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Published on: July 20, 2016
Uptake of high density lipoprotein (HDL) cholesteryl esters by human acute leukemia cells
Romelia Pinheiro Gonçalves1, Debora Garcia Rodrigues, Raul C Maranhão
1The Heart Institute (InCor) of the São Paulo University Medical School Hospital, Laboratório de Metabolismo de Lípides. Av. Dr. Enéas de Carvalho Aguiar, 44, 1 ss, São Paulo 05403-000, Brazil.
Hypocholesterolemia is a common finding in patients with acute leukemia (AL). The aim of this study is to investigate if blast myeloid and lynfoid cells take up more high density lipoprotein (HDL) cholesteryl esters than normal cells of the same origin. The HDL-cholesteryl ester uptake followed a kinetic saturation process. Higher maximal velocity rates were found in lymphoblasts and myeloblasts compared to normal cells (Vmax=3.51+/-0.30/3.61+/-0.16 and 2.54+/-0.12/2.28+/-0.12 microg/mg, respectively). High density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C) and total cholesterol were significantly lower in AL patients (p<0.05); no differences were observed in triglyceride or VLDL-C levels. In conclusion, low HDL-C levels observed in AL may be related to an overexpression of a selective HDL-cholesteryl ester putative site.
Hypocholesterolemia is a common finding in patients with acute leukemia (AL). The aim of this study is to investigate if blast myeloid and lynfoid cells take up more high density lipoprotein (HDL) cholesteryl esters than normal cells of the same origin. The HDL-cholesteryl ester uptake followed a kinetic saturation process. Higher maximal velocity rates were found in lymphoblasts and myeloblasts compared to normal cells (Vmax=3.51+/-0.30/3.61+/-0.16 and 2.54+/-0.12/2.28+/-0.12 microg/mg, respectively). High density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C) and total cholesterol were significantly lower in AL patients (p<0.05); no differences were observed in triglyceride or VLDL-C levels. In conclusion, low HDL-C levels observed in AL may be related to an overexpression of a selective HDL-cholesteryl ester putative site.
