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Continuous culture of parathyroid cells has proven difficult, regardless from which species the cells are derived. In the present study, we have used a defined serum-free low calcium containing medium to culture human parathyroid cells obtained from patients with parathyroid adenomas due to primary hyperparathyroidism. No fibroblast overgrowth occurred, and the human parathyroid chief cells proliferated until confluent. After the first passage the cells ceased to proliferate, but still retained their functional capacity up to 60 days, demonstrated by Ca(2+)-sensitive changes in the release of parathyroid hormone (PTH) and as adequate cytoplasmic calcium ([Ca2+](i)) responses to changes in ambient calcium as measured by microfluorimetry. Low calcium concentrations enhanced, and vitamin D(3) and retinoic acids (RA) dose-dependently inhibited cell proliferation during the first passage, as determined by [(3)H]thymidine incorporation, immunohistochemistry for proliferating cell nuclear antigen and cell counting. Signs of differentiation were present as the set-points, defined as the external calcium concentration at which half-maximal stimulation of [Ca2+](i) (set-point(c)), or half-maximal inhibition of PTH release (set-point(p)) occur, were higher in not proliferating compared with proliferating cells in P0. Inhibition of cell proliferation was accompanied by signs of left-shifted set-points, indicating a link between proliferation and differentiation. The results demonstrate that human parathyroid chief cells cultured in a defined serum-free medium can be kept viable for a considerable time, and that signs of differentiation occur after proliferation has ceased. The low calcium stimulated cell proliferation may also be inhibited by vitamin D and RA.
Eastern Clinical Research Unit, Department of Diabetes and Endocrinology, Biotechnology Division, Monash University, 6th Floor Burnett Tower, 89 Commercial Road, Prahran 3181, Melbourne, Victoria, Australia
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Eastern Clinical Research Unit, Department of Diabetes and Endocrinology, Biotechnology Division, Monash University, 6th Floor Burnett Tower, 89 Commercial Road, Prahran 3181, Melbourne, Victoria, Australia
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Eastern Clinical Research Unit, Department of Diabetes and Endocrinology, Biotechnology Division, Monash University, 6th Floor Burnett Tower, 89 Commercial Road, Prahran 3181, Melbourne, Victoria, Australia
Search for other papers by Richard W Simpson in
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Eastern Clinical Research Unit, Department of Diabetes and Endocrinology, Biotechnology Division, Monash University, 6th Floor Burnett Tower, 89 Commercial Road, Prahran 3181, Melbourne, Victoria, Australia
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Glucagon-like peptide-1 (GLP-1) has been proposed as a target for treatment of type 2 diabetes. GLP-1 has also been demonstrated to improve endothelial cell dysfunction in diabetic patients. Elevated plasmogen activator inhibitor-1 (PAI-1) levels have been implicated in endothelial cell dysfunction. The effect of GLP-1 on PAI-1 expression in vascular endothelial cells has not been explored. In a spontaneously transformed human umbilical vein endothelial cell (HUVEC) line, C11-spontaneously transformed HUVEC (STH) and primary HUVEC cells, GLP-1 treatment, in the presence of a dipeptidyl peptidase IV inhibitor, attenuated induction of PAI-1 protein and mRNA expression by tumour necrosis factor-α (TNF-α). GLP-1 also inhibited the effect of TNF-α on a reporter gene construct harbouring the proximal PAI-1 promoter. In addition, GLP-1 attenuated TNF-α-mediated induction of Nur77 mRNA and TNF-α-mediated binding of nuclear proteins (NPs) to the PAI-1, Nur77, cis-acting response element nerve growth factor induced clone B response element (NBRE). GLP-1 treatment also inhibited TNF-α-mediated induction of Akt phosphorylation. Taken together, these observations suggest that GLP-1 inhibits TNF-α-mediated PAI-1 induction in vascular endothelial cells, and this effect may involve Akt-mediated signalling events and the modulation of Nur77 expression and NP binding to the PAI-1 NBRE.
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Abstract
Human phaeochromocytomas abundantly express insulin-like growth factor-II (IGF-II), but its regulation and biological role in these neoplasms is not known at present. To clarify the regulation of IGF-II gene expression in phaeochromocytomas, we studied the effects of glucocorticoids, nerve growth factor (NGF), and protein kinase A and C regulators in primary cultures of human phaeochromocytoma cells. Cytoplasmic RNA was extracted and analysed by Northern and dot blotting with a 32P-labelled cDNA probe for IGF-II. Dexamethasone treatment (500 ng/ml) for 3 and 7 days resulted in a 260% and 515% increase in the accumulation of IGF-II mRNA respectively. The stimulatory effect of dexamethasone was time-and dose-dependent. The increases in the 6·0 and 2·2 kb species of IGF-II mRNAs were the most apparent. Cortisol (1 μg/ml) increased the amount of IGF-II mRNA by threefold compared with the control. NGF (200 ng/ml), dibutyryl cyclic AMP (1 mm) and 12-O-tetradecanoyl phorbol-13-acetate (a protein kinase C activator; 100 ng/ml) had no significant effect on IGF-II mRNA levels. These data suggest that IGF-II gene expression in human phaeochromocytomas may be regulated by microenvironmental glucocorticoids.
Journal of Endocrinology (1994) 142, 29–35
Australian Centre for Blood Diseases, Eastern Clinical Research Unit, Department of Diabetes and Endocrinology, Biotechnology Division, Monash University, 6th Floor Burnett Tower, 89 Commercial Road, Prahran, Melbourne, Victoria, Australia 3181
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Australian Centre for Blood Diseases, Eastern Clinical Research Unit, Department of Diabetes and Endocrinology, Biotechnology Division, Monash University, 6th Floor Burnett Tower, 89 Commercial Road, Prahran, Melbourne, Victoria, Australia 3181
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Australian Centre for Blood Diseases, Eastern Clinical Research Unit, Department of Diabetes and Endocrinology, Biotechnology Division, Monash University, 6th Floor Burnett Tower, 89 Commercial Road, Prahran, Melbourne, Victoria, Australia 3181
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Australian Centre for Blood Diseases, Eastern Clinical Research Unit, Department of Diabetes and Endocrinology, Biotechnology Division, Monash University, 6th Floor Burnett Tower, 89 Commercial Road, Prahran, Melbourne, Victoria, Australia 3181
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The thiazolidinediones (TZDs) have been reported to reduce atherogenesis in preclinical models and atherosclerosis in clinical trials in pre-diabetic and diabetic patients. Although peroxisome proliferator-activated receptor γ (PPARγ)-mediated effects on gene expression have been thought responsible for this effect, a complete understanding of the molecular mechanisms responsible remains to be fully elucidated. We have previously reported PPARγ-independent modulation of NUR77 (also known as Nr4a1), an orphan nuclear receptor deemed important in the atherogenic process, in association with TZD-mediated inhibition of tumour necrosis factor α (TNFα) induction of plasminogen activator inhibitor type 1 expression. Here, we report NUR77 mRNA expression is increased in human vascular endothelial cells (HUVEC) stimulated by TNFα and that this effect is inhibited by a TZD in a PPARγ-independent manner. TZD treatment of HUVEC also inhibited the stimulatory effects of TNFα on NUR77 promoter activity, again in a PPARγ-independent manner, confirming the transcriptional nature of this effect. TZD treatment also attenuated the binding of nuclear proteins to the nuclear factor kappa B (NF-κB)-binding site of the NUR77 promoter in HUVEC in a PPARγ-independent manner. In addition, TZD treatment also inhibited TNFα-mediated induction of NF-κB1 mRNA expression. Our results suggest a potential PPARγ-independent molecular mechanism for the anti-atherogenic effects of TZDs involving NF-κB-mediated transcriptional inhibition of cytokine-mediated induction of the orphan nuclear receptor NUR77 in HUVEC.
Australian Centre for Blood Diseases, Eastern Clinical Research Unit, Novo Nordisk A/S, Department of Diabetes and Endocrinology, Monash University, 6th Floor Burnett Tower, 89 Commercial Road, Prahran 3181, Melbourne, Victoria, Australia
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Australian Centre for Blood Diseases, Eastern Clinical Research Unit, Novo Nordisk A/S, Department of Diabetes and Endocrinology, Monash University, 6th Floor Burnett Tower, 89 Commercial Road, Prahran 3181, Melbourne, Victoria, Australia
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Australian Centre for Blood Diseases, Eastern Clinical Research Unit, Novo Nordisk A/S, Department of Diabetes and Endocrinology, Monash University, 6th Floor Burnett Tower, 89 Commercial Road, Prahran 3181, Melbourne, Victoria, Australia
Australian Centre for Blood Diseases, Eastern Clinical Research Unit, Novo Nordisk A/S, Department of Diabetes and Endocrinology, Monash University, 6th Floor Burnett Tower, 89 Commercial Road, Prahran 3181, Melbourne, Victoria, Australia
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Glucagon-like peptide-1 (GLP-1) administration attenuates endothelial cell dysfunction in diabetic patients and inhibits tumour necrosis factor α (TNF)-mediated plasminogen activator inhibitor type-1 (PAI-1) induction in human vascular endothelial cells. The short half-life of GLP-1 mediated via degradation by the enzyme dipeptidyl peptidase 4 mandates the clinical use of long-acting GLP-1 analogues. The effects of a long-acting GLP-1 analogue on PAI-1 and vascular adhesion molecule expression in vascular endothelial cells are unknown. In this report, we demonstrate for the first time that the treatment with liraglutide, a long-acting GLP-1 analogue, inhibited TNF or hyperglycaemia-mediated induction of PAI-1, intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 mRNA and protein expression in a human vascular endothelial cell line. In addition, treatment attenuated TNF- or hyperglycaemia-mediated induction of the orphan nuclear receptor Nur77 mRNA expression. Taken together, these observations indicate that liraglutide inhibits TNF- or glucose-mediated induction of PAI-1 and vascular adhesion molecule expression, and this effect may involve the modulation of NUR77. These effects suggest that liraglutide may potentially improve the endothelial cell dysfunction associated with premature atherosclerosis identified in type 2 diabetic patients.
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College of Life Sciences, Northwest Normal University, Lanzhou, China
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Gonadotropin signaling plays a pivotal role in the spermatogenesis of vertebrates, but exactly how gonadotropins regulate the process in non-mammalian species remains elusive. Using a gene knockout approach in zebrafish, we have previously demonstrated the non-canonical action of gonadotropin signaling on spermatogenesis by analyzing four single mutant lines (lhb, lhr, fshb and fshr) and three double mutant lines (lhb;fshb, lhr;fshr and fshb;lhr). In this study, we further investigated the actions of gonadotropins on the testis by establishing three other double-mutant zebrafish lines (lhb;lhr, fshb;fshr and lhb;fshr). All lhb;lhr and fshb;fshr mutant males were fertile. Analysis on the gonadosomatic index and testicular histology in these lhb;lhr and fshb;fshr mutants demonstrated that Lh signaling and Fsh signaling could functionally compensate each other in the testis. Intriguingly, it was found that the lhb;fshr mutant male fish were also morphologically and histologically normal and functionally fertile, a phenomenon which could be explained by the cross-activation of Lhr by Fsh. We have demonstrated this cross-reactivity for the first time in zebrafish. Fsh was shown to activate Lhr using three different assay systems, in which Lh-Fshr activation was also confirmed. Taken together, we conclude that the action of Lh signaling and Fsh signaling is redundant in that either alone can support zebrafish spermatogenesis based on two observations. First, that either Lh signaling or Fsh signaling alone is sufficient to support male fertility. Second, that the two gonadotropin ligands could promiscuously activate both receptors. Apart from revealing the complexity of gonadotropin signaling in controlling male reproduction in zebrafish, this study also shed light toward a better understanding on the evolution of gonadotropin signaling in vertebrates from fish to mammals.
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Danone Nutricia Research, Singapore, Republic of Singapore
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Department of Pediatrics, University Medical Centre Groningen, Groningen, The Netherlands
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Institute of Molecular and Cell Biology, A*STAR, Singapore, Republic of Singapore
School of Laboratory Medicine and Life Science, Wenzhou Medical University, Wenzhou, Zhejiang, China
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The prevalence of gestational diabetes mellitus (GDM) is estimated at 14% globally, and in some countries, such as Singapore, exceeds 20%. Both women and children exposed to GDM have an increased risk of later metabolic diseases, cardiovascular disease and other health issues. Beyond lifestyle changes and pharmaceutical intervention using existing type 2 diabetes medications for expecting women, there are limited treatment options for women with GDM; targeting better outcomes of potentially affected infants is unexplored. Numerous animal models have been generated for understanding of pathological processes of GDM development and for development of treatment strategies. These models, however, suffer from limited windows of opportunity to examine risk factors and potential intervention options. By combining short-term high-fat diet (HFD) feeding and low-dose streptozotocin (STZ) treatments before pregnancy, we have established a mouse model with marked transient gestation-specific hyperglycemia, which allows testing of nutritional and pharmacological interventions before, during and beyond pregnancy.
Laboratoire de Biologie de la Differentation et du Development, Universite Victor Segalen Bordeaux 2, 146 rue Leo Saignat 33076 Bordeaux cedex, France
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Laboratoire de Biologie de la Differentation et du Development, Universite Victor Segalen Bordeaux 2, 146 rue Leo Saignat 33076 Bordeaux cedex, France
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Laboratoire de Biologie de la Differentation et du Development, Universite Victor Segalen Bordeaux 2, 146 rue Leo Saignat 33076 Bordeaux cedex, France
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Laboratoire de Biologie de la Differentation et du Development, Universite Victor Segalen Bordeaux 2, 146 rue Leo Saignat 33076 Bordeaux cedex, France
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Laboratoire de Biologie de la Differentation et du Development, Universite Victor Segalen Bordeaux 2, 146 rue Leo Saignat 33076 Bordeaux cedex, France
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Laboratoire de Biologie de la Differentation et du Development, Universite Victor Segalen Bordeaux 2, 146 rue Leo Saignat 33076 Bordeaux cedex, France
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Laboratoire de Biologie de la Differentation et du Development, Universite Victor Segalen Bordeaux 2, 146 rue Leo Saignat 33076 Bordeaux cedex, France
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Laboratoire de Biologie de la Differentation et du Development, Universite Victor Segalen Bordeaux 2, 146 rue Leo Saignat 33076 Bordeaux cedex, France
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Laboratoire de Biologie de la Differentation et du Development, Universite Victor Segalen Bordeaux 2, 146 rue Leo Saignat 33076 Bordeaux cedex, France
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Activated signaling proteins regulate diverse processes, including the differentiation of the pancreatic islet cells during ontogeny. Here we uncover the in vivo phosphorylation status of major growth factor-activated signaling proteins in normal adult mice and during pancreatic islet regeneration. We report elevated phospho-mitogen-activated protein kinase (phospho-MAPK), phospho-c-Jun-NH2-terminal kinase (phospho-JNK), and phospho-p38 MAPK expression during pancreatic regeneration. Immunoblotting experiments demonstrated elevated phosphorylation of p52 Src-homology/collagen (SHC) in the ductal network as well, substantiating the activation of this pathway. Furthermore, protein kinase B (PKB/Akt), a key signaling protein in the anti-apoptotic pathway, was phosphorylated to a greater extent in the ductal network from regenerating pancreas. We observed fibroblast growht factor (FGF)10 and platelet-derived growth factor (PDGF)AA expression in embryonic as well as regenerating adult pancreas. Epidermal growth factor (EGF) and PDGFAA stimulated MAPK and Akt phosphorylation, while FGF10 stimulated MAPK but not Akt phosphorylation in a time-dependent manner in freshly isolated cells from the adult ductal network. These data suggest that a heightened level of expression and stimulation of key signaling proteins underlie the expansion and differentiation processes that support pancreatic ontogeny and regeneration.
Biomedical Sciences, University of Missouri, Columbia, Missouri, USA
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Informatics Institute, University of Missouri, Columbia, Missouri, USA
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Biomedical Sciences, University of Missouri, Columbia, Missouri, USA
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Biomedical Sciences, University of Missouri, Columbia, Missouri, USA
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MU Metabolomics Center, University of Missouri, Columbia, Missouri, USA
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MU Metabolomics Center, University of Missouri, Columbia, Missouri, USA
Department of Biochemistry, University of Missouri, Columbia, Missouri, USA
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MU Metabolomics Center, University of Missouri, Columbia, Missouri, USA
Department of Biochemistry, University of Missouri, Columbia, Missouri, USA
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Informatics Institute, University of Missouri, Columbia, Missouri, USA
Department of Health Management and Informatics, School of Medicine, University of Missouri, Columbia, Missouri, USA
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Biomedical Sciences, University of Missouri, Columbia, Missouri, USA
Informatics Institute, University of Missouri, Columbia, Missouri, USA
Thompson Center for Autism and Neurobehavioral Disorders, University of Missouri, Columbia, Missouri, USA
Genetics Area Program, University of Missouri, Columbia, Missouri, USA
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Human offspring encounter high amounts of phytoestrogens, such as genistein (GEN), through maternal diet and soy-based formulas. Such chemicals can exert estrogenic activity and thereby disrupt neurobehavioral programming. Besides inducing direct host effects, GEN might cause gut dysbiosis and alter gut metabolites. To determine whether exposure to GEN affects these parameters, California mice (Peromyscus californicus) dams were placed 2 weeks prior to breeding and throughout gestation and lactation on a diet supplemented with GEN (250 mg/kg feed weight) or AIN93G phytoestrogen-free control diet (AIN). At weaning, offspring socio-communicative behaviors, gut microbiota and metabolite profiles were assayed. Exposure of offspring to GEN-induced sex-dependent changes in gut microbiota and metabolites. GEN exposed females were less likely to investigate a novel female mouse when tested in a three-chamber social test. When isolated, GEN males and females exhibited increased latency to elicit their first call, suggestive of reduced motivation to communicate with other individuals. Correlation analyses revealed interactions between GEN-induced microbiome, metabolome and socio-communicative behaviors. Comparison of GEN males with AIN males revealed the fraction of calls above 20 kHz was associated with daidzein, α-tocopherol, Flexispira spp. and Odoribacter spp. Results suggest early GEN exposure disrupts normal socio-communicative behaviors in California mice, which are otherwise evident in these social rodents. Such effects may be due to GEN disruptions on neural programming but might also be attributed to GEN-induced microbiota shifts and resultant changes in gut metabolites. Findings indicate cause for concern that perinatal exposure to GEN may detrimentally affect the offspring microbiome–gut–brain axis.
