...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of cellular biochemistry. >Differential involvement of protein kinase C in basal versus acetylcholine-regulated prolactin secretion in rat anterior pituitary cells during aging.
【24h】

Differential involvement of protein kinase C in basal versus acetylcholine-regulated prolactin secretion in rat anterior pituitary cells during aging.

机译：蛋白激酶C在衰老过程中对大鼠垂体前叶基底蛋白和乙酰胆碱调节的催乳素分泌的不同参与。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Although it is well known that plasma concentration of prolactin (PRL) increases during aging in rats, how the anterior pituitary (AP) aging per se affects PRL secretion remains obscure. The objectives of this study were to determine if changes in the pituitary PRL responsiveness to acetylcholine (ACh; a paracrine factor in the AP), as compared with that to other PRL stimulators or inhibitors, contribute to the known age-related increase in PRL secretion, and if protein kinase C (PKC) is involved. We also determined if replenishment with aging-declined hormones such as estrogen/thyroid hormone influences the aging-caused effects on pituitary PRL responses. AP cells were prepared from old (23-24-month-old) as well as young (2-3-month-old) ovariectomized rats. Cells were pretreated for 5 days with diluent or 17beta-estradiol (E(2); 0.6 nM) in combination with or without triiodothyronine (T(3); 10 nM). Then, cells were incubated for 20 min with thyrotropin-releasing hormone (TRH; 100 nM), angiotensin II (AII; 0.2-20 nM), vasoactive intestinal peptide (VIP; 10(-9)-10(-5) M), dopamine (DA; 10(-9)-10(-5) M), or ACh (10(-7)-10(-3) M). Cells were also challenged with ACh, TRH, or phorbol 12-myristate 13-acetate (PMA; 10(-6) M) following PKC depletion by prolonged PMA (10(-6) M for 24 h) pretreatment. We found that estrogen priming of AP cells could reverse the aging-caused effects on pituitary PRL responses to AII and DA. In hormone-replenished cells aging enhanced the stimulation of PRL secretion by TRH and PMA, but not by AII and VIP. Aging also reduced the responsiveness of cells to ACh and DA in suppressing basal PRL secretion, and attenuated ACh inhibition of TRH-induced PRL secretion. Furthermore, ACh suppressed TRH-induced PRL secretion mainly via the PMA-sensitive PKC in the old AP cells, but via additional mechanisms in young AP cells. On the contrary, basal PRL secretion was PKC (PMA-sensitive)-independent in the old AP cells, but dependent in the young AP cells. Taken together, these results suggest differential roles of PMA-sensitive PKC in regulating basal and ACh-regulated PRL responses in old versus young AP cells. The persistent aging-induced differences in AP cell responsiveness to ACh, DA, TRH, and PMA following hormone (E(2)/T(3)) replenishment suggest an intrinsic pituitary change that may contribute, in part, to the elevated in vivo PRL secretion observed in aged rats.
机译：尽管众所周知，催乳素（PRL）的血浆浓度在大鼠衰老过程中会增加，但是垂体前叶（AP）本身的衰老本身如何影响PRL分泌仍然不清楚。这项研究的目的是确定与其他PRL刺激剂或抑制剂相比，垂体PRL对乙酰胆碱（ACh; AP中的旁分泌因子）的反应性变化是否有助于已知的与年龄相关的PRL分泌增加，以及是否涉及蛋白激酶C（PKC）。我们还确定了补充衰老的激素（例如雌激素/甲状腺激素）是否会影响衰老对垂体PRL反应的影响。从老（23-24个月大）和年轻（2-3个月大）卵巢切除大鼠制备AP细胞。将细胞用稀释剂或17β-雌二醇（E（2）; 0.6 nM）结合或不结合三碘甲状腺素（T（3）; 10 nM）预处理5天。然后，将细胞与促甲状腺激素释放激素（TRH; 100 nM），血管紧张素II（AII; 0.2-20 nM），血管活性肠肽（VIP; 10（-9）-10（-5）M）孵育20分钟，多巴胺（DA; 10（-9）-10（-5）M）或ACh（10（-7）-10（-3）M）。在通过延长的PMA（10（-6）M持续24 h）预处理PKC耗尽后，还用ACh，TRH或佛波醇12-肉豆蔻酸酯13-乙酸盐（PMA; 10（-6）M）攻击细胞。我们发现雌激素引发的AP细胞可以逆转衰老引起的对垂体PRL对AII和DA的反应。在补充激素的细胞中，衰老增强了TRH和PMA对PRL分泌的刺激，但对AII和VIP却没有促进。衰老还降低了细胞对ACh和DA在抑制基础PRL分泌中的反应能力，并减弱了ACh对TRH诱导的PRL分泌的抑制作用。此外，ACh主要通过旧AP细胞中的PMA敏感PKC抑制TRH诱导的PRL分泌，但是通过年轻AP细胞中的其他机制抑制了TRH诱导的PRL分泌。相反，基础的PRL分泌在旧的AP细胞中不依赖PKC（对PMA敏感），而在年轻的AP细胞中依赖。两者合计，这些结果表明PMA敏感PKC在调节旧的和年轻的AP细胞中基础和ACh调节的PRL反应中的不同作用。补充荷尔蒙（E（2）/ T（3））后，AP细胞对ACh，DA，TRH和PMA的响应因衰老引起的持续差异表明内在的垂体改变可能部分地导致体内升高在老年大鼠中观察到PRL分泌。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号