Opioid peptides inhibit the estradiol-induced proliferation of cultured rat uterine cells

Környei, J.; Vértes, Zsuzsanna; Oszter, Angéla; Kovács, Sándor; Vértes, Marietta

doi:10.1016/s0014-2999(97)01153-9

Cited by 11 publications

(23 citation statements)

References 40 publications

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“…In previous studies, it has been demonstrated that EOPs may be implicated in the regulation of several processes in the uterus such as: its contractility, secretory activity, local immunomodulation, cell proliferation and apoptosis (Petit et al, 1993;Cemerikic et al, 1994;Adjroud, 1995;Környei et al, 1997;Zoumakis et al, 1997;Chatzaki et al, 2001;Fanning et al, 2013). Variable data concerning the modulation of uterine muscle contractility by opioids have been reported for different species and reproductive stages.…”

Section: Discussionmentioning

confidence: 99%

“…However, DAMEA did not affect the basal proliferation of uterine cells derived from adult rats, but decreased the oestradiol-induced proliferation of these cells. It was suggested that this opioid effect is mediated mainly by μ opioid receptors (Környei et al, 1997). In turn, κ opioid receptors seem to be involved in the modulation of endometrial stromal cell apoptosis in humans since their highly specific agonist (U69593) markedly increased apoptosis of these cells.…”

Section: Discussionmentioning

confidence: 99%

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The expression of mRNAs for opioid receptors in endometrium of cyclic and early pregnant pigs; <i>in vitro</i> effects of IL-1β, IL-6 and TNFα

Dziekoński¹,

Zmijewska²,

Franczak³

et al. 2015

J. Anim. Feed Sci.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

The expression of mRNAs for opioid receptors in endometrium of cyclic and early pregnant pigs; <i>in vitro</i> effects of IL-1β, IL-6 and TNFα

Dziekoński¹,

Zmijewska²,

Franczak³

et al. 2015

J. Anim. Feed Sci.

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“…2000; Zagon et al . 2002), and with the mu (Környei et al . 1997, 1999, 2001) and kappa (Chatzaki et al .…”

Section: Introductionmentioning

confidence: 99%

“…Our laboratory also described that the opioid peptides (OP) are negative regulators of both the oestradiol‐(E 2 ) (Ördög et al . 1992; Környei et al . 1997) and epidermal growth factor‐stimulated (EGF) (Vértes et al .…”

Section: Introductionmentioning

confidence: 99%

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Developmental changes in the inhibition of cultured rat uterine cell proliferation by opioid peptides

Vértes

et al. 2003

Cell Proliferation

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Opioid peptides are negative regulators of cell proliferation in several organs including the uterus. In the present study, the ontogeny of the direct inhibitory action of opioid peptides on the proliferation of cultured rat uterine cells was investigated. Uteri of 7, 14, 21, 28, 35 and 60-day-old rats were removed in a sterile way. Tissue blocks were dispersed by limited digestions with trypsin and collagenase. Cells were cultured in enriched Dulbecco's modified Eagle's medium (DMEM). Treatments were present during the entire culture period. Cell densities of the monolayers were determined by counting the cells following trypsinization and trypan blue exclusion. Rat uterine mixed cell cultures grew to confluence within 10 days. The average population doubling time gradually increased with the age of animals. Epidermal growth factor (EGF) increased cell densities of cultures from all age groups. The oestradiol (E2)-responsiveness appeared at 21 days of age. The effect of [D-Met2-Pro5]-enkephalinamide (ENK) was biphasic. ENK and [Met5]-enkephalin (OGF) decreased cell densities of both unstimulated and EGF-stimulated cultures from 7-day-old rats to the same extent. ENK failed to act in 14-day-old animals. From 21 days of age on, the E2- or EGF-stimulated proliferation was inhibited only by ENK and DAMGO, while 30 nm DPDPE, Dynorhin-A, OGF, [Leu5]-enkephalin, beta-endorphin, and morphiceptin were ineffective. The half-inhibitory concentration of ENK was 0.3 nm. The effects of ENK were prevented by concomitant treatment with naloxone. Our novel data demonstrate two different phases of the inhibitory action of opioid peptides on rat uterine cell proliferation during ontogeny with an insensitive interval in between.

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Opioid agonists modify breast cancer cell proliferation by blocking cells to the G2/M phase of the cycle: Involvement of cytoskeletal elements

et al. 1999

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Opioids decrease cell proliferation in different systems including breast, prostate, lung, kidney, and intestine, through an interaction with opioid as well as other membrane-receptor systems (somatostatin, cholinergic), through an unidentified mechanism. Recently, we have reported an interaction of taxol with opioid membrane sites (BBRC 235, 201-204, 1997), and an involvement of opioids to the modification of actin cytoskeleton in renal OK cells (J Cell Biochem. [19981 70:60-69), indicating a possible action of the opioid effect. In the present work, we have examined the effect of two general opioid agonists (ethylketocyclazocine and etorphine) on the cell cycle, in human breast cancer T47D cells, as well as a possible modification of the cellular cytoskeleton under their action, in order to explain the antiproliferative effect of these agents. These two opioids produce a dose-dependent and reversible decrease of the proliferation of T47D cells, with a maximum attained at 10(-8) M. The addition of 10(-8) M of either opioid produced a significant increase of the number of cells arrested in the G2/M phase. Confocal laser microscopy revealed a modification of the actin and tubulin microfilaments, with a clear redistribution at the periphery of the cell, reversed by the addition of the general opioid antagonist diprenorphine. Furthermore, differences between the two opioids were obvious, attributed to the different receptor affinity of each agent. The observed redistribution of actin and tubulin cytoskeletal elements gives therefore a possible answer of the antiproliferative action of opioids. The modification of the cytoskeleton, directly involved to cell division, might provoke a "mechanical" obstacle, which could be the reason of the antiproliferative effect of these agonists. Furthermore, the observed tubulin-opioid interaction by opioids provides a possible explanation of the arrest at the G2/M phase of T47D cells under opioid treatment. Nevertheless, although the observed interaction of opioids with cytoskeletal elements gives a plausible answer of the antiproliferative effects of the agents, this might not be the only action of these agents in cell proliferation. Other, direct or indirect, genomic actions, which which remains to be elucidated, might be taken into consideration.

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Opioid peptides inhibit the estradiol-induced proliferation of cultured rat uterine cells

Cited by 11 publications

References 40 publications

The expression of mRNAs for opioid receptors in endometrium of cyclic and early pregnant pigs; <i>in vitro</i> effects of IL-1β, IL-6 and TNFα

The expression of mRNAs for opioid receptors in endometrium of cyclic and early pregnant pigs; <i>in vitro</i> effects of IL-1β, IL-6 and TNFα

Developmental changes in the inhibition of cultured rat uterine cell proliferation by opioid peptides

Opioid agonists modify breast cancer cell proliferation by blocking cells to the G2/M phase of the cycle: Involvement of cytoskeletal elements

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