“…Using a technique developed for the localization of HCG binding sites in the rat ovary in vitro (Petrusz & Uhlarik, 1973), we have demonstrated the presence of mammary gland receptor sites for HPL. Accumula¬ tion of immunoreactive HPL on the alveolar cell membrane is consistent with the localiza¬ tion of radio-iodinated prolactin as demonstrated by Birkinshaw & Falconer (1972).…”
The rate of clearance from the circulation and uptake into tissues of radioactive label was studied after i.v. injection of 125-I-labelled human placental lactogen (HPL) into rats at various stages of pregnancy. The half-life was obtained for the disappearance of the trichloroacetic acid-precipitable material from the plasma. The half-life, t1/2(S), calculated over the first 5 min after injection of the hormone was 5.4 equals or minus 1.1 (S.D.) min, while a half-life, t1/2(L), of 27.9 equals or minus 2.3 min was obtained from the decay period of 15-35 min. In the non-pregnant and pregnant rat the highest ratio of the radioactivity in an organ to that in the blood was 12-14:1 in the kidney. That the kidney is mainly involved in the uptake of exogenous HPL is further confirmed by the application of the histochemical immunoperoxidase technique. Human placental lactogen was localized in the cells of the proximal tubules of the cortex and to a lesser extent in the tubular lumen and the tubules of the medulla region. UPTAKE OF HPL in vivo occurs in the mammary gland tissue of the post-partum rat and reaches a maximum uptake between 15 and 30 min after injection of the hormone. Furthermore, specific uptake of HPL was observed on the alveolar cell membranes after the incubation of paraffin-embedded sections of formalin-fixed mammary gland and subsequent treatment by the peroxidase-labelled antibody method. These findings support the work of others who have demonstrated the presence of specific membrane receptors in the mammary gland for hormones with prolactin-like activity.
“…Using a technique developed for the localization of HCG binding sites in the rat ovary in vitro (Petrusz & Uhlarik, 1973), we have demonstrated the presence of mammary gland receptor sites for HPL. Accumula¬ tion of immunoreactive HPL on the alveolar cell membrane is consistent with the localiza¬ tion of radio-iodinated prolactin as demonstrated by Birkinshaw & Falconer (1972).…”
The rate of clearance from the circulation and uptake into tissues of radioactive label was studied after i.v. injection of 125-I-labelled human placental lactogen (HPL) into rats at various stages of pregnancy. The half-life was obtained for the disappearance of the trichloroacetic acid-precipitable material from the plasma. The half-life, t1/2(S), calculated over the first 5 min after injection of the hormone was 5.4 equals or minus 1.1 (S.D.) min, while a half-life, t1/2(L), of 27.9 equals or minus 2.3 min was obtained from the decay period of 15-35 min. In the non-pregnant and pregnant rat the highest ratio of the radioactivity in an organ to that in the blood was 12-14:1 in the kidney. That the kidney is mainly involved in the uptake of exogenous HPL is further confirmed by the application of the histochemical immunoperoxidase technique. Human placental lactogen was localized in the cells of the proximal tubules of the cortex and to a lesser extent in the tubular lumen and the tubules of the medulla region. UPTAKE OF HPL in vivo occurs in the mammary gland tissue of the post-partum rat and reaches a maximum uptake between 15 and 30 min after injection of the hormone. Furthermore, specific uptake of HPL was observed on the alveolar cell membranes after the incubation of paraffin-embedded sections of formalin-fixed mammary gland and subsequent treatment by the peroxidase-labelled antibody method. These findings support the work of others who have demonstrated the presence of specific membrane receptors in the mammary gland for hormones with prolactin-like activity.
“…A similar heterogeneity of cellular staining pattern has previously been noted in rat prostatic carcinomas (Witorsch, 1979a,b), in human prostatic carcinoma (Purnell et al, 1982) and in human breast carcinomas (Paterson et al, 1982;Purnell et al, 1982;Dhadley & Walker, 1983 (Rao et al, 1981;Rajandran & Menon, 1983). Immunoperoxidase studies have also shown that intracellular prolactin is present in rat ovaries (Dunaif et al, 1977(Dunaif et al, , 1982Nolin, 1978Nolin, , 1980 and in human breast and prostatic tissue (Purnell et al, 1982) whilst intracellular gonadotrophins have been demonstrated in rat ovary (Petrusz & Uhlarik, 1973;Petrusz, 1974;Petrusz & Sar, 1978) and human prostate (Sibley, 1981).…”
Section: Discussionmentioning
confidence: 86%
“…Biochemical studies have demonstrated specific receptors for gonadotrophins and prolactin in the normal human ovary (Poindexter et al, 1979;McNeilly et al, 1980;Kammerman, 1980Kammerman, , 1981Rao et al, 1981) and in ovarian neoplasms (Davy et al, 1977;Kammerman et al, 1980Kammerman et al, , 1981Rajaniemi et al, 1981a) whilst immunoperoxidase techniques have been used to demonstrate gonadotrophin-binding sites in rat gonads (Petrusz & Uhlarik, 1973;Petrusz, 1974;Childs et al, 1978;Rajaniemi et al, 1981b) and prolactin-binding sites in human prostate gland (Witorsch, 1978) and in normal and neoplastic human breast tissue (Paterson et al, 1982;Purnell et al, 1982;Dhadley & Walker, 1983). …”
Summary An immunoperoxidase technique has been utilised for the demonstration of follicle stimulating hormone (FSH), luteinising hormone (LH) and prolactin (PRL) binding sites in normal human ovaries and in a wide range of benign and malignant epithelial tumours of the ovary. The incidence of FSH, LH and PRL binding was, respectively, 32%, 41% and 39% in normal ovaries, 30%, 18.5% and 22.5% in benign epithelial tumours and 51%, 32% and 43% in malignant epithelial neoplasms.The incidence of FSH binding was significantly higher in malignant epithelial neoplasms than in either normal ovaries or benign epithelial tumours but otherwise no correlation was found between hormone binding capacity and the degree of malignancy of epithelial ovarian tumours, the histological type of the tumour, the degree of differentiation of the malignant epithelial tumours or the presence or absence of metastatic disease. Well differentiated malignant tumours did, however, tend to stain more strongly than did poorly differentiated neoplasms, thus suggesting that the number of binding sites per cell tends to decrease with decreasing degrees of differentiation.
“…Thin-walled blood vessels in ovaries of nonhormonetreated immature rats bore little immunoreactive hepatic lipase, while those in all steroidogenic compartments of animals receiving PMSG or PMSG-hCG displayed abundant enzyme. It is also pertinent that the parenchymal cells of all compartments possessing blood vessels strongly positive for hepatic lipase are known to be regulated by, or bear binding sites for, luteinizing hormone, a pituitary gonadotropin (Bortolussi et al, 1979;Azhar and Menon, 1979;Dyer and Erickson, 1985;Petrusz, 1973).…”
We used biochemical and structural approaches to analyze the influence of gonadotropic hormones on the association of hepatic lipase with specific subsets of ovarian blood vessels. Western blotting was used to detect this enzyme in effluent collected from heparin-perfused ovaries of nonhormone-treated immature rats and those primed with pregnant mare's serum gonadotropin (PMSG) alone or in combination with human chorionic gonadotropin (hCG). The effects of these hormones on hepatic lipase distribution among ovarian blood vessels was assessed before and after hCG and/or PMSG treatment by immunofluorescence and immunogold cytochemistry. For the latter, immunoreagents and fixative were delivered directly to chilled, unfixed ovaries by in situ vascular perfusion. Data from biochemical and structural analyses indicated that hepatic lipase was absent from nonhormone-treated ovaries. As shown by Western blotting of ovarian effluent, the enzyme appeared following treatment with PMSG and PMSG-hCG; it increased in amount in a time-dependent manner, with a transient decline in the early hours after hCG injection. Enzyme levels paralleled growth and vascularization of follicles and corpora lutea; the fall tended to coincide with early events in luteal angiogenesis. Immunogold microscopy showed that hepatic lipase was abundant in thin-walled blood vessels of theca interna of follicles, corpora lutea, and interstitial cells but sparse in those of the stroma. Moreover, during neovascularization of differentiating corpora lutea, vascular sprouts arising from hepatic lipase-laden thecal vessels appeared to lose, then regain, the enzyme as development progressed. Our findings thus suggest 1) that hormones influence the establishment of endothelial cell heterogeneity within the microvasculature of a single organ and 2) that development of novel endothelial cell properties in specific subsets of blood vessels underlies compartmentalization of function within a tissue.
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