Impaired Na⁺-K⁺-ATPase signaling in renal proximal tubule contributes to hyperuricemia-induced renal tubular injury.

ABSTRACT: 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 α1 expression vector or small interfering RNA before UA (100 μg 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 α1 subunit, Src, NOD-like receptor pyrin domain-containing protein 3 (NLRP3) and interleukin 1β (IL-1β) were measured both in vitro and in vivo. Beginning at concentrations of 100

SUBMITTER: Xiao J 

PROVIDER: S-EPMC5898891 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature