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Parathyroid hormone inhibition of Na(+)/H(+) exchanger 3 transcription: Intracellular signaling pathways and transcription factor expression.

Abstract：

:The main transport mechanism of reabsorption of sodium bicarbonate and fluid in the renal proximal tubules involves Na(+)/H(+) exchanger 3 (NHE3), which is acutely and chronically downregulated by parathyroid hormone (PTH). Although PTH is known to exert an inhibitory effect on NHE3 expression and transcription, the molecular mechanisms involved remain unclear. Here, we demonstrated that, in opossum kidney proximal tubule (OKP) cells, PTH-induced inhibition of Nhe3 gene promoter occurs even in the core promoter that controls expression of the reporter gene. We found that inhibition of the protein kinase A (PKA) and Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathways transformed PTH from an inhibitor of promoter activity into an activator of that same activity, as did point mutations in the EGR1, Sp1, and Sp3 binding consensus elements in the promoter. In nuclear extracts of PTH-treated OKP cells, we also observed increased expression of EGR1 mRNA and of some Sp3 isoforms. Electrophoretic mobility shift assay showed a supershift of the -61 to -42-bp probe with an anti-EGR1 antibody in PTH-treated cells, suggesting that EGR1 binding is relevant for the inhibitory activity of PTH. We conclude that PTH-induced inhibition of NHE3 transcription is related to higher EGR1 expression; to EGR1 binding to the proximal and core promoters; and to PKA and JAK/STAT pathway activation. This mechanism might be responsible, at least in part, for lower NHE3 expression and sodium reabsorption in renal proximal tubules in the presence of high PTH levels.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Neri EA,Bezerra CN,Queiroz-Leite GD,Polidoro JZ,Rebouças NA

doi

10.1016/j.bbrc.2015.04.049

subject

Has Abstract

pub_date

2015-06-12 00:00:00

pages

582-8

issue

4

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(15)00727-5

journal_volume

461

pub_type

杂志文章

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