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פותח על ידי קלירמאש פתרונות בע"מ -
Prolactin (prl) receptor induction in cultured rat hepatocytes: Dual regulation by prl and growth hormone
Year:
1988
Source of publication :
Endocrinology
Authors :
ברש, איתמר
;
.
Volume :
122
Co-Authors:
Barash, I., Division of Endocrinology and Department of Medicine, Royal Victoria Hospital, McGill University, Montreal, QC, H3A 1A1, Canada
Cromlish, W., Division of Endocrinology and Department of Medicine, Royal Victoria Hospital, McGill University, Montreal, QC, H3A 1A1, Canada
Posner, B.I., Division of Endocrinology and Department of Medicine, Royal Victoria Hospital, McGill University, Montreal, QC, H3A 1A1, Canada
Facilitators :
From page:
1151
To page:
1158
(
Total pages:
8
)
Abstract:
Although early work implicated PRL as the pituitary factor inducing rat hepatic PRL receptors, recent studies indicated that GH, not PRL, was responsible. The roles for these two hormones were evaluated on rat hepatocytes cultured in serum-free medium supplemented with insulin (1 μg/ml), epidermal growth factor EGF (25 ng/ml), glucagon (500 ng/ml), cholera toxin (2 ng/ml), hydrocortisone (10-8 M), and transferrin (1 μg/ml) and changed daily. Ovine (o) PRL, bovine (b) GH, or human (h) GH were introduced after 2-4 days of culture, and PRL receptors were measured by determining [125I]hGH binding in the presence and absence of excess oPRL in a total particulate fraction pretreated with 3 M MgCl2. The specific binding of hGH (% per 100 μg protein) decreased by 8- to 10-fold (♀,17.9 ± 0.2% to 1.5%; ♂, 7.0 ± 0.1% to 0.7%) after 3 days in culture. When added after 3 days, hGH induced PRL receptors in both female and male cells with the effect being more gradual in the latter. Induction occurred with 10 ng/ml hGH and was maximal [11- to 13-fold control] at 250-1000 ng/ml. bGH and oPRL also induced PRL receptors with maximal levels attained at 250-500 ng/ml oPRL (3- to 4-fold control). The combined addition of oPRL (300 ng/ml) and bGH (300 ng/ml) yielded levels of induction comparable to that seen with hGH. Although hormone treatment restored PRL receptor levels to those seen in male rats, the much higher levels of female rats were not attained. Treatment of hepatocytes with hGH, bGH, or oPRL affected neither cell number (through 10 days of culture) nor PRL receptor affinity. At supramaximal doses hGH, PRL, and bGH down-regulated PRL receptors, but this was particularly noticeable for oPRL and hGH. 17β-Estradiol and testosterone added to male and female hepatocytes simultaneously with hGH had little or no effect on receptor induction. We conclude that hepatic PRL receptors are induced by both PRL and GH, each acting through its own receptor. The failure to restore receptor levels to those seen in female rats attests to the importance of other modulators. This dual regulation of the PRL receptor explains the unusual potency of hGH which binds to both PRL and GH receptors. © 1988 by The Endocrine Society.
Note:
Related Files :
Animal
animal cell
Dose-Response Relationship, Drug
Female
liver
Male
Receptors, Prolactin
עוד תגיות
תוכן קשור
More details
DOI :
10.1210/endo-122-3-1151
Article number:
Affiliations:
Database:
סקופוס
Publication Type:
מאמר
;
.
Language:
אנגלית
Editors' remarks:
ID:
22233
Last updated date:
02/03/2022 17:27
Creation date:
16/04/2018 23:50
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Scientific Publication
Prolactin (prl) receptor induction in cultured rat hepatocytes: Dual regulation by prl and growth hormone
122
Barash, I., Division of Endocrinology and Department of Medicine, Royal Victoria Hospital, McGill University, Montreal, QC, H3A 1A1, Canada
Cromlish, W., Division of Endocrinology and Department of Medicine, Royal Victoria Hospital, McGill University, Montreal, QC, H3A 1A1, Canada
Posner, B.I., Division of Endocrinology and Department of Medicine, Royal Victoria Hospital, McGill University, Montreal, QC, H3A 1A1, Canada
Prolactin (prl) receptor induction in cultured rat hepatocytes: Dual regulation by prl and growth hormone
Although early work implicated PRL as the pituitary factor inducing rat hepatic PRL receptors, recent studies indicated that GH, not PRL, was responsible. The roles for these two hormones were evaluated on rat hepatocytes cultured in serum-free medium supplemented with insulin (1 μg/ml), epidermal growth factor EGF (25 ng/ml), glucagon (500 ng/ml), cholera toxin (2 ng/ml), hydrocortisone (10-8 M), and transferrin (1 μg/ml) and changed daily. Ovine (o) PRL, bovine (b) GH, or human (h) GH were introduced after 2-4 days of culture, and PRL receptors were measured by determining [125I]hGH binding in the presence and absence of excess oPRL in a total particulate fraction pretreated with 3 M MgCl2. The specific binding of hGH (% per 100 μg protein) decreased by 8- to 10-fold (♀,17.9 ± 0.2% to 1.5%; ♂, 7.0 ± 0.1% to 0.7%) after 3 days in culture. When added after 3 days, hGH induced PRL receptors in both female and male cells with the effect being more gradual in the latter. Induction occurred with 10 ng/ml hGH and was maximal [11- to 13-fold control] at 250-1000 ng/ml. bGH and oPRL also induced PRL receptors with maximal levels attained at 250-500 ng/ml oPRL (3- to 4-fold control). The combined addition of oPRL (300 ng/ml) and bGH (300 ng/ml) yielded levels of induction comparable to that seen with hGH. Although hormone treatment restored PRL receptor levels to those seen in male rats, the much higher levels of female rats were not attained. Treatment of hepatocytes with hGH, bGH, or oPRL affected neither cell number (through 10 days of culture) nor PRL receptor affinity. At supramaximal doses hGH, PRL, and bGH down-regulated PRL receptors, but this was particularly noticeable for oPRL and hGH. 17β-Estradiol and testosterone added to male and female hepatocytes simultaneously with hGH had little or no effect on receptor induction. We conclude that hepatic PRL receptors are induced by both PRL and GH, each acting through its own receptor. The failure to restore receptor levels to those seen in female rats attests to the importance of other modulators. This dual regulation of the PRL receptor explains the unusual potency of hGH which binds to both PRL and GH receptors. © 1988 by The Endocrine Society.
Scientific Publication
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