scholarly journals The Effects of Interleukin(IL)-4 and IL-10 on Macrophage Growth-Stimulating Activities of Oxidized Low Density Lipoprotein(LDL), Acetylated LDL and Macrophage Colony-Stimulating Factor: The Activity of Oxidized LDL Is Refractory to the Inhibitory Cytokines.

1999 ◽  
Vol 22 (9) ◽  
pp. 1002-1006
Author(s):  
Toshinori SASAKI ◽  
Seikoh HORIUCHI ◽  
Masatoshi YAMAZAKI ◽  
Satoru YUI
Keyword(s):  
Oxidized Ldl ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Colony Stimulating Factor ◽  
Oxidized Low Density Lipoprotein ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

Comparison of macrophage responses to oxidized low-density lipoprotein and macrophage colony-stimulating factor (M-CSF or CSF-1)

2001 ◽  
Vol 354 (1) ◽  
pp. 179-187 ◽  
Author(s):  
John A. HAMILTON ◽  
Robert BYRNE ◽  
Wendy JESSUP ◽  
Varuni KANAGASUNDARAM ◽  
Genevieve WHITTY
Keyword(s):  
Dna Synthesis ◽  
Essential Role ◽  
Foam Cell ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Colony Stimulating Factor ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

Modification of low-density lipoprotein (LDL), for example by oxidation, could be involved in foam cell formation and proliferation observed in atherosclerotic lesions. Macrophage colony-stimulating factor (CSF-1 or M-CSF) has been implicated in foam cell development. It has been reported previously that oxidized LDL (ox.LDL) and CSF-1 synergistically stimulate DNA synthesis in murine bone-marrow-derived macrophages (BMM). The critical signal-transduction cascades responsible for the proliferative response to ox.LDL, as well as their relationship to those mediating CSF-1 action, are unknown. We report here that ox.LDL stimulated extracellular signal-regulated protein kinase (ERK)-1, ERK-2 and phosphoinositide 3-kinase activities in BMM but to a weaker extent than optimal CSF-1 concentrations at the time points examined. Inhibitor studies suggested at least a partial role for these kinases, as well as p70 S6-kinase, in ox.LDL-induced macrophage survival and DNA synthesis. For the DNA synthesis response to CSF-1, the degree of inhibition by PD98059, wortmannin and rapamycin was significant at low CSF-1 concentrations but was reduced as the CSF-1 dose increased. Using BMM from CSF-1-deficient mice (op/op) and a neutralizing antibody approach, we found no evidence for an essential role for endogenous CSF-1 in ox.LDL-mediated survival or DNA synthesis; likewise, with the same approaches, no evidence was obtained for an essential role for endogenous granulocyte/macrophage-CSF in ox.LDL-mediated macrophage survival and, in contrast with the literature, ox.LDL-induced macrophage DNA synthesis.

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