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2018 ; 50
(3
): e452
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Impaired Na(+)-K(+)-ATPase signaling in renal proximal tubule contributes to
hyperuricemia-induced renal tubular injury
#MMPMID29497172
Xiao J
; Zhang X
; Fu C
; Yang Q
; Xie Y
; Zhang Z
; Ye Z
Exp Mol Med
2018[Mar]; 50
(3
): e452
PMID29497172
show ga
Hyperuricemia contributes to renal inflammation. We aimed to investigate the role
of Na(+)-K(+)-ATPase (NKA) in hyperuricemia-induced renal tubular injury. Human
primary proximal tubular epithelial cells (PTECs) were incubated with uric acid
(UA) at increasing doses or for increasing lengths of time. PTECs were then
stimulated by pre-incubation with an NKA ?1 expression vector or small
interfering RNA before UA (100??g?ml(-1), 48?h) stimulation. Hyperuricemic rats
were induced by gastric oxonic acid and treated with febuxostat (Feb). ATP
levels, the activity of NKA and expression of its ?1 subunit, Src, NOD-like
receptor pyrin domain-containing protein 3 (NLRP3) and interleukin 1? (IL-1?)
were measured both in vitro and in vivo. Beginning at concentrations of
100??g?ml(-1), UA started to dose-dependently reduce NKA activity. UA at a
concentration of 100??g?ml(-1) time-dependently affected the NKA activity, with
the maximal increased NKA activity at 24?h, but the activity started to decrease
after 48?h. This inhibitory effect of UA on NKA activity at 48?h was in addition
to a decrease in NKA ?1 expression in the cell membrane, but an increase in
lysosomes. This process also involved the subsequent activation of Src kinase and
NLRP3, promoting IL-1? processing. In hyperuricemic rats, renal cortex NKA
activity and its ?1 expression were upregulated at the 7th week and both
decreased at the 10th week, accompanied with increased renal cortex expression of
Src, NLRP3 and IL-1?. The UA levels were reduced and renal tubular injuries in
hyperuricemic rats were alleviated in the Feb group. Our data suggested that the
impairment of NKA and its consequent regulation of Src, NLRP3 and IL-1? in the
renal proximal tubule contributed to hyperuricemia-induced renal tubular injury.
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