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N Mairesse

Publications and source records attributed to N Mairesse.

34 records · Page 2Linked to original sources
PubMed1983

Differential blockade of estrogen-induced uterine responses by the antiestrogen nafoxidine.

We have used an experimental design described by Gardner et al. [6] for dissociating early and late uterine responses to estradiol, involving pretreatment of immature rats with 5 micrograms nafoxidine (Upjohn U-11, 100 A, UA) for 24 h, before administrating estradiol. In these conditions the authors showed that responses occurring 4-h after estradiol administration were not blocked, while 24-h responses were abolished. These findings were defined and extended in the present investigation which shows that: (1) The overall wet weight response of the uterus to estradiol in UA-pretreated animals is decreased when compared to saline pretreated rats. (2) The early increase in cGMP content induced at 2-4 h by estrogen is also decreased but not abolished by the pretreatment with UA, contrary to the late increase in cGMP, which is abolished. (3) The late estrogen-induced proliferative response, measured by the [3H]thymidine labeling index, in the myometrium, stroma and luminal epithelium is maintained after pretreatment with UA. It is remarkable that this occurs in the absence of any estrogen induced uterine hypertrophy as measured by the 24-h increase in uterine weight and RNA or protein content. These results strongly support the hypothesis proposed by Gardner et al. [6] that different control mechanisms might regulate early and late uterine responses to estrogen. Our data suggest the existence of the following dissociable groups of response: (1) Wet weight increase and early increase in cGMP content, (2) Late hypertrophy and second rise in cGMP content and (3) Proliferative response; which are respectively, moderately depressed, abolished or unaffected by UA pretreatment.

Animals↗
PubMed1981

Nafoxidine-responsive uterine protein: further characterization and distinction from the "estrogen-induced" protein (IP).

In a previous paper, we reported that nafoxidine (UA) stimulated the synthesis of a uterine protein showing the same electrophoretic mobility as the "estrogen-induced protein" (E2-IP) first described by Notides and Gorski. In the present work, we analyzed the IP-containing electrophoretic zone by SDS polyacrylamide-gel electrophoresis, and found that estradiol-17 beta (E2) and nafoxidine stimulated the synthesis of different proteins. As expected, estradiol-17 beta stimulated the synthesis of the E2-IP of 46 000 Mr. On the other hand, UA stimulated the synthesis of 27 000 and 30 000 Mr proteins (UA-IP). These UA-IP were not precipitated by an antiserum raised against E2-IP. Therefore, UA-IP appear to be independent entities and not degradation or precursor products of E2-IP. Both UA-IP are constitutively present in the uterus and even in higher relative amounts in rat brain. The present finding, that an "anti-estrogen", such as nafoxidine, stimulates the synthesis of different proteins than estrogen, provides a new approach to the study of the molecular mechanism of estrogen action.

Animals↗
PubMed1979

Comparison between the action of estradiol and that of the antiestrogen U 11-100 A on the induction in the rat uterus of a specific protein (the induced protein).

When measured by an in vitro approach, involving incubation in the presence of labeled leucine, the rate of synthesis of the specific estrogen-induced protein (IP) after in vivo stimulation of the rat uterus by the antiestrogens U 11-100 A (UA; 1-(2-[p-(3,4-dihydro-6-methoxy-2-phenyl-1-naphtyl)-phenoxy]ethyl)pyrrolidine hydrochloride) or CI-628 (alpha-[4-pyrrolidinoethyoxy]phenyl-4-methoxy-d-nitrostilbene) was very low compared to the response measured under the same conditions after in vivo stimulation with 17 beta-estradiol (E2). In the course of investigations aimed at clarifying the role of IP in estrogen action, we have conducted similar experiments, but the labeling step aimed at detecting and measuring IP synthesis was carried out in vivo. We have observed that UA promoted a full IP response which is lost or missed in incubated uteri. Similar results were obtained with CI-628 and tamoxifen. A comparison between IP responses obtained and measured in vivo after E2 and those after UA action revealed that the responses paralleled the number of receptors that are translocated to the nucleus by each compound. Thus, while transient after E2 treatment, the IP (or IP-like) response was maintained for as long as 12 h (as is the nuclear receptor occupancy) when UA was used as inducer. Several explanations for the disappearance of the UA-induced IP response under in vitro conditions are considered.

Animals↗
PubMed1978

Effect of the skin chalone on the epidermis and other tissues in the mouse. A reappraisal of the concept of chalone specificity.

Effect of a pig skin extract (72-81/ethanol precipitate from crude waterextract) was investigated on the ear epidermis, vaginal and uterine mucosae of spayed mice. This extract has a strong inhibitory effect on the epidermis. Inhibition was less marked on the vaginal mucosa while uterine epithelium was not affected. After stimulation of the proliferative activity by oestrogen a pronounced inhibition was detected in the three tissues. Purification of the crude extract by pronase treatment followed by chromatography on Sephadex G200 allowed the separation of three fractions. Two of these fractions (phenol extract and low molecular fraction) were active on epidermis vagina and uterine. The high molecular weight fraction has mainly a marked action on uterine epithelium. No effect was detectable on intestinal tissues with any fraction.

Animals↗
PubMed1977

Effect of propranolol on various parameters of estrogen stimulation in the rat uterus.

Pretreatment with propranolol does not modify the estrogen-induced uterine eosinophilia, the water imbibition effect, nor the increase in uterine RNA and protein content. This confirms the independence of these parameters from the estrogen-induced early increase in uterine cAMP, since, when observed, the latter is suppressed by propranolol pretreatment.

Animals↗
PubMed1977

Oestrogen-induced uterine protein: presence of associated phosphoprotein phosphatase activity before oestrogen treatment.

The phosphoprotein phosphatase (PPPase) activity that is found associated with oestrogen-induced protein(s) is not itself induced by oestrogen. Indeed, this activity was found at the same electrophoretic position (i.e. the position of the oestrogen-induced protein) and in equal amounts relative to the total PPPase activity, whether the cytosol fraction from control or from stimulated uteri was tested.

Animals↗
PubMedDate not supplied

Estrogen-induced proteins in luminal epithelium, endometrial stroma and myometrium of the rat uterus.

The early effect of estrogen on the synthesis of cytosolic proteins was investigated in the luminal epithelium, endometrial stroma and myometrium of the uterus in adult ovariectomized rats. The procedure of Reiss and Kaye (1981) was followed (involving two-step fractionation of 35S-labelled proteins and fluorographic analysis) except that the uteri were fractionated into their three main tissue components before homogenization. The results show that E2 stimulates the synthesis of BB-CK (brain-type creatine kinase), the major component of IP (estrogen-induced protein), in the three tissues. This suggests that BB-CK is related to a function that is common to the estrogen responses (such as hypertrophy) of all three uterine tissues in ovariectomized adult animals. The synthesis of two unidentified proteins of 37000 and 27000 Mr was markedly stimulated in the epithelium. These proteins are probably rate-limiting in responses to estrogen treatment that are specific to the epithelium. The 27000 Mr protein has the same charge as that of the 27000 Mr nafoxidine-induced protein described previously (Mairesse et al., 1981) and is probably therefore the same protein.

Animals↗