β-estradiol (E2) stimulates synthesis of cyclic ADP ribose (cADPR) in rat uterus

E. N. Chini, F. G.S. De Toledo, T. P. Dousa

Research output: Contribution to journalArticlepeer-review

Abstract

Administration of E2 is known to increase sensitivity of myometrium to contractile stimuli, that are mediated by an increase of intracellular Ca2 (Cai2+). Recently discovered nucleotide, cADPR, was shown to promote smooth muscle contraction. We investigated whether administration of E2 to ovarectomized (OVX) rats changes activity of ADP-ribose cyclase, an enzyme that catalyzes synthesis of cADPR from β-NAD in uterus. OVX rats were injected with E2 (200 μg/kg/day for 7 days, s.c.), and ADPR cyclase activity was determined in homogenates from uterus by measurement of cADPR synthesis from β-NAD. In uteri from E2-rats cADPR synthesis was greatly (> Δ + 300%) increased. cADPR (nmol/mg protein); mean ± SEM controls: 1.5 ± 0.1 (4); E2-treated: 6.5 ± 0.5(4); (P < 0.05) Authenticity of cADPR product was verified with the use of sea urchin homogenate bioassays. Tamoxifen, E2-receptor antagonist (8 mg/kg/day), blocked stimulatory effect of E2 upon uterine ADPR-cyclase. Conclusions: a) E2 stimulates, via action on its receptor, activity of ADPR-cyclase in uterus; b) E2 is the first hormone found to increase cADPR synthesis in vivo; c) we surmise that increased cADPR generation caused by E2 may be the main or contributing factor that accounts for enhanced Cai2+ release and contractility of uterus in response to oxytocin and prostaglandin F.

Original languageEnglish (US)
Pages (from-to)A323
JournalFASEB Journal
Volume11
Issue number3
StatePublished - Dec 1 1997

ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

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