ピットの好物はほるもんです in メタボ研究室

本ブログは製薬会社の研究者である筆者が【研究者としてよりよく生きていくための日々の学び】を綴る日記です。世界中の人々の健康に貢献するため、働きたいと考えています。現在、筋骨格系疾患に対応する薬の基礎研究を進行中。人生一度きり、太く、ユニークに生きたいと考えています。

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5/23/09 抄読会 

Egashira N et al

Pituitary changes in Prop1 transgenic mice: hormone producing tumors and signet-ring type gonadotropes.
(Acta Histochem Cytochem. 2008 Jun 27;41(3):47-57.)

Prophet of Pit-1 (Prop1) is an early transcription factor that delays the appearance of gonadotropin in the developing pituitaries. Prop1 transgenic (Tg) mice have been shown to generate pituitary tumors that either produce TSH or are non-hormone producing. In our series of Prop1 Tg mice, only 5 out of 9 female mice produced pituitary adenomas, and the adenomas were only GH, PRL, GH and PRL, PRL and gonadotropin or TSH producing. The pituitary cells that surrounded these adenomas showed hyperplasia of the corresponding hormone producing cells; i.e. the GH cells were increased in the pituitary that contained GH producing adenoma. In addition, although the adenomas lacked the expression of Prop1, the non-neoplastic pituitary cells showed expression of Prop1.The Prop1 Tg mice also showed vacuolated cells with eccentric nuclei, which are characteristic of "signet-ring hypertrophic cells". Using immunohistochemistry, these signet ring hypertrophic cells were found to be positive for gonadotropin.Taken together, our results suggest a (1) tumorigenic effect of Prop1 in the pituitaries, and (2) causative effects of signet ring-type gonadotropes.
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[ 2009/05/23 11:36 ] 論文 | TB(0) | CM(0)

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PARP-1 is involved in autophagy induced by DNA damage.Muñoz-Gámez JA, Rodríguez-Vargas JM, Quiles-Pérez R, Aguilar-Quesada R, Martín-Oliva D, de Murcia G, Menissier de Murcia J, Almendros A, Ruiz de Almodóvar M, Oliver FJ.
Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (Ciberehd) and Laboratory of Medical Research, Academical Hospital San Cecilio, Granada, Spain.

Autophagy is a lysosome-dependent degradative pathway frequently activated in tumor cells treated with chemotherapy or radiation. PARP-1 has been implicated in different pathways leading to cell death and its inhibition potentiates chemotherapy-induced cell death. Whether PARP-1 participates in the cell's decision to commit to autophagy following DNA damage is still not known. To address this issue PARP-1 wild-type and deficient cells have been treated with a dose of doxorubicin that induces autophagy. Electron microscopy examination and GFP-LC3 transfection revealed autophagic vesicles and increased expression of genes involved in autophagy (bnip-3, cathepsin b and l and beclin-1) in wild-type cells treated with doxo but not in parp-1(-/-) cells or cells treated with a PARP inhibitor. Mechanistically the lack of autophagic features in PARP-1 deficient/PARP inhibited cells is attributed to prevention of ATP and NAD(+) depletion and to the activation of the key autophagy regulator mTOR. Pharmacological or genetical inhibition of autophagy results in increased cell death, suggesting a protective role of autophagy induced by doxorubicin. These results suggest that autophagy might be cytoprotective during the response to DNA damage and suggest that PARP-1 activation is involved in the cell's decision to undergo autophagy.

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[ 2009/01/07 21:39 ] 論文 | TB(0) | CM(0)

12/20/08 抄読会 

Seale P. et al.

PRDM16 controls a brown fat/skeletal muscle switch.
(Nature. 2008 Aug 21;454(7207):961-7)


Brown fat can increase energy expenditure and protect against obesity through a specialized program of uncoupled respiration. We show here by in vivo fate mapping that brown but not white fat cells arise from precursors that express myf5, a gene previously thought to be expressed only in the myogenic lineage. Notably, the transcriptional regulator, PRDM16 controls a bidirectional cell fate switch between skeletal myoblasts and brown fat cells. Loss of PRDM16 from brown fat precursors causes a loss of brown fat characteristics and promotes muscle differentiation. Conversely, ectopic expression of PRDM16 in myoblasts induces their differentiation into brown fat cells. PRDM16 stimulates brown adipogenesis by binding to PPARγ and activating its transcriptional function. Finally, PRDM16-deficient brown fat displays an abnormal morphology, reduced thermogenic gene expression and elevated expression of muscle-specific genes. Taken together, these data indicate that PRDM16 specifies the brown fat lineage from a progenitor that expresses myoblast markers and is not involved in white adipogenesis.

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[ 2008/12/20 21:23 ] 論文 | TB(0) | CM(0)
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山本 大輔

Author:山本 大輔
製薬会社 研究者
保健学博士

1981年長崎県生まれ
2005年臨床検査技師免許取得
2010年神戸大学 博士課程修了
2010年4月より現職

学生時代は下垂体前葉ホルモンの分泌機構や関連因子および栄養素の生体に及ぼす作用について研究していました。現在は内分泌代謝学の視点を基に、抗加齢学の観点から筋骨格系疾患に対応する薬の研究を行っています。

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