification of programmed cell death in situ via specific labeling of nuclear DNA fragmentation. J Cell Biol 119: 493-501, 1992 – reference: 24. Fanidi A, Harrington EA, Evan G1: Cooperative interaction between c-myc and bcl - 2 proto-oncogenes. Nature 359: 554-556, 1992 – reference: 14. Falchetti A, Bale AE, Amorosi A, Bordi C, Cicci P, Bandini S, Marx SJ, Brandi ML: Progression of uremic hyperparathyroidism involves allelic loss on chromosome 11. J Clin Endocrinol Metab 76: 139-144, 1993 – reference: 3. Raff MC: Social controls on cell survival and cell death. Nature 356: 397-400, 1992 – reference: 23. Bissonnette RP, Echeverri F, Mahboubi A, Green DR: Apoptotic cell death induced by c-myc is inhibited by bcl-2. Nature 359: 552-554, 1992 – reference: 2. Wyllie AH, Kerr JFR, Currie AR: Cell death: the significance of apoptosis. Int Rev Cytol 68: 251-306, 1980 – reference: 13. Duh QY, Gum ET, Sancho JJ, Levin KE, Raper SE, Clark OH: Epidermal growth factor receptors in parathyroid tumors. J Surg Res 40: 569-573, 1986 – reference: 6. Borzillo GV, Endo K, Tsujimoto Y: Bcl-2 confers growth and survival advantage to interleukin 7-dependent early pre-B cells which become factor independent by a multiple process in culture. Oncogene 7: 869-876, 1992 – reference: 5. Vaux DL, Cory S, Adams JM: Bcl-2 gene promotes haemopoietic cell survival and cooperates with c-myc to immortalize pre-B cells. Nature 335: 440-442, 1988 – reference: 4. Tsujimoto Y, Cossman J, Jaffe E, Croce CM: Involvement of the bcl-2 gene in follicular lymphoma. Science 228: 1440-1443, 1985 – reference: 8. Uda S, Yoshimura A, Inui K, Sugenoya Y, Nabeshima K, Taira T, Ideura T: Glomerular expression of apoptosis-related molecules in rats with mesangial proliferative nephritis (abstract). J Am Soc Nephrol 5: 797, 1994 – reference: 9. Yoshimura A, Sugenoya Y, Uda S, Inui K, Iwasaki S, Taira T, Ideura T: Expression of apoptosis-preventing Bcl-2 protein and -inducing Fas antigen in glomeruli of IgA nephropathy. Contrib Nephrol 118: 48-53, 1996 – reference: 10. Thiele J, Fischer R: Bone marrow tissue and proliferation markers: results and general problems. Virchows Archiv A Pathol Anat 423: 409-416, 1993 – reference: 12. Szabo A, Merke J, Beier E, Mall G, Ritz E: 1, 25(OH)2 vitamin D3 inhibits parathyroid cell proliferation in experimental uremia. Kidney Int 35: 1049-1956, 1989 – reference: 16. Motokura T, Bloom T, Kim HG, Juppner H, Ruderman JV, Kronenberg HM, Arnold A: A novel cyclin encoded by a bcl 1-linked candidate oncogene. Nature 350: 512-515, 1991 – reference: 18. Oltvai ZN, Milliman CL, Korsmeyer SJ: Bcl - 2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programed cell death. Cell 74: 609-619, 1993 – reference: 19. Yin XM, Oltvai ZN, Korsmeyer SJ: BH 1 and BH2 domeins of Bcl - 2 are required for inhibition of apoptosis and heterodimerization with Bax. Nature 369: 321-323, 1994 – reference: 22. Shi Y, Glynn JM, Guilbert LJ, Cotter TG, Bissonnette RP, Green DR: Role for c-myc in activation-induced apoptotic cell death in Tcell hybridomas. Science 257: 212-214, 1992 – reference: 20. Fukagawa M, Yi H, Kurokawa K: Calcitriol induces apoptosis of hyperplastic parathyroid cells in uremic rats. (abstract) J Am Soc Nephrol 2: 635, 1991 |
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| SubjectTerms | Adult Apoptosis - physiology Cell Division Female Humans Hyperparathyroidism, Secondary - pathology Ki-67 Antigen - analysis Male Middle Aged Parathyroid Glands - pathology Proto-Oncogene Proteins - analysis secondary hyperparathyroidism, primary hyperparathyroidism, apoptosis, Ki-67, Bcl-2 |
| Title | Role of apoptosis in the progression of secondary hyperparathyroidism |
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