PubMed · 7036061
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R Fienberg. 1981. Thecosis.. https://pubmed.ncbi.nlm.nih.gov/7036061/
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Expression of 3beta-hydroxysteroid dehydrogenase (3beta-HSD) is mainly found in the Leydig cells from which steroid hormones are biosynthesized in the testes. To investigate whether endocrine disruptors affect the microenvironment of the testes, the mRNA expression of 3beta-HSD as a molecular marker for androgen biosynthesis was analyzed in rat testes exposed to several endocrine disruptors using a reverse transcription-polymerase chain reaction technique. Testosterone [50, 200 and 1,000 microg/kg body weight (BW)], flutamide (1, 5 and 25 mg/kg BW), ketoconazole (0.2, 1, 5 and 25 mg/kg BW), diethylhexyl phthalate (10, 50 and 250 mg/kg BW), nonylphenol (10, 50, 100 and 250 mg/kg BW), octylphenol (10, 50 and 250 mg/kg BW), and diethylstilbestrol (10, 20 and 40 microg/kg BW) were orally administered to 4-week-old Sprague-Dawley rats for 3 weeks daily. Although testosterone at a low dose (50 microg/kg/day) increased the expression of 3beta-HSD mRNA, it was significantly decreased in the rats treated with 200 or 1,000 microg/kg/day testosterone compared with the control group (P<0.05). Furthermore, ketoconazole, diethylhexyl phthalate, nonylphenol, octylphenol and diethylstilbestrol caused significant downregulation of 3beta-HSD mRNA in the testes at all doses (P<0.05). However, flutamide remarkably increased the level of 3beta-HSD mRNA in the testes (P<0.05). These results suggest that endocrine disruptors may influence androgen biosynthesis in the testes by alteration of 3beta-HSD mRNA expression.
In the central nervous system, transferrin (Tf) is produced by oligodendroglial cells (OLGcs) and is essential for their development. Recently, using the complete cDNA of the human Tf gene, we obtained clones overexpressing Tf in two OLGc lines, N19 and N20.1, which represent different stages of differentiation. We showed that the overexpression of this glycoprotein promotes the maturation and myelinogenic capacity of both cell lines. In this work, using cDNA array technology, we examined changes induced by Tf in 1,176 genes. We found 41 genes differentially expressed in both cell lines, all of them involved in OLGc development. In the less mature cells (N19) overexpressing Tf, there was a significant increase in key enzymes of neurosteroid metabolism, such as cholesterol side chain cleavage cytochrome P450, 3beta-hydroxysteroid dehydrogenase and 5alpha-reductase type 1. In the more mature cell line (N20.1), Tf overexpression produced an induction of several mRNAs of the GABA(A) receptor subunits, of thyroid hormone receptors and of proteins involved in axon-glia interactions such as F3/contactin. In addition, in both cell lines, Tf overexpression induced an increase in the expression of different isoforms of transforming growth factor beta receptors and in several genes related to mitochondrial function and to complex lipid metabolism, crucial steps in myelin synthesis. Differentiation produced by Tf in both cell lines seems to occur by modulation of different genes depending on the maturational stage of the cells. Our findings provide new insights into the molecular basis of OLGc differentiation and on the role played by Tf in this process.
Although the human and the nonhuman primate fetal adrenal glands undergo a highly unique pattern of cortical zone-specific intrauterine growth and development, studies of the regulatory components of the cell cycle responsible for this growth have not been conducted. Therefore, the present study determined expression of the cell cycle regulators, cyclin D1 and cyclin E, and their cyclin-dependent kinases, Cdk2, Cdk4, and Cdk6, and Ki67 a marker of cell proliferation within the baboon fetal adrenal cortex during advancing stages of gestation. Fetal adrenal glands were obtained on days 60 (early), 100 (mid), and 160-170 (late) of gestation (term = 184 days). Mean (+/- s.e.) cyclin D1 mRNA levels, determined by RT-PCR and expressed relative to 18S rRNA, were similar at early (0.85 +/- 0.09) and mid (1.04 +/- 0.08) gestation, then decreased (P < 0.001, ANOVA) approximately 50% by late gestation (0.57 +/- 0.04). Cyclin E mRNA levels were also similar at early (2.03 +/- 0.07) and mid (1.63 +/- 0.31) gestation, and decreased by 70% (P < 0.001) in late gestation (0.53 +/- 0.09). Coinciding with the decrease in cyclin D1 and cyclin E, the percentage of Ki67 positive cells in the definitive zone decreased twofold (P < 0.01) between mid (28.2 +/- 3.6) and late (13.8 +/- 1.7) gestation. The cyclin D1 and cyclin E proteins, determined by immunocytochemistry, were expressed at high levels in the definitive zone of baboon fetal adrenal gland, where they decreased between mid- and late gestation. In contrast, immunocytochemical expression of the functionally important steroidogenic enzyme Delta(5)-3beta-hydroxysteroid dehydrogenase (3beta-HSD) became abundant in the definitive and transitional zones with advancing pregnancy. However, fetal adrenal Cdk2, Cdk4, and Cdk6 mRNA levels and protein immunoexpression were similar in the baboon fetal adrenal at early-, mid-, and late gestation. In summary, expression of cyclin D1, cyclin E, and Ki67 decreased, while 3beta-HSD expression increased, in the fetal adrenal cortex, particularly in the definitive zone, between mid- and late-baboon gestation. We propose that a developmental decline in cellular proliferation permits functional differentiation of fetal adrenal cortical cells, leading to increased production of steroid hormones important for placental estrogen synthesis and maturation of organ systems within the developing fetus.