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Estrogen induces transient intracellular Ca 2+ signals in distal renal tubules
Author(s) -
Praetorius Jeppe,
Fenton Robert A,
Hofmeister Marlene Vind
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.606.23
Subject(s) - gper , estrogen receptor , intracellular , medicine , extracellular , estrogen , transient receptor potential channel , endocrinology , receptor , chemistry , microbiology and biotechnology , signal transduction , agonist , membrane potential , biophysics , biology , biochemistry , cancer , breast cancer
The renal late distal convoluted tubules (DCT2s) and connecting tubules (CNTs) are sites for fine‐regulating the urinary excretion of various ions including Na + and Ca 2+ . Accumulating evidence suggests that estrogen has the ability to induce rapid signaling through activation of plasma membrane‐associated receptors such as GPCR30. We hypothesized that estrogen may evoke acute signaling in the distal renal tubules through such mechanism. DCT2s and CNTs were isolated from transgenic mice expressing enhanced green fluorescent protein (EFGP) driven by the transient receptor potential subfamily V, member 5 (TRPV5) promoter. Intracellular Ca 2+ levels ([Ca 2+ ] i ) of freshly isolated DCT2s and CNTs increased after 1 min superfusion with 17β‐estradiol (E2, 10 −9 M to10 −7 M) using live cell Fluo‐4 imaging. The E2‐induced [Ca 2+ ] i signal was dependent on extracellular Ca 2+ and was enhanced rather than inhibited by the classical antagonists ICI 182 780. G‐1, an agonist of the membrane associated E2 receptor GPR30, induced a similar response as E2. Preliminary data indicate enhanced TRPV5 immunoreactivity in the apical domain of the cells upon estrogen treatment, while the transepithelial Ca 2+ flux in primary cultures of DCT2/CNT did not seem affected. We suggest that E2 can act through non‐genomic signaling pathways in DCT2 and CNT and may acutely alter tubular function.