Prolactin and Leydig Cell Responsiveness to LH/hCG in the Rat

Purvis, K.; Clausen, O. P. F.; Olsen, Ambre L.; Haug, Egil; Hansson, V.

doi:10.3109/01485017908988408

Cited by 72 publications

(29 citation statements)

References 24 publications

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“…11). Both forms of PRL increased expression of the LHR, a result consistent with positive effects of PRL administration in prepubescent and hypophysectomized animals (2,10,32,36,54) because this would be expected to increase sensitivity to LH. Making the assumption that the mRNA was translated into protein displayed on the plasma membrane, one might also have expected this to normalize 3␤-HSD by increasing sensitivity to LH when LH levels were normal in the adult animals, but this was not the case in the presence of either form of PRL.…”

Section: Discussionsupporting

confidence: 53%

“…In studies by other investigators, PRL has been shown to be responsible for the induction of Leydig cell proliferation and differentiation in prepubertal hypophysectomized rats (10) and the maintenance of Leydig cell morphology, upregulation of luteinizing hormone receptor (LHR) expression, and potentiation of luteinizing hormone (LH)-induced steroidogenesis in hypophysectomized rats (2,10,32,36,54). In vitro approaches, utilizing murine Leydig tumor cell lines and isolated rodent primary Leydig cell cultures, have concluded that PRL exerts trophic effects on Leydig cell steroidogenic function, mostly through an effect on LH-induced testosterone production (23,32,33,45), although some of these effects have been shown to have biphasic dose-response curves, with high concentrations actually exerting an inhibitory effect (33).…”

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confidence: 99%

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Common and specific effects of the two major forms of prolactin in the rat testis

Williams¹,

Guzmán²,

Dang³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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Williams VL, DeGuzman A, Dang H, Kawaminami M, Ho TW, Carter DG, Walker AM. Common and specific effects of the two major forms of prolactin in the rat testis. Am J Physiol Endocrinol Metab 293: E1795-E1803, 2007. First published October 2, 2007; doi:10.1152/ajpendo.00541.2007.-Prolactin (PRL) has both stimulatory and inhibitory effects on testicular function, a finding we hypothesized may be related in some part to the form of the hormone present or administered. In the analysis of the pituitary secretion profiles of early pubescent vs. mature male rats, we found PRL released from early pubescent pituitaries had about twice the degree of phosphorylation. Treatment of mature males with either unmodified PRL (U-PRL) or phosphorylated PRL (via the molecular mimic S179D PRL) for a period of 4 wk (circulating level of ϳ50 ng/ml) showed serum testosterone decreased by ϳ35% only by treatment with the phospho-mimic S179D PRL. Given the specificity of this effect, it was initially surprising that both forms of PRL decreased testicular expression of 3␤-hydroxysteroid dehydrogenase and steroidogenic acute regulatory protein. Both forms also increased expression of the luteinizing hormone receptor, but only S179D PRL increased the ratio of short to long PRL receptors. Endogenous PRL and luteinizing hormone levels were unchanged in all groups in this time frame, suggesting that effects on steroidogenic gene expression were directly on the testis. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling analysis combined with staining for 3␤-hydroxysteroid dehydrogenase and morphometric analysis showed that S179D PRL, but not U-PRL, increased apoptosis of Leydig cells, a finding supported by increased staining for Fas and Fas ligand in the testicular interstitium, providing an explanation for the specific effect on testosterone. S179D PRL, but not U-PRL, also increased apoptosis of primary spermatogonia, and U-PRL, but not S179D PRL, decreased apoptosis of elongating spermatids. Thus, in mature males, hyperprolactinemic levels of both forms of PRL have common effects on steroidogenic proteins, but specific effects on the apoptosis of Leydig and germ cells. phosphorylated prolactin; S179D prolactin; apoptosis; Leydig cells; testosterone; 3␤-hydroxysteroid dehydrogenase; steroidogenic acute regulatory protein; luteinizing hormone receptor; luteinizing hormone; short prolactin receptor PROLACTIN (PRL) is a 23-kDa polypeptide hormone produced and secreted in largest quantity by lactotropes of the anterior pituitary (reviewed in Ref. 13). It has a broad range of functions in the male reproductive system, but its role in testes remains poorly understood and is somewhat species specific (reviewed in Ref. 1).In studies by other investigators, PRL has been shown to be responsible for the induction of Leydig cell proliferation and differentiation in prepubertal hypophysectomized rats (10) and the maintenance of Leydig cell morphology, upregulation of luteinizing hormone receptor (LHR) expression, and ...

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Section: Discussionsupporting

confidence: 53%

mentioning

confidence: 99%

Common and specific effects of the two major forms of prolactin in the rat testis

Williams¹,

Guzmán²,

Dang³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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“…In the rat, Belanger et al [4] showed that PRL treatment increased serum and testicular androgen levels as early as 2 h after injection. In vivo treatment with PRL stimulates in vitro androgen production by testicular interstitial cells [23]. Mild chronic hyperprolactinaemia also results in an increase in serum LH levels [2] as well as in testicular LH receptors [23].…”

Section: Introductionmentioning

confidence: 99%

Acute Effect of Prolactin on Ornithine Decarboxylase Activity in the Rat Testis

Heras

Calandra

1992

Archives of Andrology

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A study was conducted to evaluate the effect of the acute treatment with prolactin (PRL) on ornithine decarboxylase (ODC) activity in the rat testis. Injection of a single SC dose of ovine PRL to puberal rats resulted in the activation of ODC from whole testis. This effect was maximal at 4 h after injection, and statistically significant at the dose of 500 fig. The effect of PRL was confined to the interstitial space; no change was observed in seminiferous tubules. PRL was unable to further increase testicular ODC activity when injected together with a stimulatory dose of human chorionic gonadotropin (hCG). The effect of PRL was mimicked by injection of a single dose of the dopamine antagonist sulpiride, which provoked a ninefold increase in serum PRL levels. In contrast, PRL did not stimulate testicular ODC activity in hypophysectomized rats, either under basal conditions or during treatment with PRLhCG, indicating the requirement of a functional hypophysis for the expression of PRL action. These results suggest that the stimulation of testicular ODC activity by PRL is a marker of the trophic response of the testis to this hormone, different from the stimulation of steroidogenesis. This activity could be useful for the study of PRL action on the testis as well as of the interaction between PRL and LH at the testicular level.

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“…Moreover, many studies generally suggest that PRL positively modulates testicular functions in several ways, as follows: PRL is involved in the upregulation of LH receptor on Leydig cells [2,3], in the increase in FSH receptors in Sertoli cells [4], and in the meiosis of germ cells [5]. In contrast, none of the parameters or functions of the male reproductive organs are affected in PRL knockout (KO) or PRL receptor (PRLR) KO mice [6,7].…”

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confidence: 99%

“…Dev. 56: [567][568][569][570][571][572][573][574] 2010) he various functions of prolactin (PRL) in vertebrates include the growth and differentiation of the mammary epithelium, lactation in mammals, osmoregulation and parental behavior in teleosts, amphibian development, broodiness in hens, crop sac production in pigeons and immunoregulation [1].Moreover, many studies generally suggest that PRL positively modulates testicular functions in several ways, as follows: PRL is involved in the upregulation of LH receptor on Leydig cells [2,3], in the increase in FSH receptors in Sertoli cells [4], and in the meiosis of germ cells [5]. In contrast, none of the parameters or functions of the male reproductive organs are affected in PRL knockout (KO) or PRL receptor (PRLR) KO mice [6,7].…”

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confidence: 99%

Analysis of Prolactin Gene Expression and Cleaved Prolactin Variants in the Mouse Testis and Spermatozoa

Ishida

Yoshida

Fukuta

et al. 2010

Journal of Reproduction and Development

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Abstract. Prolactin (PRL) has long been known to be a hormone responsible for mammary gland development and lactation in females, whereas its role in males is still unclear. Thus, we investigated male mouse (m) PRL protein and mRNA expression in spermatozoa at various differentiation stages in the testes. Quantitative RT-PCR and in situ hybridization detected the expression of PRL not only in Leydig cells but also in germ cells, in particular in spermatogonia. The nucleotide sequence of testis PRL mRNA was the same as that in the pituitary. The mPRL was detected in Leydig cells and in round and elongated spermatids of the testes by immunohistochemistry. Immunoblotting detected 2 forms of mPRL in the testes, one form was 23-kDa PRL, and the other form was smaller than full-length PRL. Based on these results, we focused on N-terminal cleaved PRL to determine its involvement in spermatogenesis. Immunohistochemistry using two sets of antibodies, one that recognized full-length PRL and Nterminal cleaved PRL and another that recognized full-length PRL and C-terminal cleaved PRL, suggested that intact PRL was localized in the nucleus of round spermatids, while N-terminal cleaved PRL variants were localized in the Golgi apparatus of the sperrmatid nuclei of round spermatids, cytoplasms of elongated spermatids and in the spermatozoa tails. These findings suggest that PRL is ectopically expressed in the spermiogenesis and spermatogenesis and that cleaved PRL variants were localized in the Golgi apparatus of spermatids and in spermatozoa tails. Key words: Ectopic expression, Mouse, Prolactin, Testis (J. Reprod. Dev. 56: [567][568][569][570][571][572][573][574] 2010) he various functions of prolactin (PRL) in vertebrates include the growth and differentiation of the mammary epithelium, lactation in mammals, osmoregulation and parental behavior in teleosts, amphibian development, broodiness in hens, crop sac production in pigeons and immunoregulation [1].Moreover, many studies generally suggest that PRL positively modulates testicular functions in several ways, as follows: PRL is involved in the upregulation of LH receptor on Leydig cells [2,3], in the increase in FSH receptors in Sertoli cells [4], and in the meiosis of germ cells [5]. In contrast, none of the parameters or functions of the male reproductive organs are affected in PRL knockout (KO) or PRL receptor (PRLR) KO mice [6,7]. Thus, the exact role of PRL in the regulation of testicular function is still unclear. It is unknown why the lack of PRL signaling in PRLR KO and PRL KO mice affects the reproductive function of the male mouse in such a way that the expected results are marginal compared with those obtained in hypophysectomized or PRL deficient hereditary dwarf mice or even absent. Perhaps normal or near-normal reproductive function in PRLR KO and PRL KO animals is due to compensatory mechanisms and/or alternate signaling pathw a y s ( e . g . , gr o w t h h or m o n e) t ha t a r e a b s e n t i n b o t h hypophysectomized animals and hereditary dwarf mic...

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Prolactin and Leydig Cell Responsiveness to LH/hCG in the Rat

Cited by 72 publications

References 24 publications

Common and specific effects of the two major forms of prolactin in the rat testis

Common and specific effects of the two major forms of prolactin in the rat testis

Acute Effect of Prolactin on Ornithine Decarboxylase Activity in the Rat Testis

Analysis of Prolactin Gene Expression and Cleaved Prolactin Variants in the Mouse Testis and Spermatozoa

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