Article

Prolactin-gene expression in human ovarian follicular cells

Johns Hopkins University, Baltimore, Maryland, United States
Fertility and Sterility (Impact Factor: 4.59). 02/2003; 79(1):182-5. DOI: 10.1016/S0015-0282(02)04536-3
Source: PubMed

ABSTRACT To investigate prolactin gene expression in human ovarian follicular cells.
RNA was isolated from follicular cells obtained at the time of transvaginal oocyte retrieval from patients after controlled ovarian hyperstimulation. The RNA was subjected to reverse transcription and polymerase chain reaction (RT-PCR) using prolactin-specific primers. The RT-PCR products were analyzed by gel electrophoresis, followed by Southern blot analysis using prolactin-specific probes.
Department of gynecology and obstetrics research laboratory.
Women undergoing controlled ovarian hyperstimulation followed by transvaginal oocyte retrieval.
Controlled ovarian hyperstimulation followed by transvaginal oocyte retrieval. Expression of prolactin mRNA by follicular cells.
The presence of prolactin-specific cDNA amplified by RT-PCR from RNA isolated from human follicular cells was confirmed by Southern blot analysis.
Human ovarian follicular cells are an extrapituitary site of prolactin gene expression.

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    • "It has, for instance been located in a variety of reproductive tissues (in ovaries, the deciduas, placenta, mammary glands, testes, prostate and germ cells), immune tissues (leucocytes , bone marrow, thymus, spleen, tonsils, lymph nodes), neural tissues (brain and spinal cord, in sense organs and vitreous fluid), integumentary tissues (skin, sweat glands, sebaceous glands, hair and hair follicles) and other locations (in lachrymal glands, kidneys, in adipose and in blood endothelial cells) (see Table 1). These studies include those that show the presence of prolactin mRNA (eg. by in situ in the neural retina; Aranda et al., 2005; by RT-PCR in hair follicles, Foitzik et al., 2006; by RT-PCR in ovarian follicles, Phelps et al., 2003) and those that show the presence of immunoreactive proteins (eg. by immunohistochemistry and western blotting in capillary endothelial cells, Ochoa et al., 2001; by radioimmunoassay in adipose tissue explants, Hugo et al., 2008). "
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    ABSTRACT: Growth hormone (GH) and prolactin (PRL) are both endocrines that are synthesized and released from the pituitary gland into systemic circulation. Both are therefore hormones and both have numerous physiological roles mediated through a myriad of target sites and both have pathophysiological consequences when present in excess or deficiency. GH or PRL gene expression is not, however, confined to the anterior pituitary gland and it occurs widely in many of their central and peripheral sites of action. This may reflect "leaky gene" phenomena and the fact that all cells have the potential to express every gene that is present in their genome. However, the presence of GH or PRL receptors in these extrapituitary sites of GH and PRL production suggests that they are autocrine or paracrine sites of GH and PRL action. These local actions often occur prior to the ontogeny of pituitary somatotrophs and lactotrophs and they may complement or differ from the roles of their pituitary counterparts. Many of these local actions are also of physiological significance, since they are impaired by a blockade of local GH or PRL production or by an antagonism of local GH or PRL action. These local actions may also be of pathophysiological significance, since autocrine or paracrine actions of GH and PRL are thought to be causally involved in a number of disease states, particularly in cancer. Autocrine GH for instance, is thought to be more oncogenic than pituitary GH and selective targeting of the autocrine moiety may provide a therapeutic approach to prevent tumor progression. In summary, GH and PRL are not just endocrine hormones, as they have autocrine and/or paracrine roles in health and disease. Copyright © 2014 Elsevier Inc. All rights reserved.
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    • "), im Myometrium (Gellersen et al., 1991) und in den Follikelzellen des Ovars (Phelps et al., 2003). Auch die Follikelflüssigkeit enthält Prolaktin (Lebedeva et al., 1998). "
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    • "However, our data demonstrating the presence of prolactin peptide in lysates and supernatants of granulosa cells suggest that the ovary could be an additional extrapituitary source of prolactin. This ®nding is in contrast to an earlier study (Ohwaki et al., 1992) but is in agreement with more recent data, which demonstrated that prolactin gene expression was evident in homogenized whole ovarian samples (Schwarzler et al., 1997) and in human luteinized granulosa cells (Phelps et al., 2003). If prolactin is a local product, then its levels might be expected to exceed those in serum, and indeed the levels were found to range from 9 to 180% of serum levels in a range of matched follicles (McNatty et al., 1975). "
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    ABSTRACT: The role of prolactin in the regulation of ovarian folliculogenesis and corpus luteal function and in particular its relationship to atresia in these structures is as yet unclear. We established a model of apoptosis in which to examine the actions of prolactin. Granulosa cells collected from IVF-flush were cultured at 0.1-0.3 x 10(6) cells/well in growth media for 48 h, placed into serum-free media for 24 h prior to dosing for 24 h. Dose responses to C2-ceramide and prolactin were performed. Cells were then treated with an apoptotic dose of C2-ceramide alone, prolactin (100 ng/ml) alone or a combination of the two. Cell death was assessed by Trypan Blue cell counting and MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; Thiazolyl Blue] assay and apoptosis confirmed by morphological assessment and flow cytometry. C2-ceramide (0-40 micro mol/l) induced a dose-dependent increase in cell death (63.8% increase at 40 micro mol/l) and, morphologically, cells exhibited classical features of apoptosis. Prolactin alone had no effect on metabolic activity or total cell number. On co- incubation, prolactin alone had no effect on cell death, whereas C2-ceramide induced an approximately 62.6% increase in apoptosis, which was inhibited in the presence of prolactin. Prolactin may contribute significantly to early corpus luteum formation and survival by acting as a potent antiapoptotic factor for human granulosa cells.
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