Modulation of the cellular expression of circulating advanced glycation end-product receptors in type 2 diabetic nephropathy
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Modulation of the cellular expression of circulating advanced glycation end-product receptors in type 2 diabetic nephropathy. / Sourris, Karly C; Harcourt, Brooke E; Penfold, Sally A; Yap, Felicia Y T; Morley, Amy L; Morgan, Philip E; Davies, Michael Jonathan; Baker, Scott T; Jerums, George; Forbes, Josephine M.
In: Journal of Diabetes Research, Vol. 2010, 2010, p. 974681.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Modulation of the cellular expression of circulating advanced glycation end-product receptors in type 2 diabetic nephropathy
AU - Sourris, Karly C
AU - Harcourt, Brooke E
AU - Penfold, Sally A
AU - Yap, Felicia Y T
AU - Morley, Amy L
AU - Morgan, Philip E
AU - Davies, Michael Jonathan
AU - Baker, Scott T
AU - Jerums, George
AU - Forbes, Josephine M
PY - 2010
Y1 - 2010
N2 - BACKGROUND: Advanced glycation end-products (AGEs) and their receptors are prominent contributors to diabetic kidney disease.METHODS: Flow cytometry was used to measure the predictive capacity for kidney impairment of the AGE receptors RAGE, AGE-R1, and AGE-R3 on peripheral blood mononuclear cells (PBMCs) in experimental models of type 2 diabetes (T2DM) fed varied AGE containing diets and in obese type 2 diabetic and control human subjects.RESULTS: Diets high in AGE content fed to diabetic mice decreased cell surface RAGE on PBMCs and in type 2 diabetic patients with renal impairment (RI). All diabetic mice had elevated Albumin excretion rates (AERs), and high AGE fed dbdb mice had declining Glomerular filtration rate (GFR). Cell surface AGE-R1 expression was also decreased by high AGE diets and with diabetes in dbdb mice and in humans with RI. PBMC expression of AGE R3 was decreased in diabetic dbdb mice or with a low AGE diet.CONCLUSIONS: The most predictive PBMC profile for renal disease associated with T2DM was an increase in the cell surface expression of AGE-R1, in the context of a decrease in membranous RAGE expression in humans, which warrants further investigation as a biomarker for progressive DN in larger patient cohorts.
AB - BACKGROUND: Advanced glycation end-products (AGEs) and their receptors are prominent contributors to diabetic kidney disease.METHODS: Flow cytometry was used to measure the predictive capacity for kidney impairment of the AGE receptors RAGE, AGE-R1, and AGE-R3 on peripheral blood mononuclear cells (PBMCs) in experimental models of type 2 diabetes (T2DM) fed varied AGE containing diets and in obese type 2 diabetic and control human subjects.RESULTS: Diets high in AGE content fed to diabetic mice decreased cell surface RAGE on PBMCs and in type 2 diabetic patients with renal impairment (RI). All diabetic mice had elevated Albumin excretion rates (AERs), and high AGE fed dbdb mice had declining Glomerular filtration rate (GFR). Cell surface AGE-R1 expression was also decreased by high AGE diets and with diabetes in dbdb mice and in humans with RI. PBMC expression of AGE R3 was decreased in diabetic dbdb mice or with a low AGE diet.CONCLUSIONS: The most predictive PBMC profile for renal disease associated with T2DM was an increase in the cell surface expression of AGE-R1, in the context of a decrease in membranous RAGE expression in humans, which warrants further investigation as a biomarker for progressive DN in larger patient cohorts.
KW - Animals
KW - Diabetes Mellitus, Type 2
KW - Diabetic Nephropathies
KW - Flow Cytometry
KW - Glycosylation End Products, Advanced
KW - Male
KW - Mice
KW - Mice, Inbred C57BL
KW - Receptors, Immunologic
U2 - 10.1155/2010/974681
DO - 10.1155/2010/974681
M3 - Journal article
C2 - 21318189
VL - 2010
SP - 974681
JO - Journal of Diabetes Research
JF - Journal of Diabetes Research
SN - 2314-6745
ER -
ID: 129669850