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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Am+J+Physiol+Renal+Physiol
2016 ; 310
(10
): F1000-7
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Macrophage-derived IL-6 contributes to ANG II-mediated angiotensinogen
stimulation in renal proximal tubular cells
#MMPMID27009340
O'Leary R
; Penrose H
; Miyata K
; Satou R
Am J Physiol Renal Physiol
2016[May]; 310
(10
): F1000-7
PMID27009340
show ga
The development of ANG II-dependent hypertension involves increased infiltration
of macrophages (M?) and T cells into the kidney and the consequent elevation of
intrarenal cytokines including IL-6, which facilitates the progression of
hypertension and associated kidney injury. Intrarenal renin-angiotensin system
(RAS) activation, including proximal tubular angiotensinogen (AGT) stimulation,
has also been regarded as a cardinal mechanism contributing to these diseases.
However, the interaction between immune cells and intrarenal RAS activation has
not been fully delineated. Therefore, the present study investigated whether ANG
II-treated M? induce AGT upregulation in renal proximal tubular cells (PTCs). M?
were treated with 0-10(-6) M ANG II for up to 48 h. PTCs were incubated with the
collected medium from M?. In ANG II-treated M?, IL-6 mRNA and protein levels were
increased (1.86 ± 0.14, protein level, ratio to control); moreover, IL-6 levels
were higher than TNF-? and IL-1? in culture medium isolated from ANG II-treated
M?. Elevated AGT expression (1.69 ± 0.04, ratio to control) accompanied by
phosphorylated STAT3 were observed in PTCs that received culture medium from ANG
II-treated M?. The addition of a neutralizing IL-6 antibody to the collected
medium attenuated phosphorylation of STAT3 and AGT augmentation in PTCs.
Furthermore, a JAK2 inhibitor also suppressed STAT3 phosphorylation and AGT
augmentation in PTCs. These results demonstrate that ANG II-induced IL-6
elevation in M? enhances activation of the JAK-STAT pathway and consequent AGT
upregulation in PTCs, suggesting involvement of an immune response in driving
intrarenal RAS activity.
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