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  • 1
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 128 (1986), S. 105-112 
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Stimulation of cultured rabbit endometrial cells by one of the rabbit endometrial cell culture proliferation factors, prostaglandin F2α (PGF2α), resulted in a very rapid increase in the intracellular levels of [3H]-inositol triphosphate (IP3), [3H]-inositol biphosphate (IP2), and [3H]-inositol monophosphate (IP1) in cells prelabeled with [3H]-inositol. These increases in inositol phosphate levels were detected in periods of stimulation as short as 30 seconds, reached a maximum by 1 1/2-2 min and declined to control levels by 6-10 min. The stimulation was dose-dependent with maximal increases observed near 10-6 M PGF2α. The cholinergic agent, carbachol, also led to time and dose-independent increases in IP3. Lithium, cadmium, silver, copper, and zinc ions had no effect either on the breakdown of IP3 or on the accumulation of IP1. In contrast, vanadate at 10-6 or 10-5 M did lead to a decrease in the breakdown of IP1 and a concomitant increase in IP1, IP2, and IP3. PGF2α was found previously to induce an increase in rabbit endometrial cell DNA synthesis which was inhibited by concomitant or prior addition of prostaglandin E1 (PGE1). PGE1, in a dose-dependent manner, was found to inhibit the observed IP3 increase by PGF2α at 1 1/2 min of stimulation. PGF2α treated and control cultures did not differ in cAMP or cGMP levels, cellular 45Ca uptake, nor cellular 22Na uptake. We propose that IP3 may be one of the intracellular messenger(s) synthesized following the treatment of rabbit endometrial cell cultures with the proliferation agent PGF2α and that it may play a crucial role with cAMP in growth regulation.
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 130 (1987), S. 292-300 
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: We have hypothesized that two of the endogenously synthsized endometrial prostaglandins (PGs), prostaglandin F2α (PGF2α), and prostaglandin E1 (PGE1), play a regulatory role in growth control of the rabbit endometrium. PGF2α increases DNA synthesis and PGE1 inhibits that effect. Primary cultures of rabbit endometrial cells were used to examine the possible role of these PGs in the mechanism of action of 17β-estradiol on DNA synthesis. Towards this end, binding, second messenger and DNA synthesis experiments were performed. 17β-estradiol stimulation restulted in a time dependent (optimal: approximately 6 h) and 17β-estradiol concentration dependent (optimal: approximately 10-7 M 17β-estradiol in phenol red-containing medium) increase in [3H]PGF2α binding. Scatchard type analysis of the binding data revealed an increase in receptor number while the receptor affinity for [3H]PGF2α remained the same as in the control treated cultures. This 17β-estradiol stimulated increase in PGF2α receptor allowed a suboptimal concentration of PGF2α (10-9M) to increase intracellular levels of inositol polyphosphates, while by itself this concentration of PGF2α caused no significant change in intracellular inositol polyphosphate levels. 17β-estradiol, alone among the several studied steroid hormones, could increase [3H]PGF2α binding. Proliferation studies revealed that, in these primary cultures of rabbit endometrium, 17β-estradiol could increase DNA synthesis but not in the presence of indomethacin, unless PGF2α was addd to the medium at a concentration (10-9M) near or above what is normally accumulated in the medium by these cultures. In the absence of 17β-estradiol stimulation, addition of these same low concentrations of PGF2α had no effect on DNA synthesis. Apparently, through its effect on the PGF2α receptor, 17β-estradiol enhances the PGF2α stimulated DNA synthesis response approximately 100 fold. The DNA synthesis inducd by 17β-estradiol can be inhibited by PGE1, as can PGF2α-induced DNA synthesis. We propose that 17β-estradiol may be mediating its mitogenic effect through an alteration of the prostglandin agonist:antagonist control of proliferation in rabbit endometrial cultures. In additon we suggest that, if 17β-estradiol acts to increase PGF2α receptors as part of its mode of action, this may be of importance in other tissues possessing both prostaglandin and 17β-estradiol receptos.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    New York, NY : Wiley-Blackwell
    Journal of Electron Microscopy Technique 1 (1984), S. 311-312 
    ISSN: 0741-0581
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Natural Sciences in General
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
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