Role of apoptosis in the progression of secondary hyperparathyroidism

• Published in: Nihon Jinzo Gakkai shi Vol. 38; no. 8; pp. 323 - 328
• Main Authors: INUI, Kiyoko, UDA, Susumu, YOSHIMURA, Ashio, SUGENOYA, Youichi, TAIRA, Takayasu, IDEURA, Terukuni, IWASAKI, Shigeki
• Format: Journal Article
• Language: Japanese
• Published: Japan Japanese Society of Nephrology 1996
• Subjects: 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
• ISSN: 0385-2385; 1884-0728
• DOI: 10.14842/jpnjnephrol1959.38.323

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.