Co-Expression of BCL-2 and CD44S in Basal Layers of Human Ocular Surface Epithelia

Abstract

The regulating mechanism of life and death of cells is a closely coordinated process of adaptation and survival. Selective and controlled cell death is a dominant force in renewing the tissue composition of complex organisms. Elimination of unwanted cells occurs during the normal course of tissue differentiation and also when cells are damaged by various noxious forces.¹ The two major mechanisms of cell death are apoptosis (programmed cell death) and necrosis.² Apoptosis is an active process in which a central biochemical “program” is activated causing nuclear fragmentation, formation of a rigid apoptotic envelope, and shrinkage of the cells into small fragments that are then phagocytosed, often by surrounding parenchymal cells not usually involved in phagocytosis. In necrosis, cells are passive targets of extensive membrane damage, cell swelling, colloidal osmotic lysis, and release of cellular contents. In the development and differentiation of multicellular organisms, apoptosis is the preferred mechanism for eliminating unwanted cell population. In actively cycling cells, proliferation and apoptosis are two opposing pathways for regulating cellular activities. Dysregulation of apoptosis is an important factor in cancer, leading to proliferation of cells, with a mutation in genes favoring proliferation or blocking apoptosis.³ The cell cycle, which includes cellular proliferation and differentiation pathways, is regulated by multiple genes, some of which are oncogenes.^4,5 Oncogenes have been divided into two categories: genes that promote cellular proliferation and growth, and genes that regulate apoptosis.