Immunocytochemical localization of prolactin receptors in rat liver cells: I. Dependence on sex and sex steroids

Смирнова, О. В.; Petraschuk, O.M.; Kelly, Paul A.

doi:10.1016/0303-7207(94)90037-x

Cited by 31 publications

(25 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, during puberty, when the production and secretion of gonadal steroid hormones increase, the hepatic level of PRL binding sites was found to increase in female but decrease in male rats (Maes et al 1983). It was also shown immunocytochemically that the amount of PRLR in the liver of gonadectomized rats was increased by estrogen treatment and decreased by androgen treatment (Smirnova et al 1994). Furthermore, it was recently shown that the levels of mRNA for the long and short forms of PRLR in rat liver decreased in males but increased in females during the course of sexual maturation (Sakaguchi et al 1994).…”

Section: Discussionmentioning

confidence: 91%

Involvement of gonadal steroid hormone disturbance in altered prolactin receptor gene expression in the liver of diabetic mice

Murakami¹,

Maeda²,

Oka³

1999

Journal of Endocrinology

View full text Add to dashboard Cite

The levels of mRNA for long and three short forms of prolactin receptor (PRLR) were examined in the livers of normal (db+/db ) and insulin-resistant diabetic (db+/ db+) mice to assess the role of gonadal steroid hormones in the regulation of PRLR gene expression in diabetes mellitus. In females, plasma levels of testosterone in diabetic mice were higher, and those of 17 -estradiol were lower when compared with levels in normal mice. By contrast, diabetic male mice had lower plasma levels of testosterone than normal males and showed no significant difference in the low circulating level of 17 -estradiol compared with normal males. The short 3 form of PRLR (PRLR3) mRNA was the most abundant in the liver of both normal and diabetic mice. In addition, the level of PRLR3 mRNA in normal females was 8-fold higher than in normal males. The level of PRLR3 mRNA in diabetic females was approximately a quarter lower than in normal females, whereas the level of PRLR3 mRNA in diabetic males was approximately 2-fold higher than in normal males. During postnatal development, the level of PRLR3 mRNA increased during puberty in normal females, while the level in diabetic females decreased to a nadir at 7 weeks of age followed by a progressive rise. On the other hand, the levels of PRLR3 mRNA in both normal and diabetic males decreased gradually during 5 to 14 weeks of age. Testosterone treatment of diabetic males and females resulted in a 49·1 and 49·8% decrease of PRLR3 mRNA respectively. 17 -Estradiol treatment slightly (18%) increased levels of PRLR3 mRNA in diabetic males. These results suggest that the hepatic level of PRLR mRNA is regulated by the inhibitory effect of testosterone and the stimulatory effect of estrogen in both normal and diabetic mice.

show abstract

Section: Discussionmentioning

confidence: 91%

Involvement of gonadal steroid hormone disturbance in altered prolactin receptor gene expression in the liver of diabetic mice

Murakami¹,

Maeda²,

Oka³

1999

Journal of Endocrinology

View full text Add to dashboard Cite

show abstract

“…It has been shown that PRL-R is largely expressed in hepatocytes in the rat liver with higher levels in the female than in the male and that the PRL-R levels increase and decrease in both sexes with oestrogen and androgen treatments respectively (Smirnova et al 1994). More recently, PRL-R gene expression has been observed in Kupffer cells as well as in hepatocytes in the male rat liver (Yokoyama et al 2003).…”

Section: Discussionmentioning

confidence: 99%

Differential effects of sex steroid hormones on the expression of multiple first exons including a novel first exon of prolactin receptor gene in the rat liver

Tanaka¹,

Suzuki²,

Kawana³

et al. 2005

Journal of Molecular Endocrinology

View full text Add to dashboard Cite

In addition to the known four alternative first exons E1 1 , E1 2 , E1 3 and E1 4 of the rat prolactin receptor (PRL-R) gene, a novel first exon, E1 5 , was identified by cDNA cloning of the 58-end region of PRL-R mRNA in the rat liver. Genomic fragments containing E1 5 and its 58-or 38-flanking regions were also cloned from rat kidney genomic DNA. A sequence search for E1 5 revealed that E1 5 is located 49 kb upstream of exon 2 of the PRL-R gene in rat chromosome 2q16. RT-PCR analysis revealed that E1 5 was preferentially expressed in the liver, brain and kidney. Expression profiles of E1 2 -, E1 3 -and E1 5 -PRL-R mRNAs in the liver of male and female rats at 5 days of age and those at 8 weeks of age were examined by RT-PCR. The levels of E1 2 -PRL-R mRNA in the female rat increased remarkably in rats at 8 weeks of age compared with those at 5 days of age, and the levels of E1 5 -PRL-R mRNA in the male rat decreased markedly at 8 weeks of age compared with those at 5 days of age. In the female rat, the levels of E1 2 -PRL-R mRNA at 8 weeks of age decreased with ovariectomy performed at 4 weeks of age and recovered with the administration of -oestradiol. On the contrary, the levels of E1 5 -PRL-R mRNA increased with ovariectomy and decreased with the oestrogen treatment. In the male rat liver, the levels of E1 2 -PRL-R mRNA at 8 weeks of age increased strikingly with castration performed at 4 weeks of age and became undetectable with the administration of testosterone. The levels of E1 5 -PRL-R mRNA increased slightly with castration and were restored by testosterone treatment. Removal of gonadal tissues and sex steroid hormone treatment had no effect on the expression levels of E1 3 -PRL-R mRNA in both female and male rat livers. These results indicated that the expression of the PRL-R gene in the liver is regulated by the differential effects of sex steroid hormones on the transcription of the multiple first exons including the novel one.

show abstract

“…3A and B), which is also well established Table 2. (Sakaguchi et al 1994, Smirnova et al 1994, Bogorad et al 2004: male sex hormones decrease and female sex hormones increase PrlR level. In contrast, immunohistochemistry did not reveal any pronounced PrlR-positive signal in cholangiocytes (Fig.…”

Section: Parameters Of Prlr Expression In the Cholangiocytes Of Normamentioning

confidence: 99%

Long isoform of prolactin receptor predominates in rat intrahepatic bile ducts and further increases under obstructive cholestasis

Bogorad

Ostroukhova²,

Orlova³

et al. 2006

Journal of Endocrinology

View full text Add to dashboard Cite

Prolactin participates in the regulation of liver function. However, prolactin receptor (PrlR) expression and its regulation have been described only for hepatocytes. In this study, we investigated the expression and regulation of PrlR isoforms in the other important intrahepatic cellular compartment: the biliary epithelial cells, or cholangiocytes. Our aim was to determine whether prolactin should be considered as a potential regulator of cholangiocyte function under normal and pathological conditions. Cholangiocytes and hepatocytes were differentially isolated from rat liver. PrlR expression was analysed at the mRNA level by isoform-specific semiquantitative PCR, and at the protein level by immunostaining of liver sections. Hormonal regulation of PrlR expression was evaluated by comparing intact rats with gonadectomized, pituitary-grafted or bromocriptine-treated animals. Common bile-duct ligation was used as the experimental model of cholestasis. Our results demonstrate that the expression pattern and regulation of PrlR isoforms is totally different in cholangiocytes compared with hepatocytes: (1) mature rat cholangiocytes express low levels of PrlR, while it is very high in hepatocytes, (2) only the long isoform is detected in cholangiocytes, while the short isoform predominates in hepatocytes and (3) PrlR levels in cholangiocytes are induced by obstructive cholestasis, but not by sex hormones or prolactin, while it is the opposite in hepatocytes. From these data, the actions of prolactin on liver are anticipated to exhibit strong cell-type specificity in both normal and pathological conditions.

show abstract

Immunocytochemical localization of prolactin receptors in rat liver cells: I. Dependence on sex and sex steroids

Cited by 31 publications

References 18 publications

Involvement of gonadal steroid hormone disturbance in altered prolactin receptor gene expression in the liver of diabetic mice

Involvement of gonadal steroid hormone disturbance in altered prolactin receptor gene expression in the liver of diabetic mice

Differential effects of sex steroid hormones on the expression of multiple first exons including a novel first exon of prolactin receptor gene in the rat liver

Long isoform of prolactin receptor predominates in rat intrahepatic bile ducts and further increases under obstructive cholestasis

Contact Info

Product

Resources

About