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Paracrine control by immune cells on the expression of gonadal function

Paracrine control by immune cells on the expression of gonadal function
免疫细胞旁分泌对性腺功能表达的控制
批准号:
62480078
负责人:
KOHMOTO Kaoru
金额:
$4.22万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for General Scientific Research (B)
财政年份:
1987
资助国家:
日本
项目状态:
已结题
起止时间:
1987 至 1988

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中文摘要
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英文摘要
It can be taken that ovulation and luteinization are a local inflamatory reaction and succeeding trauma formation, respectively. At ovulation, macrophages invade into and stay in corpora lutea after luteinization. However, their function is not yet clear. To clarify the function, rats were splenectomized on different days of cycle, and the effect on ovulation was examined. Rats splenectomized in the morning of metestrus showed delay of ovulation by one day. On the day of diestrus their blood concentrations of progesterone and 20alpha-dihydroprogesterone were higher and lower than those in normally cycling rats, respectively. As high progesterone concentrations in the morning of diestrus prolong the appearance of LH surge which induces ovulation, the delay of ovulation after splenectomy may be caused by this high progesterone level.This delay of ovulation by splenectomy on the day of metestrus is overcome by grafting of spleens from metestrous rats. These results suggest that splenocytes which invade into corpora lutea promote luteolysis. In rats, prolactin inhibits the regression of luteal function by inhibition of the activity of 20alpha-hydroxysteroid dehydrogenase in corpora lutea. This luteotropic actitivity of prolactin has not been confirmed in vitro. We examined this prolactin action by culturing luteal cells with macrophages. When luteal cells from pseudopregnant rats were cultured for 48 h with macrophages from metestrous rats, the inhibition of 20 -hydroxysteroid dehydrogenase by prolactin was observed. All these data suggest that function of luteal cells are under paracrine control of splenocytes including macrophages.
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Imataka,H.,Suzuki,K.,Inano,H.,Kohmoto,K.,Tamaoki,: Gen.Comp.Endocrinol.71. 413-418 (1988)
Imataka,H.,Suzuki,K.,Inano,H.,Kohmoto,K.,Tamaoki,:Gen.Comp.Endocrinol.71。
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通讯作者:
Shigemi MATSUYAMA;Mitsuaki OHTA;Michio TAKAHASHI: Endocrinologia Japonica. 34. 849-855 (1987)
松山茂美;太田光明;高桥道夫:日本内分泌学。
DOI: --
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作者: []
通讯作者:
Imataka,H.;Suzuki,K.;Inano,H.;Kohmoto,K.;Tamaoki,B.: General and Comparative Endocrinology. 71. 413-418 (1988)
Imataka,H.;Suzuki,K.;Inano,H.;Kohmoto,K.;Tamaoki,B.:一般和比较内分泌学。
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通讯作者:
Imataka,H.;Suzuki,K.;Inano,H.;Kohmoto,K.;Tamaoki,: Gen.Comp.Endocrinl.69. 153-162 (1988)
Imataka,H.;Suzuki,K.;Inano,H.;Kohmoto,K.;Tamaoki,:Gen.Comp.Endocrinl.69。
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22
    Regulation of signal transduction for growth factors in mammary epithelial cells.
    • 批准号:
      06454124
    • 项目类别:
      Grant-in-Aid for General Scientific Research (B)
    • 资助金额:
      $4.61万
    • 财政年份:
      1994
    • 负责人:
      KOHMOTO Kaoru
    • 依托单位:
    Interaction between the substratum and mesenchyme and regulation by growth factor in mammary glands and reproductive organs.
    • 批准号:
      04304023
    • 项目类别:
      Grant-in-Aid for Co-operative Research (A)
    • 资助金额:
      $7.68万
    • 财政年份:
      1992
    • 负责人:
      KOHMOTO Kaoru
    • 依托单位:
    Molecular biology of the proliferation of mammary epithelial cells
    • 批准号:
      04454105
    • 项目类别:
      Grant-in-Aid for General Scientific Research (B)
    • 资助金额:
      $4.22万
    • 财政年份:
      1992
    • 负责人:
      KOHMOTO Kaoru
    • 依托单位:
    海外基金