Altered Phosphorylation of a 91-kDa Protein in Particulate Fractions of Rat Kidney after Protracted 1,25-Dihydroxyvitamin D3or Estrogen Treatment

Qin, Xu‐Jie; Siaw, E. K. O.; Cheung, Anthony; Walters, Marian R.

doi:10.1006/abbi.1997.0354

Cited by 1 publication

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“…Because E 2 and P 4 rapidly regulate protein phosphorylation in other organs, tissues, and cell lines [28][29][30][31][32], 0.5 h was the first point in time selected, and a second point at 2.5 h was considered appropriate for detection of a change along time. A total of 96 rats on C1 and P1 were treated with vehicle, P 4 (5 mg), E 2 (1 g), or E 2 ϩ P 4 .…”

Section: Methodsmentioning

confidence: 99%

Acceleration of Oviductal Transport of Oocytes Induced by Estradiol in Cycling Rats Is Mediated by Nongenomic Stimulation of Protein Phosphorylation in the Oviduct1

Orihuela

Croxatto

2001

Biology of Reproduction

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In order to explore nongenomic actions of estradiol (E2) and progesterone (P4) in the oviduct, we determined the effect of E2 and P4 on oviductal protein phosphorylation. Rats on Day 1 of the cycle (C1) or pregnancy (P1) were treated with E2, P4, or E2 + P4, and 0.5 h or 2.5 h later their oviducts were incubated in medium with 32P-orthophosphate for 2 h. Oviducts were homogenized and proteins were separated by SDS-PAGE. Following autoradiography, protein bands were quantitated by densitometry. The phosphorylation of some proteins was increased by hormonal treatments, exhibiting steroid specificity and different individual time courses. Possible mediation of the E2 effect by mRNA synthesis or protein kinases A (PK-A) or C (PK-C) was then examined. Rats on C1 treated with E2 also received an intrabursal (i.b.) injection of alpha-amanitin (Am), or the PK inhibitors H-89 or GF 109203X, and 0.5 h later their oviducts were incubated as above plus the corresponding inhibitors in the medium. Increased incorporation of 32P into total oviductal protein induced by E2 was unchanged by Am, whereas it was completely suppressed by PK inhibitors. Local administration of H-89 was utilized to determine whether or not E2-induced egg transport acceleration requires protein phosphorylation. Rats on C1 or P1 were treated with E2 s.c. and H-89 i.b. The number and distribution of eggs in the genital tract assessed 24 h later showed that H-89 blocked the E2-induced oviductal egg loss in cyclic rats and had no effect in mated rats. It is concluded that E2 and P4 change the pattern of oviductal protein phosphorylation. Estradiol increases oviductal protein phosphorylation in cyclic rats due to a nongenomic action mediated by PK-A and PK-C. In the absence of mating, this action is essential for its oviductal transport accelerating effect. Mating changes the mechanism of action of E2 in the oviduct by waiving this nongenomic action as a requirement for E2-induced embryo transport acceleration.

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Section: Methodsmentioning

confidence: 99%