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2016 ; 68
(1
): 167-74
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Interleukin-17A Regulates Renal Sodium Transporters and Renal Injury in
Angiotensin II-Induced Hypertension
#MMPMID27141060
Norlander AE
; Saleh MA
; Kamat NV
; Ko B
; Gnecco J
; Zhu L
; Dale BL
; Iwakura Y
; Hoover RS
; McDonough AA
; Madhur MS
Hypertension
2016[Jul]; 68
(1
): 167-74
PMID27141060
show ga
Angiotensin II-induced hypertension is associated with an increase in T-cell
production of interleukin-17A (IL-17A). Recently, we reported that IL-17A(-/-)
mice exhibit blunted hypertension, preserved natriuresis in response to a saline
challenge, and decreased renal sodium hydrogen exchanger 3 expression after 2
weeks of angiotensin II infusion compared with wild-type mice. In the current
study, we performed renal transporter profiling in mice deficient in IL-17A or
the related isoform, IL-17F, after 4 weeks of Ang II infusion, the time when the
blood pressure reduction in IL-17A(-/-) mice is most prominent. Deficiency of
IL-17A abolished the activation of distal tubule transporters, specifically the
sodium-chloride cotransporter and the epithelial sodium channel and protected
mice from glomerular and tubular injury. In human proximal tubule (HK-2) cells,
IL-17A increased sodium hydrogen exchanger 3 expression through a serum and
glucocorticoid-regulated kinase 1-dependent pathway. In mouse distal convoluted
tubule cells, IL-17A increased sodium-chloride cotransporter activity in a serum
and glucocorticoid-regulated kinase 1/Nedd4-2-dependent pathway. In both cell
types, acute treatment with IL-17A induced phosphorylation of serum and
glucocorticoid-regulated kinase 1 at serine 78, and treatment with a serum and
glucocorticoid-regulated kinase 1 inhibitor blocked the effects of IL-17A on
sodium hydrogen exchanger 3 and sodium-chloride cotransporter. Interestingly,
both HK-2 and mouse distal convoluted tubule 15 cells produce endogenous IL-17A.
IL17F had little or no effect on blood pressure or renal sodium transporter
abundance. These studies provide a mechanistic link by which IL-17A modulates
renal sodium transport and suggest that IL-17A inhibition may improve renal
function in hypertension and other autoimmune disorders.
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