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  • 1.
    Berg, Håkan
    et al.
    Örebro University, School of Science and Technology. Marine Science Institute, University of Texas, Austin, United States .
    Rice, Charles
    Department of Biology, Clemson University, United States .
    Rahman, Saydur
    Marine Science Institute, University of Texas, Austin, United States .
    Dong, Jing
    Marine Science Institute, University of Texas, Austin, United States .
    Thomas, Peter
    Marine Science Institute, University of Texas, Austin, United States .
    Identification and characterization of membrane androgen receptors in the ZIP9 zinc transporter subfamily: I. Discovery in female Atlantic croaker and evidence ZIP9 mediates testosterone-induced apoptosis of ovarian follicle cells2014In: Endocrinology, ISSN 0013-7227, E-ISSN 1945-7170, Vol. 155, no 11, p. 4237-4249Article in journal (Refereed)
    Abstract [en]

    Rapid, cell surface-initiated, pregenomic androgen actions have been described in various vertebrate cells, but the receptors mediating these actions remain unidentified.We report here cloning and expression of a cDNA from Atlantic croaker (Micropogonias undulatus) ovaries encoding a 33kDa, 7-transmembrane protein with binding and signaling characteristics of a membrane androgen receptor (mAR) that is unrelated to any previously described steroid receptor. Instead croaker mAR has 81–93 % amino acid sequence identity with zinc transporter ZIP9 (SLC39A9) subfamily members, indicating it is a ZIP9 protein. Croaker ZIP9 is expressed in gonadal tissues and in brain, and is upregulated in the ovary by reproductive hormones. ZIP9 protein is localized to plasma membranes of croaker granulosa cells and human breast cancer (SKBR-3) cells stably transfected with ZIP9. Recombinant croaker ZIP9 has a high affinity (Kd 12.7 nM), limited capacity (Bmax 2.8nM/mgprotein), displaceable, single binding site specific for androgens, characteristic of steroid receptors. Testosterone activates a stimulatory G protein coupled to ZIP9, resulting in increased cAMP production. Testosterone promotes serum starvation-induced cell death and apoptosis in transfected cells and in croaker ovarian follicle cells that is associated with rapid increases in intracellular free zinc concentrations, suggesting an involvement of zinc in this nonclassical androgen action to promote apoptosis. These responses to testosterone are abrogated by treatment with ZIP9 siRNA. The results provide the first evidence that zinc transporter proteins can function as specific steroid membrane receptors and indicate a previously unrecognized signaling pathway mediated by steroid receptors involving alterations in intracellular zinc.

  • 2. Brönnegård, M.
    et al.
    Arner, P.
    Hellström, L.
    Akner, Gunnar
    Örebro University, School of Health and Medical Sciences.
    Gustafsson, J. A.
    Glucocorticoid receptor messenger ribonucleic acid in different regions of human adipose tissue1990In: Endocrinology, ISSN 0013-7227, E-ISSN 1945-7170, Vol. 127, no 4, p. 1689-1696Article in journal (Refereed)
    Abstract [en]

    The expression of glucocorticoid receptor (GR) messenger RNA (mRNA) was investigated in sc adipose tissue and isolated adipocytes from the abdominal and gluteal regions in men and women using a human GR complementary RNA probe. GR mRNA levels were 2-fold higher in female than in male abdominal tissue or adipocytes, whereas in gluteal tissue or adipocytes no sex differences were observed. GR mRNA levels in female abdominal adipocytes were 50% higher than in corresponding female gluteal adipocytes; the opposite was observed corresponding in males. Northern blot analysis of total cellular RNA isolated from abdominal and gluteal adipocytes showed hybridization of the human GR probe to an RNA species of approximately 7.1 kilobases in both regions. No sex or regional differences in GR mRNA stability were observed. The human metallothionein II (hMTII) mRNA, which is regulated by glucocorticoids at the transcriptional level, showed an opposite sex and regional pattern as GR mRNA. However, in gluteal adipose tissue no sex differences were observed in hMTII mRNA levels. The expression of beta-actin mRNA, which is not regulated by glucocorticoids, showed no sex or regional variation. By immunocytochemistry, using an anti-GR-monoclonal antibody, cytoplasmic as well as nuclear staining for GR was demonstrated in both sexes and both regions. In conclusion, variations in GR mRNA levels between sexes and body regions may explain the well known sex and tissue differences in effects of glucocorticoids on human adipose tissue.

  • 3.
    Hogh, K-Lynn N.
    et al.
    Northern Medical Program, University of Northern British Columbia, Prince George BC, Canada.
    Craig, Michael N.
    Northern Medical Program, University of Northern British Columbia, Prince George BC, Canada.
    Uy, Christopher E.
    Northern Medical Program, University of Northern British Columbia, Prince George BC, Canada.
    Nygren, Heli
    VTT Technical Research Centre of Finland, Espoo, Finland; Steno Diabetes Center A/S, Gentofte, Denmark.
    Asadi, Ali
    Department of Cellular and Physiological Sciences and Faculty of Medicine, University of British Columbia, Vancouver BC, Canada.
    Speck, Madeline
    Child and Family Research Institute, Vancouver BC, Canada.
    Fraser, Jordie D.
    Rudecki, Alexander P.
    Northern Medical Program, University of Northern British Columbia, Prince George BC, Canada.
    Baker, Robert K.
    Department of Cellular and Physiological Sciences and Faculty of Medicine, University of British Columbia, Vancouver BC, Canada.
    Oresic, Matej
    Örebro University, School of Medical Sciences. VTT Technical Research Centre of Finland, Espoo, Finland; Steno Diabetes Center A/S, Gentofte, Denmark.
    Gray, Sarah L.
    Northern Medical Program, University of Northern British Columbia, Prince George BC, Canada.
    Overexpression of PPARγ specifically in pancreatic β-cells exacerbates obesity-induced glucose intolerance, reduces β-cell mass, and alters islet lipid metabolism in male mice2014In: Endocrinology, ISSN 0013-7227, E-ISSN 1945-7170, Vol. 155, no 10, p. 3843-3852Article in journal (Refereed)
    Abstract [en]

    The contribution of peroxisomal proliferator-activated receptor (PPAR)-γ agonism in pancreatic β-cells to the antidiabetic actions of thiazolidinediones has not been clearly elucidated. Genetic models of pancreatic β-cell PPARγ ablation have revealed a potential role for PPARγ in β-cell expansion in obesity but a limited role in normal β-cell physiology. Here we overexpressed PPARγ1 or PPARγ2 specifically in pancreatic β-cells of mice subjected to high-fat feeding using an associated adenovirus (β-PPARγ1-HFD and β-PPARγ2-HFD mice). We show β-cell-specific PPARγ1 or PPARγ2 overexpression in diet-induced obese mice exacerbated obesity-induced glucose intolerance with decreased β-cell mass, increased islet cell apoptosis, and decreased plasma insulin compared with obese control mice (β-eGFP-HFD mice). Analysis of islet lipid composition in β-PPARγ2-HFD mice revealed no significant changes in islet triglyceride content and an increase in only one of eight ceramide species measured. Interestingly β-PPARγ2-HFD islets had significantly lower levels of lysophosphatidylcholines, lipid species shown to enhance insulin secretion in β-cells. Gene expression profiling revealed increased expression of uncoupling protein 2 and genes involved in fatty acid transport and β-oxidation. In summary, transgenic overexpression of PPARγ in β-cells in diet-induced obesity negatively impacts whole-animal carbohydrate metabolism associated with altered islet lipid content, increased expression of β-oxidative genes, and reduced β-cell mass.

  • 4.
    Jee, Youn Hee
    et al.
    Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda MD, United States.
    Wang, Jinhee
    Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda MD, United States.
    Yue, Shanna
    Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda MD, United States.
    Jennings, Melissa
    Eunice Kennedy Shriver National Institute of Child Health and Human Development, NIH, Bethesda, United States.
    Clokie, Samuel J. H.
    Birmingham Women's and Children's NHS Foundation Trust, Birmingham, United Kingdom.
    Nilsson, Ola
    Örebro University, School of Medical Sciences. Department of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden.
    Lui, Julian
    Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda MD, United States.
    Baron, Jeffrey
    Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda MD, United States.
    Mir-374-5p, mir-379-5p, and mir-503-5p regulate proliferation and hypertrophic differentiation of growth plate chondrocytes in male rats2018In: Endocrinology, ISSN 0013-7227, E-ISSN 1945-7170, Vol. 159, no 3, p. 1469-1478Article in journal (Refereed)
    Abstract [en]

    Growth plate chondrocytes undergo sequential differentiation to form the resting (RZ), proliferative (PZ), and hypertrophic zones (HZ). The important role of microRNAs (miRNAs) in the growth plate was previously revealed by cartilage-specific ablation of Dicer, an enzyme essential for biogenesis of many miRNAs. To identify specific miRNAs that regulate differentiation of PZ chondrocytes to HZ chondrocytes, we microdissected individual growth plate zones from juvenile rats and performed miRNA profiling using a solution hybridization method and also miRNA-seq. Thirty-four miRNAs were differentially expressed between PZ and HZ and we hypothesized that some of the miRNAs that are preferentially expressed in PZ may serve to promote proliferation and inhibit hypertrophic differentiation. Consistent with this hypothesis, transfection of inhibitors for four of these miRNAs (mir-369-3p, mir-374-5p, mir-379-5p, mir-503-5p) decreased proliferation in primary epiphyseal chondrocytes. The inhibitors for three of these miRNAs (mir-374-5p, mir-379-5p, mir-503-5p) also increased expression of multiple genes that are associated with chondrocyte hypertrophic differentiation. We next hypothesized that preferential expression of these miRNAs in PZ is driven by the PTHrP concentration gradient across the growth plate. Consistent with this hypothesis, treatment of primary chondrocytes with a PTH/PTHrP receptor agonist, PTH1-34, increased expression of mir-374-5p, mir-379-5p, and mir-503-5p. Taken together, our findings suggest that the PTHrP concentration gradient across the growth plate induces differential expression of mir-374-5p, mir-379-5p and mir-503-5p between PZ and HZ. In PZ, the higher expression levels of these miRNAs promote proliferation and inhibit hypertrophic differentiation. In HZ, downregulation of these miRNAs inhibits proliferation and promotes hypertrophic differentiation.

  • 5.
    Thomas, Peter
    et al.
    Marine Science Institute, University of Texas, Austin, USA.
    Pang, Yefei
    Marine Science Institute, University of Texas, Austin, USA.
    Dong, Jing
    Marine Science Institute, University of Texas, Austin, USA.
    Berg, Håkan
    Örebro University, School of Science and Technology. Marine Science Institute, University of Texas, Austin, USA.
    Identification and characterization of membrane androgen receptors in the ZIP9 zinc transporter subfamily: II. Role of human ZIP9 in testosterone-induced prostate and breast cancer cell apoptosis2014In: Endocrinology, ISSN 0013-7227, E-ISSN 1945-7170, Vol. 155, no 11, p. 4250-4265Article in journal (Refereed)
    Abstract [en]

    Recently we discovered a cDNA in teleost ovarian follicle cells belonging to the zinc transporter ZIP9 subfamily encoding a protein with characteristics of a membrane androgen receptor (mAR). Here we demonstrate that human ZIP9 expressed in MDA-MB-468 breast cancer cells and stably overexpressed in human prostate cancer PC-3 cells (PC-3-ZIP9) also displays the ligand binding and signaling characteristics of a specific, high-affinity mAR. Testosterone treatment of MDA-MB-468 and PC-3-ZIP9 cells caused activation of G proteins and second messenger pathways as well as increases in intracellular free zinc concentrations that were accompanied by induction of apoptosis. [3H]-Testosterone binding and these responses were abrogated in MDA-MB-468 cells after ZIP9 siRNA treatment and absent in PC-3 cells transfected with empty vector, confirming that ZIP9 functions as an mAR. Testosterone treatment caused upregulation of proapoptotic genes Bax, p53 and JNK in both cell lines and increased expression of Bax, Caspase 3 and cytochrome C proteins. Treatment with a zinc chelator (TPEN) or a MAP kinase inhibitor (PD98059) blocked testosterone induced increases in Bax, p53 and JNK mRNA expression. The results suggest that both androgen signaling and zinc transporter functions of ZIP9 mediate testosterone promotion of apoptosis. ZIP9 is widely expressed in human tissues and upregulated in malignant breast and prostate tissues, suggesting it is a potential therapeutic target for treating breast and prostate cancers. These results provide the first evidence for a mechanism mediated by a single protein through which intracellular steroidandzinc signaling pathways interact to regulate physiological functions in mammalian cells.

1 - 5 of 5
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