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POMC Gene (pomc + gene)

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Medical Sciences50%

Terms modified by POMC Gene

  • pomc gene expression
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    Selected Abstracts

    High glucose activates pituitary proopiomelanocortin gene expression: possible role of free radical-sensitive transcription factors

    DIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 4 2007
    Koichi Asaba
    Abstract Background Hyperglycemia is recognized as a metabolic stress, and indeed it is known to stimulate hypothalamo-pituitary-adrenal (HPA) axis, a representative anti-stress system, in patients with diabetes mellitus or in animal models of hyperglycemia. Thus, we tried to clarify the molecular mechanism of glucose-induced HPA axis activation. Methods We studied the effect of high glucose on the transcriptional regulation of proopiomelanocortin (POMC) gene that encodes adrenocorticotropic hormone, a central mediator of HPA axis, using AtT20 corticotroph cell line in vitro. Results We found that high glucose concentration (24 mM) significantly stimulated the 5,-promoter activity of POMC gene. The effect was promoter-specific, and was mimicked by nuclear factor-kappaB (NF-,B)- or AP1-responsive promoters but not by cAMP-responsive element or serum-response element-containing promoters. Furthermore, the stimulatory effect of high glucose on POMC gene was eliminated by NF-,B and AP1 inhibitors, suggesting the involvement of the transcriptional factors. The POMC 5,-promoter has the canonical NF-,B consensus sequence, and gel shift assay showed the binding of NF-,B to the element. Finally, the effect of high glucose was completely abolished by treatment with a radical quencher 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (TEMPOL). Conclusions Our data suggest that hyperglycemia activates POMC gene expression, at least partly, via NF-,B/AP1, and that high-glucose-induced free radical generation may mediate the activation of these transcription factors, which in turn stimulates the transcription of POMC gene. Copyright © 2006 John Wiley & Sons, Ltd. [source]

    The Melanocortin Receptor-1 Gene but not the Proopiomelanocortin Gene is Expressed in Melanoblasts and Contributes their Differentiation in the Mouse Skin

    PIGMENT CELL & MELANOMA RESEARCH, Issue 6 2004
    Tomohisa Hirobe
    Alpha-melanocyte stimulating hormone (, -MSH) added to serum-free primary culture of melanoblasts derived from epidermal cell suspensions of 0.5 d old C57BL/10JHir mice induced their differentiation. Analysis using the reverse transcription-polymerase chain reaction showed that the expression of the melanocyte-specific , -MSH receptor gene, melanocortin receptor-1 (MC1-R), had already been initiated before addition of , -MSH, and, in addition, no up-regulation of the MC1-R gene was observed after addition of , -MSH. However, no expression of the proopiomelanocortin (POMC) gene was observed before or after the addition of , -MSH. The expression of the MC1-R and POMC genes in the epidermis and dermis of the dorsal skin was surveyed from 13 d old embryos to 5.5 d old neonates. The expression of the MC1-R gene was first observed in the epidermis of 13 d old embryos, and gradually increased up to 0.5 d after birth, and thereafter remained constant. By contrast, the expression of the MC1-R gene in the dermis was first observed in 16 d old embryos, and gradually increased up to 3.5 d after birth, and thereafter remained constant. However, no expression of the POMC gene was observed in the epidermis or dermis of the dorsal skin at any age of mice tested. These results suggest that the expression of the MC1-R gene, but not of the POMC gene, plays an important role in the regulation of melanocyte differentiation in mouse skin. [source]

    Pro-Opiomelanocortin Expression in a Metastatic Breast Carcinoma with Ectopic ACTH Secretion

    THE BREAST JOURNAL, Issue 4 2004
    Marie-Françoise Pelte MD
    Abstract: Cushing's syndrome secondary to ectopic adrenocorticotropic hormone (ACTH) secretion is rarely observed in breast carcinoma and only four cases have been previously published. We report here the case of a 50-year-old woman who presented with a history of diffuse bone pain associated with multiple hepatic, pulmonary, and bone metastases. A core needle biopsy specimen revealed an invasive ductal carcinoma in the right breast. The patient subsequently developed an ACTH-dependent paraneoplastic Cushing's syndrome and she died of arrhythmia and heart failure, despite treatment. At autopsy, immunohistochemical staining showed chromogranin A and ACTH positivity in the breast tumor and a lung metastasis. The mRNA expression of the pro-opiomelanocortin (POMC) gene was detected in tumoral cells by reverse transcriptase polymerase chain reaction (RT-PCR). This is the first case of Cushing's syndrome secondary to ectopic ACTH secretion where the presence of ACTH by immunohistochemistry and the expression of the POMC gene by RT-PCR have both been demonstrated in a breast carcinoma with metastases. The clinical history and the pathologic findings are presented with the methods and results of the molecular analysis. This case illustrates an example of ectopic ACTH syndrome in a breast carcinoma with neuroendocrine (NE) differentiation. This NE phenotype is directly related to the synthesis of ACTH by the tumoral cells. It should be kept in mind that an ectopic ACTH syndrome may be produced not only by small cell carcinoma or endocrine tumors but also by breast cancer. No relationship has been established between NE features and prognostic factors or patient outcome for this peculiar type of breast carcinoma. The demonstration of mRNA POMC in breast carcinoma with NE features suggests a depression and/or an activation of the POMC gene linked to the NE differentiation., [source]

    The Melanocortin Receptor-1 Gene but not the Proopiomelanocortin Gene is Expressed in Melanoblasts and Contributes their Differentiation in the Mouse Skin

    PIGMENT CELL & MELANOMA RESEARCH, Issue 6 2004
    Tomohisa Hirobe
    Alpha-melanocyte stimulating hormone (, -MSH) added to serum-free primary culture of melanoblasts derived from epidermal cell suspensions of 0.5 d old C57BL/10JHir mice induced their differentiation. Analysis using the reverse transcription-polymerase chain reaction showed that the expression of the melanocyte-specific , -MSH receptor gene, melanocortin receptor-1 (MC1-R), had already been initiated before addition of , -MSH, and, in addition, no up-regulation of the MC1-R gene was observed after addition of , -MSH. However, no expression of the proopiomelanocortin (POMC) gene was observed before or after the addition of , -MSH. The expression of the MC1-R and POMC genes in the epidermis and dermis of the dorsal skin was surveyed from 13 d old embryos to 5.5 d old neonates. The expression of the MC1-R gene was first observed in the epidermis of 13 d old embryos, and gradually increased up to 0.5 d after birth, and thereafter remained constant. By contrast, the expression of the MC1-R gene in the dermis was first observed in 16 d old embryos, and gradually increased up to 3.5 d after birth, and thereafter remained constant. However, no expression of the POMC gene was observed in the epidermis or dermis of the dorsal skin at any age of mice tested. These results suggest that the expression of the MC1-R gene, but not of the POMC gene, plays an important role in the regulation of melanocyte differentiation in mouse skin. [source]