Effect of exposure of human monocyte-derived macrophages to high, versus normal, glucose on subsequent lipid accumulation from glycated and acetylated low-density lipoproteins
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Effect of exposure of human monocyte-derived macrophages to high, versus normal, glucose on subsequent lipid accumulation from glycated and acetylated low-density lipoproteins. / Moheimani, Fatemeh; Tan, Joanne T M; Brown, Bronwyn E; Heather, Alison K; van Reyk, David M; Davies, Michael Jonathan.
In: Journal of Diabetes Research, Vol. 2011, 2011, p. 851280.Research output: Contribution to journal › Journal article › Research › peer-review
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T1 - Effect of exposure of human monocyte-derived macrophages to high, versus normal, glucose on subsequent lipid accumulation from glycated and acetylated low-density lipoproteins
AU - Moheimani, Fatemeh
AU - Tan, Joanne T M
AU - Brown, Bronwyn E
AU - Heather, Alison K
AU - van Reyk, David M
AU - Davies, Michael Jonathan
PY - 2011
Y1 - 2011
N2 - During atherosclerosis monocyte-derived macrophages accumulate cholesteryl esters from low-density lipoproteins (LDLs) via lectin-like oxidised LDL receptor-1 (LOX-1) and class AI and AII (SR-AI, SR-AII) and class B (SR-BI, CD36) scavenger receptors. Here we examined the hypothesis that hyperglycaemia may modulate receptor expression and hence lipid accumulation in macrophages. Human monocytes were matured into macrophages in 30 versus 5 mM glucose and receptor expression and lipid accumulation quantified. High glucose elevated LOX1 mRNA, but decreased SR-AI, SR-BI, LDLR, and CD36 mRNA. SR-BI and CD36 protein levels were decreased. Normo- and hyperglycaemic cells accumulated cholesteryl esters from modified LDL to a greater extent than control LDL, but total and individual cholesteryl ester accumulation was not affected by glucose levels. It is concluded that, whilst macrophage scavenger receptor mRNA and protein levels can be modulated by high glucose, these are not key factors in lipid accumulation by human macrophages under the conditions examined.
AB - During atherosclerosis monocyte-derived macrophages accumulate cholesteryl esters from low-density lipoproteins (LDLs) via lectin-like oxidised LDL receptor-1 (LOX-1) and class AI and AII (SR-AI, SR-AII) and class B (SR-BI, CD36) scavenger receptors. Here we examined the hypothesis that hyperglycaemia may modulate receptor expression and hence lipid accumulation in macrophages. Human monocytes were matured into macrophages in 30 versus 5 mM glucose and receptor expression and lipid accumulation quantified. High glucose elevated LOX1 mRNA, but decreased SR-AI, SR-BI, LDLR, and CD36 mRNA. SR-BI and CD36 protein levels were decreased. Normo- and hyperglycaemic cells accumulated cholesteryl esters from modified LDL to a greater extent than control LDL, but total and individual cholesteryl ester accumulation was not affected by glucose levels. It is concluded that, whilst macrophage scavenger receptor mRNA and protein levels can be modulated by high glucose, these are not key factors in lipid accumulation by human macrophages under the conditions examined.
KW - Antigens, CD36
KW - Atherosclerosis
KW - Base Sequence
KW - Cell Differentiation
KW - Cells, Cultured
KW - Cholesterol Esters
KW - DNA Primers
KW - Glucose
KW - Humans
KW - Lipid Metabolism
KW - Lipoproteins, LDL
KW - Macrophages
KW - RNA, Messenger
KW - Receptors, LDL
KW - Scavenger Receptors, Class A
KW - Scavenger Receptors, Class B
KW - Scavenger Receptors, Class E
U2 - 10.1155/2011/851280
DO - 10.1155/2011/851280
M3 - Journal article
C2 - 21904540
VL - 2011
SP - 851280
JO - Journal of Diabetes Research
JF - Journal of Diabetes Research
SN - 2314-6745
ER -
ID: 129669420