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2013 ; 61
(6
): 433-43
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Losartan affects glomerular AKT and mTOR phosphorylation in an experimental model
of type 1 diabetic nephropathy
#MMPMID23456824
Mavroeidi V
; Petrakis I
; Stylianou K
; Katsarou T
; Giannakakis K
; Perakis K
; Vardaki E
; Stratigis S
; Ganotakis E
; Papavasiliou S
; Daphnis E
J Histochem Cytochem
2013[Jun]; 61
(6
): 433-43
PMID23456824
show ga
The AKT-mTOR pathway is activated in diabetic nephropathy. Renin-angiotensin
system modulators exert beneficial effects on the diabetic kidney. We explored
the action of losartan on AKT-mTOR phosphorylation in glomeruli and podocytes.
Diabetes mellitus was induced to Sprague-Dawley rats by streptozotocin. Five
months later, the rats were commenced on losartan and euthanized 2 months later.
Kidneys were processed for immunofluorescence studies. Glomeruli were isolated
for Western blot analysis. Diabetes increased activated forms of AKT and mTOR
both in glomeruli and podocytes. In diabetic rats, losartan decreased
phosphorylated/activated forms of AKT (Thr308) and mTOR (Ser2448) in glomeruli
but decreased only activated mTOR in podocytes. However, in both glomeruli and
podocytes of healthy animals, an inverse pattern was evident. In conclusion, a
new body of evidence indicates the differential activation of AKT-mTOR in
glomeruli and podocytes of healthy and diabetic animals in response to losartan.
|*Disease Models, Animal
[MESH]
|Animals
[MESH]
|Diabetes Mellitus, Type 1/*drug therapy/metabolism/pathology
[MESH]