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Search for other papers by Y. D. Li in
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ABSTRACT
The effect of transferrin on basal and FSH-stimulated aromatase activity of granulosa cells from immature female rats treated with diethylstilboestrol (DES) was examined in vitro by a radiometric method. The basal activity of the enzyme was very low after 3 days of incubation. Treatment with FSH (20 ng/ml) resulted in a 9·6-fold increase in activity, whereas coincubation with increasing doses of transferrin (3–300 μg/ml) produced a dose-dependent inhibition of FSH-stimulated aromatase activity with a projected minimal effective dose of < 2 μg/ml. A time-course study showed that the inhibitory effect of transferrin on aromatase activity has become significant at 48 h of incubation.
The inhibitory action of transferrin on the enzyme complex was further confirmed by showing that the FSH dose–response curve was significantly suppressed by concomitant treatment with 100 μg transferrin/ml with a maximum suppression of 54·1 % at a dose of 30 ng FSH/ml.
The possibility that transferrin may act through a non-specific inhibitory effect seems unlikely, as no changes in cell number and DNA content per well were observed. In fact, protein synthesis was enhanced after treatment with transferrin. Aromatase activity, stimulated by several promoters of cyclic AMP (cAMP), such as prostaglandin E2 (PGE2), forskolin and 8-bromo-cAMP, was significantly suppressed by 100 μg transferrin/ml (36·6, 47·4 and 23·4% inhibition respectively), suggesting that the effect of transferrin on FSH action may involve a site(s) distal to cAMP generation.
These findings indicated that transferrin, present in follicular fluid, may play an important role in the regulation of granulosa cell differentiation.
Journal of Endocrinology (1991) 131, 245–250
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Search for other papers by Z. X. Zhou in
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Search for other papers by Y. D. Zhang in
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Search for other papers by M. G. Parker in
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ABSTRACT
Prostatic steroid-binding protein (PSBP) mRNAs transcribed from the three genes C1, C2 and C3 were quantitated in neonatal rat ventral prostate by Northern blot analysis. Transcription was initiated at day 14 for C1 and C2 and day 10 for C3, and reached mature levels by day 21 for C1 and C2 and day 28 for C3. The changes of both cytoplasmic and nuclear prostatic androgen receptors in 10- to 150-day-old rats were investigated by radioligand assay and showed a fivefold transient increase between days 10 and 28. Thus there was a good correlation between the onset of PSBP gene expression and the transient increase in androgen receptors; increases in receptor concentration may be a prerequisite for changes in gene expression.
J. Endocr. (1988) 117, 361–366
Department of Zoology and Physiology, University of Wyoming, Laramie, Wyoming 82071, USA
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Department of Zoology and Physiology, University of Wyoming, Laramie, Wyoming 82071, USA
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Department of Zoology and Physiology, University of Wyoming, Laramie, Wyoming 82071, USA
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Department of Zoology and Physiology, University of Wyoming, Laramie, Wyoming 82071, USA
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Department of Zoology and Physiology, University of Wyoming, Laramie, Wyoming 82071, USA
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Department of Zoology and Physiology, University of Wyoming, Laramie, Wyoming 82071, USA
Search for other papers by Z Zhang in
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Department of Zoology and Physiology, University of Wyoming, Laramie, Wyoming 82071, USA
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Department of Zoology and Physiology, University of Wyoming, Laramie, Wyoming 82071, USA
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The level of the obese gene product leptin is often positively correlated with body weight, supporting the notion that hyperleptinemia contributes to obesity-associated cardiac dysfunction. However, a link between leptin levels and cardiac function has not been elucidated. This study was designed to examine the role of leptin deficiency (resulting from a point mutation of the leptin gene) in cardiomyocyte contractile function. Mechanical properties and intracellular Ca2 + transients were evaluated in ventricular myocytes from lean control and leptin-deficient ob/ob obese mice at 12 weeks of age. Cardiac ultrastructure was evaluated using transmission electron microscopy. ob/ob mice were overtly obese, hyperinsulinemic, hypertriglycemic, hypoleptinemic and euglycemic. Ultrastructural examination revealed swelling and disorganization of cristae in mitochondria from ob/ob mouse ventricular tissues. Cardiomyocytes from ob/ob mice displayed reduced expression of the leptin receptor Ob-R, larger cross-sectional area, decreased peak shortening and maximal velocity of shortening/relengthening, and prolonged relengthening but not shortening duration compared with lean counterparts. Consistent with mechanical characteristics, myocytes from ob/ob mice displayed reduced intracellular Ca2 + release upon electrical stimulus associated with a slowed intracellular Ca2 + decay rate. Interestingly, the contractile aberrations seen in ob/ob myocytes were significantly improved by in vitro leptin incubation. Contractile dysfunction was not seen in age- and gender-matched high fat-induced obese mice. These results suggested that leptin deficiency contributes to cardiac contractile dysfunction characterized by both systolic and diastolic dysfunction, impaired intracellular Ca2 + hemostasis and ultrastructural derangement in ventricular myocytes.
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Hypothalamic Integration Mechanisms, Netherlands Institute for Neuroscience (NIN), Amsterdam, Amsterdam, the Netherlands
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In addition to the direct effects of thyroid hormone (TH) on peripheral organs, recent work showed metabolic effects of TH on the liver and brown adipose tissue via neural pathways originating in the hypothalamic paraventricular and ventromedial nucleus (PVN and VMH). So far, these experiments focused on short-term administration of TH. The aim of this study is to develop a technique for chronic and nucleus-specific intrahypothalamic administration of the biologically active TH tri-iodothyronine (T3). We used beeswax pellets loaded with an amount of T3 based on in vitro experiments showing stable T3 release (∼5 nmol l−1) for 32 days. Upon stereotactic bilateral implantation, T3 concentrations were increased 90-fold in the PVN region and 50-fold in the VMH region after placing T3-containing pellets in the rat PVN or VMH for 28 days respectively. Increased local T3 concentrations were reflected by selectively increased mRNA expression of the T3-responsive genes Dio3 and Hr in the PVN or in the VMH. After placement of T3-containing pellets in the PVN, Tshb mRNA was significantly decreased in the pituitary, without altered Trh mRNA in the PVN region. Plasma T3 and T4 concentrations decreased without altered plasma TSH. We observed no changes in pituitary Tshb mRNA, plasma TSH, or plasma TH in rats after placement of T3-containing pellets in the VMH. We developed a method to selectively and chronically deliver T3 to specific hypothalamic nuclei. This will enable future studies on the chronic effects of intrahypothalamic T3 on energy metabolism via the PVN or VMH.
Search for other papers by Laura E Pascal in
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Transcriptomics Lab, Division of Plant Biotechnology, Sher-e-Kashmir University of Agricultural Sciences and Technology of Kashmir, Shalimar, Srinagar, Jammu and Kashmir, India
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School of Medicine, Tsinghua University, Beijing, China
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Center for Translational Medicine, Guangxi Medical University, Nanning, Guangxi, China
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Department of Urology, The Second Affiliated Hospital of Soochow University, Suzhou, China
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Department of Urology, Henan Cancer Hospital, Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou, China
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Department of Urology, China-Japan Hospital of Jilin University, Changchun, Jilin, China
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Department of Biology, Southern University of Science and Technology School of Medicine, Shenzhen, Guangdong, China
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Department of Biology, Southern University of Science and Technology School of Medicine, Shenzhen, Guangdong, China
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University of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA
Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA
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Elongation factor, RNA polymerase II, 2 (ELL2) is an RNA Pol II elongation factor with functional properties similar to ELL that can interact with the prostate tumor suppressor EAF2. In the prostate, ELL2 is an androgen response gene that is upregulated in benign prostatic hyperplasia (BPH). We recently showed that ELL2 loss could enhance prostate cancer cell proliferation and migration, and that ELL2 gene expression was downregulated in high Gleason score prostate cancer specimens. Here, prostate-specific deletion of ELL2 in a mouse model revealed a potential role for ELL2 as a prostate tumor suppressor in vivo. Ell2-knockout mice exhibited prostatic defects including increased epithelial proliferation, vascularity and PIN lesions similar to the previously determined prostate phenotype in Eaf2-knockout mice. Microarray analysis of prostates from Ell2-knockout and wild-type mice on a C57BL/6J background at age 3 months and qPCR validation at 17 months of age revealed a number of differentially expressed genes associated with proliferation, cellular motility and epithelial and neural differentiation. OncoPrint analysis identified combined downregulation or deletion in prostate adenocarcinoma cases from the Cancer Genome Atlas (TCGA) data portal. These results suggest that ELL2 and its pathway genes likely play an important role in the development and progression of prostate cancer.
