apoptosis in cell turnover

• Published in: Journal of the Japan Society of the Reticuloendothelial System Vol. 35; no. 5; pp. 223 - 228
• Main Authors: Nagura, Hiroshi, Kimura, Kenji, Imatani, Akira, Sasano, Hironobu
• Format: Journal Article
• Language: Japanese
• Published: The Japanese Society for Lymphoreticular Tissue Research 1995
• Subjects: adrenal; apoptosis; cell turnover; proliferation; stomach
• ISSN: 0386-9725; 1883-6801
• DOI: 10.3960/jslrt1961.35.223

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.