PMN Apoptosis Research Articles

Macrophage Vitronectin Receptor, CD36, and Thrombospondin Cooperate in Recognition of Neutrophils Undergoing Programmed Cell Death

Macrophage phagocytosis of intact senescent neutrophils (PMNs) is an important mechanism of PMN clearance from the resolving inflamed site which is determined by programmed cell death or apoptosis in the aging PMN. 1 J Clin Invest. 1989; 83: 865-875 Crossref PubMed Scopus (1349) Google Scholar This leads to recognition of the aged PMN as “senescent self” and phagocytosis by macrophages via a mechanism in which the Arg-Gly-Asp adhesion signal and a macrophage β3 integrin, the vitronectin receptor (VnR), play critical roles. 2 Nature. 1990; 343: 170-173 Crossref PubMed Scopus (700) Google Scholar

The electro-pneumatic brake system for steam road service

A flow cytometric technique was used to detect apoptosis and necrosis of bovine polymorphonuclear neutrophil leukocytes (PMN) using fluorescein isothiocyanate labeled annexin-V and propidium iodide (PI). Isolation of PMN from the blood following lysis by water or NH4Cl resulted in false positive results for apoptosis. Therefore, a method was developed to identify living, apoptotic and necrotic PMN simultaneously in a single 100 μl blood sample. To establish a positive control for PMN apoptosis, the effect of cycloheximide, actinomycin D, diamide, buthionine sulfoximine and sodium arsenite, that have been described to induce apoptosis by various mechanisms was tested. Only actinomycin D induced a significant increase in the percentage of apoptotic PMN after 2 h. Incubation of blood for 6 h with cycloheximide, actinomycin D and buthionine sulfoximine resulted in a significant increase of apoptotic PMN compared to control values. Sodium arsenite, mainly caused necrosis after 6 h of incubation.