Cell surface modifications are fundamental for the correct and fast removal of apoptotic cells. These changes include the appearance of tethering molecules on the surface of apoptotic cells, the externalization of PS, oxidation of phospholipids and qualitative and quantitative changes in surface sugars and ICAM-3. Phagocytes, both professional and non-professional, use specific receptors that bind to the apoptotic cells either directly or through bridging molecules. In non-pathological conditions, apoptotic cells are normally cleared via an anti-inflammatory pathway. In contrast, the uptake and removal of necrotic cells normally involves inflammation and an immune response. Besides the “eat me” signals on the dying cells, phagocytes can also recognize “leave-me-alone” signals on healthy cells. The correct repertoire of molecules exposed on the cell surfaces prevents the engulfment of living undamaged cells. Thus, any factors influencing cell surface molecule expression on both phagocytes and/or apoptotic cells can in turn affect recognition of living and/or apoptotic cells. One such factor is cigarette smoke, which contain highly reactive carbonyls, which can modify proteins that directly or indirectly affect cellular functions. Moreover cigarette smoke is a major etiological factor in the development of COPD, in which apoptosis and defective PACs play a fundamental role. Another environmental factor that may interfere with the normal correct exposure of molecules on cell surfaces is exposure to (S)MFs. Despite the multiplicity of experimental conditions (i.e. in vitro or in vivo models, intensity and type of field, time of exposure, metabolic state of the cells, etc), converging data indicate that the primary site of action of (S)MFs and (E)MFs is the plasma membrane: i.e. they affect the electrochemical balance of the membrane, the distribution of membrane proteins and membrane receptors, cell-cell and cell-matrix junctions, sugar residues

Environmental Factors Affecting Phagocytosisof Dying Cells: Smoking and StaticMagnetic Fields

DINI, Luciana;
2009-01-01

Abstract

Cell surface modifications are fundamental for the correct and fast removal of apoptotic cells. These changes include the appearance of tethering molecules on the surface of apoptotic cells, the externalization of PS, oxidation of phospholipids and qualitative and quantitative changes in surface sugars and ICAM-3. Phagocytes, both professional and non-professional, use specific receptors that bind to the apoptotic cells either directly or through bridging molecules. In non-pathological conditions, apoptotic cells are normally cleared via an anti-inflammatory pathway. In contrast, the uptake and removal of necrotic cells normally involves inflammation and an immune response. Besides the “eat me” signals on the dying cells, phagocytes can also recognize “leave-me-alone” signals on healthy cells. The correct repertoire of molecules exposed on the cell surfaces prevents the engulfment of living undamaged cells. Thus, any factors influencing cell surface molecule expression on both phagocytes and/or apoptotic cells can in turn affect recognition of living and/or apoptotic cells. One such factor is cigarette smoke, which contain highly reactive carbonyls, which can modify proteins that directly or indirectly affect cellular functions. Moreover cigarette smoke is a major etiological factor in the development of COPD, in which apoptosis and defective PACs play a fundamental role. Another environmental factor that may interfere with the normal correct exposure of molecules on cell surfaces is exposure to (S)MFs. Despite the multiplicity of experimental conditions (i.e. in vitro or in vivo models, intensity and type of field, time of exposure, metabolic state of the cells, etc), converging data indicate that the primary site of action of (S)MFs and (E)MFs is the plasma membrane: i.e. they affect the electrochemical balance of the membrane, the distribution of membrane proteins and membrane receptors, cell-cell and cell-matrix junctions, sugar residues
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11587/332951
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