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At least 19 recordsLinked to original sources
PubMed1990

Prostatein C3-mRNA: a sensitive marker of androgen-responsiveness in prostate explant cultures.

Prostatein is an androgen-dependent protein which is secreted by the rat ventral prostate. To determine if prostatein or its mRNA were responsive to androgen in vitro, prostate explants were cultured in media containing 0 or 25 nM dihydrotestosterone (DHT), estradiol (E2), or cortisol (F). Prostatein concentrations in medium were measured by radioimmunoassay at 2 and 4 days and in homogenates at 4 days. They were not changed significantly by any of these steroids. The concentration of the mRNA for the C3-subunit of prostatein was determined by dot hybridization at 0, 2, 4, 6, and 8 days. It was decreased significantly by 2 days when compared with explants cultured in the presence of DHT and significant differences persisted through 8 days. In conclusion, quantitation of the mRNA for the C3-subunit of prostatein in short-term cultures of ventral prostate explants appears to be more sensitive to changes in androgen concentration than does measurement of prostatein, per se. Prostatein C3-mRNA may be a useful marker for in vitro studies of androgen agonists and antagonists.

Androgen-Binding Protein↗
PubMed2003

Effect of prostatein, the major protein produced by the rat ventral prostate, on phagocytic cell functions.

PROBLEM: To determine whether prostatein, the major protein produced and secreted into the seminal fluid by the rat ventral prostate has any effect on the phagocytic cell functions in vitro. METHOD OF STUDY: Analysis was done by determining if purified prostatein added to cells obtained from the peritoneal cavity has any effect on their phagocytic and intracellular killing capacity. Also, we analyzed the effect of prostatein on the production of oxygen and nitrogen intermediates, measuring these metabolites by Nitroblue tetrazolium assay and by the Griess reaction respectively. RESULTS: Prostatein possess the ability to inhibit in vitro the phagocytic and killing properties of peritoneal rat leukocytes in a dose-dependent manner. The addition of a polyclonal antiserum against prostatein specifically blocks this inhibitory effect. Moreover, prostatein inhibits the production of oxygen and nitrogen intermediates by these cells. CONCLUSION: Regulation of the production of reactive oxygen species in the reproductive tract is extremely necessary to avoid their deleterious effects on the sperm motility and the fertilization process. We propose that prostatein, a protein supplied by an accessory gland like prostate, can inhibit the macrophage function, showing an important antioxidant effect.

Androgen-Binding Protein↗
PubMed1998

Prostatein (or rat prostatic steroid binding protein) is a major autoantigen in experimental autoimmune prostatitis.

Experimental autoimmune prostatitis (EAP) is a disease that could be considered an experimental model of human non-bacterial prostatitis. In this experimental model, male rats are intradermally immunized with a saline extract of male sex accessory glands (RAG) in an adequate adjuvant. The prostatitis observed in the immunized animals develops as a consequence of the immune response against RAG antigens, and the histological lesion is strikingly similar to the pattern of prostatic inflammation observed in the human disease. In this study, we purified one of the prostatic autoantigens recognized by the autoantibodies in our model. Amino acid sequence analysis identified the purified protein as prostatein or rat prostatic steroid binding protein, a member of the uteroglobin superfamily. Prostatein was recognized not only by the humoral autoimmune response, but also by the cellular autoimmune response. Certainly, the DTH response and lymph node cell proliferative assays against prostatein in immunized animals yielded positive results. Prostatein is not only the target of the autoimmune response in animals immunized with the whole extract, but also an inducing antigen of the disease. Purified prostatein, when incorporated to an adequate adjuvant, elicited cellular and humoral autoimmune response and lesion in the prostate gland. The identification of one of the target antigens in autoimmune prostatitis has provided a further refinement and characterization of our model, which could serve for a better understanding of the aetiology, pathogenesis and pathophysiology of non-bacterial prostatitis.

Androgen-Binding Protein↗
PubMed1987

Multihormonal control of synthesis and secretion of prostatein in cultured rat ventral prostate.

The synthesis and accumulation of prostatein, a major secretory protein of the rat ventral prostate, was examined in organ culture conditions. For the quantitation of this protein in the medium, a sensitive enzyme immunoassay was developed. The rat ventral prostate could be maintained in organ culture in defined medium for at least 2 weeks. Morphologically the changes in explants cultured without hormones resembled those of castration. These involutive changes could be postponed by testosterone and totally prevented by a combination of testosterone, corticosterone, and insulin in the culture medium. Newly synthesized prostatein, studied by fluorography of [35S] methionine-labeled proteins, accumulated only in the presence of testosterone. Its synthesis also took place in cultured prostate derived from castrated rats. Neither corticosterone nor insulin alone could sustain prostatein synthesis. Insulin increased the testosterone-dependent prostatein synthesis in the beginning of culture, but later, inhibition, rather than stimulation, could be noted. Corticosterone increased the testosterone-dependent synthesis of prostatein throughout the culture. The results show that organ culture of adult rat ventral prostate provides an in vitro model for studies of differentiated prostatic function.

Androgen-Binding Protein↗
PubMed1983

Isolation of two genomic sequences encoding the Mr = 14,000 subunit of rat prostatein.

Complementary DNAs to rat ventral prostate poly(A) RNA were cloned into pBR322 by the "dG-dC tailing" procedure. Clones containing cDNAs to the mRNAs coding for each of the three subunits of a major secretory protein (prostatein) were identified by hybrid-arrested translation. A 457-nucleotide base pair cDNA (E45) and a portion of a 365-base pair cDNA (E85) were analyzed to determine the composite complete DNA coding sequence for the Mr = 14,000 (C3) subunit of prostatein. A sequence of 12-nucleotide bases (TTTGCTGCTATG) in the signal peptide of C3 was noted to be homologous to signal peptide nucleotide sequences reported in cDNAs coding for the other two prostatein subunits, Mr = 6,000 (C1) and 10,000 (C2). Complementary DNA coding for the C3 subunit was used as a hybridization probe to screen an EcoRI rat genomic DNA library. Two unique 12-kilobase genomic clones, each containing mRNA coding sequences within 2.5-3-kilobase fragments, were identified by restriction enzyme mapping and Southern blot analysis. Restriction enzyme sites within the coding regions of both genes were analogous to the cDNA. Differences in restriction enzyme sites in regions of intervening sequences and flanking DNA established the uniqueness of the two genes. It is suggested that both genes may be transcribed in vivo.

Amino Acid Sequence↗
PubMedDate not supplied

4-MAPC, a 5 alpha-reductase inhibitor, reduces rat ventral prostate weight, DNA, and prostatein concentrations.

Several compounds, such as 4-MAPC (4-methyl-3-oxo-4-aza-5 alpha-pregnane-20- carboxylate), that inhibit conversion of testosterone (T) to dihydrotestosterone (DHT) by 5 alpha-reductase have been demonstrated to reduce prostate size in rats and dogs. The current studies were undertaken to determine if this effect is due to a reduction in cell number, in epithelial cell synthetic activity, or both. Eight-week-old intact rats were treated daily for 14 days with sesame seed oil, 4-MAPC (10 mg/kg), 4-MAPC + testosterone propionate (TP, 1 mg/kg), or 4-MAPC + TP (3 mg/kg). Rats were killed 24 hours after the last injection. In the animals treated only with 4-MAPC, ventral prostate weight was reduced 37%, but the 14% reduction in total DNA was not significant. The mean intraprostatic concentration of prostatein, a major secretory protein, was reduced 45% (P less than 0.05). The 3 mg/kg dose of TP increased ventral prostate weight, prostatein concentrations, and acid phosphatase activity, even though DNA/ventral prostate was similar to that in control animals. These observations indicate that the reduction in ventral prostate weight in adult rats is due in part to a reduction in cell number, but the primary effect was due to a reduction in synthetic activity, and possibly atrophy of the epithelial cells. Furthermore, TP in pharmacologic doses increased ventral prostate weight and synthetic activity without increasing DNA.

5-alpha Reductase Inhibitors↗
PubMed1999

Lipophilins: human peptides homologous to rat prostatein.

Lipophilin components A, B and C are human homologues of prostatein, the major secreted protein of rat prostate. This report describes their cDNA sequences, tissue expression and chromosomal localization. Lipophilin gene products were widely expressed in normal tissues, especially in endocrine-responsive organs. The gene for lipophilin C (also called mammaglobin b) is located on chromosome 11q12-q13.1, near the mammaglobin gene, a homologue overexpressed in many breast cancers. The lipophilin B gene resides on chromosome 10q23, a region deleted in many tumors, and the lipophilin A gene is on chromosome 15q12-q13.

Amino Acid Sequence↗
PubMed2002

Prostatein or steroid binding protein (PSBP) induces experimental autoimmune prostatitis (EAP) in NOD mice.

In a previous study, we showed that nonobese diabetic (NOD) mice, a strain that present an inherited predisposition to develop both spontaneous and induced autoimmune lesions, are susceptible to the induction of experimental autoimmune prostatitis (EAP), developing a severe inflammatory reaction in the prostate, accompanied by humoral and T-cell-mediated responses. In this study we asked whether the protein steroid binding protein (PSBP) or prostatein (a major autoantigen in the rat model of EAP) is a potential autoantigen in the NOD mouse model and examined the ability of purified PSBP to induce EAP in this strain. Our results indicate clearly that NOD male mice react immunologically to PSBP by developing lymphocytic inflammatory lesions in prostatic tissue and producing both a cellular- and humoral-specific autoimmune response. But our results suggest also the existence of other prostatic autoantigens present only in total prostate extract. Such additional antigens could enhance the autoimmune response and result in more severe forms of inflammation. We also analyzed the respective contributions of MHC antigens and CD4/CD8 T-cell subsets in NOD mice lacking expression of beta 2-microglobulin (NOD.beta2m degrees/degrees) or MHC class II beta chain (NOD.Abeta degrees/degrees) and demonstrate an essential role for CD4(+) T cells in the development of EAP in the NOD model. In conclusion, we demonstrate that PSBP is an autoantigen recognized by the NOD immune system, capable of generating humoral and cellular autoimmune responses and of inducing EAP. Moreover, using selected knock-out NOD mice we demonstrate an essential role for CD4(+) T cells in the development of EAP.

Androgen-Binding Protein↗
PubMed1987

Androgen regulation of c-myc messenger ribonucleic acid levels in rat ventral prostate.

Androgens regulate growth of the rat ventral prostate gland. In a search for possible mediators of androgen stimulated growth we have studied c-myc proto-oncogene expression in ventral prostate after androgen withdrawal and replacement. Steady state levels of c-myc mRNA were determined by Northern hybridization and compared with mRNA levels for prostatein, the major androgen dependent protein of ventral prostate. C-myc mRNA in ventral prostate increased nearly 4-fold within 1 day and 6- to 7-fold within 2 days after castration. Administration of androgen at the time of castration prevented this increase in c-myc mRNA levels. Androgen treatment of 4-day castrate rats caused c-myc mRNA levels to decrease within 4 h. Cycloheximide increased c-myc mRNA severalfold within 2 h. The net increase in c-myc mRNA after cycloheximide treatment was greater in the castrate than in the noncastrate or in androgen-treated castrate rats. These results suggest that androgen may influence both transcription and turnover of c-myc mRNA. Prostatein C3 mRNA decreased rapidly after castration and increased after androgen treatment of the castrate but was only slightly influenced by cycloheximide. Steady state levels of c-myc mRNA were higher in the 10-day-old rat and decreased with age while prostatein C3 mRNA increased with age. In situ hybridization demonstrated that both c-myc and prostatein mRNAs are expressed in the epithelial cells of ventral prostate acinar glands. These data indicate that androgens regulate the expression of c-myc in the ventral prostate.

Aging↗
PubMed1987

Interaction of male and female sex hormones in cultured rat prostate.

The organ culture of the rat ventral prostate was chosen as a model to determine whether any of the estrogen effects in vivo on the prostate are direct and expressed at the hormone concentrations normally found in the male. During 2 weeks of culture, estradiol at the high concentration of 10(-5) M blocked the androgenic activation of [3H]thymidine incorporation into DNA. The inhibition was localized in epithelium. Protein content of testosterone-treated explants and the accumulation of prostatein in the medium were considerably decreased, indicating inhibition of secretion. Antiandrogenic effects were not seen in morphology of estrogen-treated explants. The lower concentrations (from 10(-9) M to 10(-6) M) of estradiol increased the volume density of epithelium from day 7 onwards. The height of epithelium was concomitantly increased. The volume density of epithelium as well as the percentage of acini with metaplastic changes were significantly increased. These epithelial changes were less pronounced in the presence of androgen, suggesting that physiological concentrations of androgen prevent the expression of estrogen action in the morphology of the prostate. A change in staining with peanut (PNA)- and wheat germ agglutinin (WGA)-lectins indicated defective secretory capacity in metaplastic epithelium. In spite of the increased protein content in the explants, no constant pattern of the changes in prostatein accumulation could be recorded. Although the concentrations of estrogen required to induce squamous metaplasia were still unphysiological, the occurrence of this abnormal differentiation of the prostatic epithelium suggests that the cooperative action of estrogen is involved in androgen-dependent normal epithelial growth and possibly also in promoting growth of prostatic neoplasia.

Androgen-Binding Protein↗
PubMed1998

Lipophilin, a novel heterodimeric protein of human tears.

We identified a novel heterodimeric protein, lipophilin AC, in human tears. One of its components, lipophilin A (69 residues; mass, 7575.1; pI, 9.47) was homologous to the C1 and C2 components of prostatein ('estramustine-binding protein'), the major secreted protein of rat prostate. Human lipophilin C (77 residues; mass, 8854.1; pI, 4.94) was homologous to the rat prostatein C3 component and to human mammaglobin, a protein overexpressed in some mammary carcinomas. Tear lipophilins A and C expand the roster of human uteroglobin superfamily members and provide models for exploring these typically steroid-regulated and steroid-binding molecules.

Amino Acid Sequence↗
PubMed2004

Purification and characterization of pheromaxein, the porcine steroid-binding protein. A member of the secretoglobin superfamily.

Low molecular mass proteins are implicated in chemical communication throughout mammalian species, being involved in both perception and delivery of pheromonal compounds. In boars, pheromones are secreted in saliva to cause oestrous sows to take up the mating stance. These pheromones are the 16-androstene steroids, 5alpha-androsten-3alpha-ol and 5alpha-androsten-3-one. The submaxillary glands of boars contain a low molecular mass protein, pheromaxein, which is capable of binding these 16-androstene pheromones. Pheromaxein was purified, cloned and characterized. It was found to be a nonglycosylated heterodimeric protein, belonging to the secretoglobin superfamily and the major 16-androstene-binding protein present in submaxillary salivary glands of the boar. One subunit, pheromaxein A, was found to be homologous to prostatein peptides, C1 and C2 and lipophilin A and B, whereas the other subunit, pheromaxein C, was homologous to prostatein peptide C3 and lipophilin C. Transcription of pheromaxein A was limited to the prostate and submaxillary salivary glands from both the boar and sow, whereas transcription of the other subunit, pheromaxein C, was more widespread. This is similar to the transcription distribution of lipophilin in humans. Many isoforms of pheromaxein were found to exist, with a molecular mass range of 17,415-18,159 Da; these are probably products of a multigene family. Post-translational modifications, to generate mature pheromaxein isoforms, probably include C-terminal cleavage of pheromaxein A, followed by additional modifications.

Amino Acid Sequence↗
PubMed1995

Growth hormone directly affects the function of the different lobes of the rat prostate.

In this study, we investigated the involvement of GH in rat prostate function. First, we demonstrated that specific transcripts corresponding to the GH receptor (4.5 kilobases) and to the GH-binding protein (1.2 kilobases) were expressed in the normal rat prostate, but also in all prostatic carcinoma cell lines tested (LNCaP, PC-3, MAT-Lu, MAT-LyLu, and Pif-1). Moreover, these transcripts were much more abundant in the human and rat carcinoma cells than in the normal tissue. One-year-old dwarf rats were supplemented for 7 days with saline (group DR1) or highly purified rat GH (group DR2). Northern blotting and quantitation of prostatic messenger RNAs (mRNAs) revealed that GH increases the steady state levels of transcripts coding for androgen receptor (2.4-fold), type I and II 5 alpha-reductases (2.6- and 2.2-fold), and several androgen-dependent proteins [prostatein C3 subunit (3.6-fold), probasin (11.0-fold), and R. W. B. (Royal Winnipeg Ballet) (12.5-fold)]. This suggests that GH might either potentiate the action of androgens on the prostate or act directly on this gland by a mechanism that does not depend on testicular androgens. To address this question, we supplemented hypophysectomized and castrated adult rats for 7 days with saline (group HC1), rat GH (group HC2), testosterone propionate (group HC3), or GH plus testosterone (group HC4), starting 3 days after castration. In this animal model, the abundance of C3 mRNA increased in all hormone-treated rats; the stimulation factors were 3.5 (group HC2), 25.5 (group HC3), and 9.5 (group HC4) compared to group HC1. Analysis of prostatein synthesis by Western blotting confirmed these results at the protein level. The same trend was observed for probasin and RWB mRNA levels. Probasin mRNA increased 4.5-fold in group HC2 and 12-fold in group HC3, but did not increase in group HC4 (both hormones combined); enhancement of RWB mRNA was, respectively, 5.0-, 28.0-, and 15.0-fold in groups HC2, HC3, and HC4. GH did not affect the abundance of androgen receptor mRNA. As described previously, the level of this mRNA dropped significantly in group HC3. GH alone did not significantly alter the level of either 5 alpha-reductase mRNA, whereas testosterone, alone or with GH, produced a 2-fold increase in type II 5 alpha-reductase mRNA (groups HC3 and HC4). Type I isoenzyme mRNA reached 1.6 times the control level (group HC1) in groups HC3 and HC4.(ABSTRACT TRUNCATED AT 400 WORDS)

Androgens↗
PubMed1997

Vinclozolin and p,p'-DDE alter androgen-dependent gene expression: in vivo confirmation of an androgen receptor-mediated mechanism.

Vinclozolin and p,p'-DDE induce antiandrogenic developmental effects in vivo and are potent inhibitors of androgen receptor (AR) binding and AR-dependent gene expression in vitro. To determine whether this molecular mechanism is operative in vivo, the effects of these compounds on two androgen-regulated prostatic mRNAs were studied. Rats were sham operated or castrated and immediately implanted with one or two empty 2.5-cm silastic capsules or with one (1x) or two (2x) 2.5-cm capsules containing testosterone (T). T-implanted rats were treated by gavage for 4 days with vehicle (corn oil), vinclozolin (200 mg/kg/day), p,p'-DDE (200 mg/kg/day), or the antiandrogen flutamide (100 mg/kg/day) as a positive control. Vinclozolin, p,p'-DDE, and flutamide all induced a reciprocal decline in seminal vesicle (p < 0.01) and prostate (p < 0.01) weight as well as a reduction in immunohistochemical staining of AR in epididymal nuclei compared to vehicle-treated T-implanted controls. Specific AR antagonism was assessed by determining the ability of these chemicals to induce a testosterone-repressed prostatic message (i.e., TRPM-2) and/or repress a testosterone-induced prostatic message (i.e., prostatein subunit C3). Densitometry scans of Northern blots indicated that vinclozolin, p,p'-DDE, and flutamide each induced TRPM-2 mRNA and repressed C3 mRNA compared to vehicle-treated T-implanted controls. These antiandrogenic effects were competitively reduced in castrate rats implanted with two 2.5-cm T capsules (2x), where serum T levels were elevated more than twofold above physiological levels. Taken together, these data indicate that vinclozolin and p,p'-DDE act as antiandrogens in vivo by altering the expression of androgen-dependent genes.

Androgen Antagonists↗
PubMed1995

Androgen-independent effects of prolactin on the different lobes of the immature rat prostate.

In this study, we have examined the respective roles of androgens and prolactin (Prl) on rat prostate development and function. Hypophysectomized immature rats, castrated or not after hypophysectomy and treated or not with a 5 alpha-reductase inhibitor, were used to study the different aspects of Prl action on the rat prostate and its synergy with androgens in vivo. Using Northern blot analysis and quantitation of prostatic mRNAs, we have shown that Prl significantly increases the steady-state levels of transcripts coding for several lobe-specific proteins: the C3 subunit of prostatein, probasin, and RWB. We have confirmed these observations in vitro, on explants of immature rat prostate treated with either saline, Prl, or testosterone. In addition, we have demonstrated by a nuclear run-on assay that Prl significantly enhances the transcription rate of the C3 gene in the rat prostate. We conclude that the effects of Prl concern all lobes of the organ and are, at least in part, androgen-independent. Moreover, Prl is able, via an androgen-independent pathway, to increase the rate of transcription of the C3 gene, one of the major products of the rat prostate.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1985

Circadian rhythms in accessory sex gland function in the male rat.

Alterations in various parameters of accessory sex gland function were monitored during two separate 24 h periods in adult male rats, and compared to fluctuations in the circulating levels of testosterone, prolactin, corticosterone and LH. Bimodal circadian rhythms in ventral prostate prolactin binding, cytosolic oestrogen binding and seminal vesicle weight could be discerned which appeared to be related to a similar rhythmicity in circulating testosterone levels, but with a phase shift of 3 h. Prostatic membrane bound adenylyl cyclase activities (basal and hormone stimulated) and prostatein concentrations followed different patterns possibly correlated to other endocrine changes.

Adenylyl Cyclases↗
PubMed1985

Short-term effects of prolactin on prostatic function in rats with lisuride-induced hypoprolactinaemia.

The effects of a single injection of ovine prolactin on prostatic function were monitored in intact, intact androgenized and castrated-androgenized rats rendered hypoprolactinaemic after 7 days of treatment with a potent dopamine agonist, lisuride. Hypoprolactinaemia was associated with reductions in ventral prostate weight, polyamine levels, lateral lobe zinc and the concentration of the ventral prostate protein prostatein, but an elevation in the level of cytosolic oestradiol binding. Whether these differences attained statistical significance depended on whether the animals were intact, intact-androgenized or castrated-androgenized. With the exception of ventral prostate weight and lateral lobe zinc concentrations, a single injection of prolactin restored or reversed these changes towards control levels within 12 h, which could not be explained by an indirect effect of the hormone on adrenal or testicular function. No effects of lisuride or prolactin were observed with regard to the content of fructose in the coagulating gland or in the degree of prolactin binding to prostatic membranes.

Androgen-Binding Protein↗