apoptosis in cell turnover
Cell proliferation and programmed cell death play an important roles in the maintenance of tissue dynamics in both physiologic and pathologic status. Increased proliferation and/or decreased programmed cell death or apoptosis can result in “abnormal proliferation”. On the other hand, decreased proli...
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Published in | Journal of the Japan Society of the Reticuloendothelial System Vol. 35; no. 5; pp. 223 - 228 |
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Main Authors | , , , |
Format | Journal Article |
Language | Japanese |
Published |
The Japanese Society for Lymphoreticular Tissue Research
1995
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Subjects | |
Online Access | Get full text |
ISSN | 0386-9725 1883-6801 |
DOI | 10.3960/jslrt1961.35.223 |
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Abstract | Cell proliferation and programmed cell death play an important roles in the maintenance of tissue dynamics in both physiologic and pathologic status. Increased proliferation and/or decreased programmed cell death or apoptosis can result in “abnormal proliferation”. On the other hand, decreased proliferation and/or increased apoptosis may cause “loss of the cells”. Therefore, simultaneous analysis of both cell proliferation and apoptosis can provide important information on understanding physiology and pathology of various tissues. Recent advent in immunohistochemistry including ki67 immunostain with microwave irradiation for antigen retrieval and MIB-1 monoclonal antibody and development of 3'-OH nick end labeling technique or TUNEL method made it possible to assess cell proliferation and apoptosis in formalin-fixed and paraffin-embedded materials with reasonable accuracy. We applied these methods to human adrenal cortex and its disor-ders and gastric mucosa with or without atrophy or intestinal metaplasia in order to understand tissue dynamics. In the human adrenal glands, apoptosis appears to play important roles in the maintenance of organized cortical cell turnover, i.e., centripetal movement of the cortical cells or cell proliferation in the outer fasciculata and cell death in the zona glomerulosa and the zona reticularis, and in tumor cell dynamics in adrenocortical neoplasms. In non-neoplastic human gastric mucosa, marked increase of the number of the cells positive for both Ki67 and 3'-OH nick end labeling was observed in the gastric glands associated with incomplete intestinal metaplasia. In addition, marked mRNA hybridization signals of p53 was detected in the cells undergoing apoptosis in these glands. Gastric glands associated with incomplete intestinal metaplasia are therefore characterized by increased cells turnover and possibly p53 induced apoptosis. |
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AbstractList | Cell proliferation and programmed cell death play an important roles in the maintenance of tissue dynamics in both physiologic and pathologic status. Increased proliferation and/or decreased programmed cell death or apoptosis can result in “abnormal proliferation”. On the other hand, decreased proliferation and/or increased apoptosis may cause “loss of the cells”. Therefore, simultaneous analysis of both cell proliferation and apoptosis can provide important information on understanding physiology and pathology of various tissues. Recent advent in immunohistochemistry including ki67 immunostain with microwave irradiation for antigen retrieval and MIB-1 monoclonal antibody and development of 3'-OH nick end labeling technique or TUNEL method made it possible to assess cell proliferation and apoptosis in formalin-fixed and paraffin-embedded materials with reasonable accuracy. We applied these methods to human adrenal cortex and its disor-ders and gastric mucosa with or without atrophy or intestinal metaplasia in order to understand tissue dynamics. In the human adrenal glands, apoptosis appears to play important roles in the maintenance of organized cortical cell turnover, i.e., centripetal movement of the cortical cells or cell proliferation in the outer fasciculata and cell death in the zona glomerulosa and the zona reticularis, and in tumor cell dynamics in adrenocortical neoplasms. In non-neoplastic human gastric mucosa, marked increase of the number of the cells positive for both Ki67 and 3'-OH nick end labeling was observed in the gastric glands associated with incomplete intestinal metaplasia. In addition, marked mRNA hybridization signals of p53 was detected in the cells undergoing apoptosis in these glands. Gastric glands associated with incomplete intestinal metaplasia are therefore characterized by increased cells turnover and possibly p53 induced apoptosis. |
Author | Nagura, Hiroshi Kimura, Kenji Imatani, Akira Sasano, Hironobu |
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References | 1) Thompson CB: Apoptosis in the pathogenesis and treatment of disease Science. 267: 1456-1462 1995 3) Sasano H, Imatani A, Shizawa S, Suzuki T, Nagura H: Cell proliferation and apoptosis in normal and pathologic human adrenal. Modern Pathol 8: 11-17 1995 2) 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 4) Fritsche M, Haessler C, Brandner G: Induction of nuclear accumulation of the tumor suppressor protein p 53 by DNA damaging agents. Oncogene 8: 307-318 1993 5) Sasano H, Goukon Y, Nishihira T, Nagura H, In situ hybridization of p 53 tumur suppressor gene in human esophageal carcinoma. Am J Pathol 141: 545-550 1992 |
References_xml | – reference: 1) Thompson CB: Apoptosis in the pathogenesis and treatment of disease Science. 267: 1456-1462 1995 – reference: 3) Sasano H, Imatani A, Shizawa S, Suzuki T, Nagura H: Cell proliferation and apoptosis in normal and pathologic human adrenal. Modern Pathol 8: 11-17 1995 – reference: 5) Sasano H, Goukon Y, Nishihira T, Nagura H, In situ hybridization of p 53 tumur suppressor gene in human esophageal carcinoma. Am J Pathol 141: 545-550 1992 – reference: 2) 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: 4) Fritsche M, Haessler C, Brandner G: Induction of nuclear accumulation of the tumor suppressor protein p 53 by DNA damaging agents. Oncogene 8: 307-318 1993 |
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