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Transcript
anism. 37 Tox Appi Haslett C, RAF, Hanson Wound SJ, Ross Am J Pathol Leslie CC, Respir CC, growth The 1975; Dis York: role Plenum of the Clark n Biology Publishing of Cor- factors K, Cook JL, in rat alveolar DNA synthesis 132:1246-52 DNA Mol ml were 12.9% type Mac- II cells. RJ. Heparin-binding in rat alveolar synthesis Biol RJ. 1990; 25.9%±4.5% ± 2.9% Similar which type and are present II We M.D.; A. Lee, M.D.; M.D.; Despite and the before alternative from ptosis, which senescent described blood or the stimulate mediators. effect of apoptosis control N.’ via number of with populations have shape change, but there was nonapoptotic to the apoptosis may also proinflammatory senting an contents inflammatory agents rate to in in pure were inhibit, of PMN aggregation or exclusion). For in loss vitro 13 mersmith 6S the Respiratory Hospital, Division, London, h in Department England. is cell PMN a modulatable contents, leads without the products, disposal to mac- release of thus repre- mechanism impor- 83:865-75 343:170-73 by programmed This leads mechanism M.D. PMN trypan blue resolving to recognition cell of intact senescent site or apoptosis inflamed death of the vitronectin the possible of PMN in the aged clear- is determined which aging PMN by macrophages adhesion signal the neutrophils mechanism important as PMN.’ “senescent via a mechanism and a macrophage receptor (VnR), sugars ties of activated and sought play in critical major 80%, indicating ml in the that PMN enhanced and TSP the aged acts of aged we with of aged maneuver) mechanism. Indeed, TSP on there the a was between in solution whether TSP PMNs played bridge” (1) ad- structures this uptake, secrete CD36, coated TSP-binding as a “molecular PMN to proper- PMNs. recognition macrophage: by known both include surfaces by recognition PMNs intercellular to that specific adhesive which recognition (downregulated evidence aged macrophages subsequent cell- by molecules of TSP/CD36-mediated inhibited role aged Since of macrophages macrophage of acids, for TSP, in macrophage specifically additional of suggested (TSP)-dependent receptors evidence over amino platelets. bear Attachment by involvement and basic thrombospondin amino hesion in fashion, (by Haslett, signaling mechanisms was of macrophage phagocytosis inhibition When aging the However, that culture, Chris phagocytosis is an 13:, integrin, suggested causing and self” and phagocytosis which the Arg-Gly-Asp TSP PMNs Hogg, acrophage the at 5 s.g/ in solution in the untreated *From 5From of inflamma- resolution. Nancy from to be without integrity after at sites macrophage 1989; 1990; surface (LPS), granulocyte-mac(GM-CSF), and chemotaccounterpart FMLP were of membrane example, Invest Savill, appeared removal. with John inhibit a concentration-dependent in was apoptosis Macrophage Vitronectin Receptor, CD36, and Thrombospondin Cooperate in Recognition of Neutrophils Undergoing Programmed Cell Death* were and packaging included apoptosis ± 0.9% roles. included stimulated aged PMNs into apoptotic to macrophage vitro, bacterial lipopolysaccharide rophage colony-stimulating factor t/c peptide C5a and its synthetic the the declined which as an “inert” prior of apoptosis intact injury-limiting in inflammatory ance for cells loss fraction, serve for neutrophil all found functions functional apoptotic rate PMN of the (PMNs) PMNs and the rate of PMN apoptotic exclusion. When centrifugation subpopulations, restricted appear and stimulated release of granule enzymes, no evidence of loss of membrane integrity as by trypan blue by counterflow PMN “packaging” further M apoptotic not implications of the were 6.1% intact proinflammatory of aging on the PMN appearance apo- the of does release important PMNs, of of PM Ns aging in vitro. These functions phagocytosis of opsonized zymosan, chemotaxis, assessed separated undergo that properties mediators important the aging sites, recognition to in concentration that by removal 1 J Clin (PMN) which ingestion macrophage would also of inflammation. concert by mechanisms The functional inflammatory neutrophil inflamed Macrophage a novel in high that, 2 Nature sites is poorly underthat PMNs inevitably local macrophages, an by from 1 ig/ml were M.D.; of to macrophage leads occurs A removal been PM PMNs to their has fate derived potential fate at inflamed it is widely assumed Although at g/ml REFERENCES in M.D. their disintegrate 10 at Mediators j S. Savill, K. Whyte, injurious contents, stood. M. at reductions hypothesize process Apoptosis (Programmed Cell Death) and Functional Changes Aging Neutrophils* L. Meagher, LPS with GM-CSF, C5a, and FMLP, that the process of apoptosis can be PMN longevity can be prolonged by factors suggested tant C. Haslett, and ± SE; 100 ng/ (mean with tion. 2:99-106 by Inflammatory apoptotic treated treatment modulated rophage Modulation ± 4.8% apoptotic, apoptotic, following that K, Mason stimulate Mason were cell apoptotic. in wound 78:71-91 1985; Cell macrophage 43.3% populations populations 7) whereas = seen McCormick-Shannon Am J Respir cells. In: and Cellular Molecular 7. New B. stimulate Rev Leslie PMN of inflammation. McCormick-Shannon rophages 40 The eds. Chapter repair. Am 51:475-87 Resolution 1988:185-211 Leibovich 39 1979; PM. PM, Repair, poration, 38 Pharm Hanson of Medicine, Ham- School (N.H.), the Department of Medicine, (IS., C.H.). and London, England. 33rd the Annual Imperial Thomas Downloaded From: http://journal.publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21626/ on 05/03/2017 Royal Postgraduate Cancer L Petty Aspen Medical Research Lung Fund Conference