...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Cellular Physiology >cAMP activation by PACAP/VIP stimulates IL-6 release and inhibits osteoblastic differentiation through VPAC2 receptor in osteoblastic MC3T3 cells.
【24h】

cAMP activation by PACAP/VIP stimulates IL-6 release and inhibits osteoblastic differentiation through VPAC2 receptor in osteoblastic MC3T3 cells.

机译：营激活PACAP /贵宾刺激il - 6释放,抑制成骨细胞的分化通过在成骨细胞MC3T3 VPAC2受体细胞。

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

The neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP), a member of the glucagon/vasoactive intestinal peptide (VIP) superfamily, stimulates cyclic AMP accumulation initiating a variety of biological processes such as: neurotropic actions, immune and pituitary function, learning and memory, catecholamine biosynthesis and regulation of cardiopulmonary function. Both osteoclasts and osteoblasts have been shown to express receptors for PACAP/VIP implicated in their role in bone metabolism. To further understand the role of PACAP/VIP family in controlling bone metabolism, we investigated differentiation model of MC3T3-E1 cells, an osteoblastic cell line derived from mouse calvaria. Quantitative RT-PCR analysis demonstrated that MC3T3-E1 cells expressed only VPAC2 receptor and its expression was upregulated during osteoblastic differentiation, whereas VPAC1 and PAC1 receptors were not expressed. Consistent with expression of receptor subtype, both PACAP and VIP stimulate cAMP accumulation in a time- and dose-dependent manner with the similar potency in undifferentiated and differentiated cells, while Maxadilan, a specific agonist for PAC1-R, did not. Furthermore, downregulation of VPAC2-R by siRNA completely blocked cAMP response mediated by PACAP and VIP. Importantly, PACAP/VIP as well as forskolin markedly suppressed the induction of alkaline phosphatase mRNA upon differentiation and the pretreatment with 2',5'-dideoxyadenosine, a cAMP inhibitor, restored its inhibitory effect of PACAP. We also found that PACAP and VIP stimulated IL-6 release, a stimulator of bone resorption, and VPAC2-R silencing inhibited IL-6 production. Thus, PACAP/VIP can activate adenylate cyclase response and regulate IL-6 release through VPAC2 receptor with profound functional consequences for the inhibition of osteoblastic differentiation in MC3T3-E1 cells.
机译：神经肽垂体腺苷酸cyclase-activating多肽(PACAP)成员胰高糖素/——血管活性肠肽(VIP)总科,刺激环腺苷酸积累发起各种各样的生物过程如:亲神经的行动,免疫和垂体功能,学习和记忆,儿茶酚胺的生物合成和调控心肺功能。成骨细胞表达受体已被证明PACAP /贵宾卷入他们的角色在骨头新陈代谢。PACAP /贵宾家庭在控制骨代谢,我们研究了微分MC3T3-E1模型细胞,成骨细胞的细胞系来源于老鼠头顶。仅证明MC3T3-E1细胞表达VPAC2受体表达和调节在成骨细胞的分化,而受体VPAC1和PAC1并不表示。与受体亚型的表达一致,PACAP和VIP刺激营地积累时间和剂量依赖性的方式在未分化的能力,类似分化细胞,虽然Maxadilan,一个特定的PAC1-R受体激动剂,没有。完全downregulation VPAC2-R的核阻塞营地响应由PACAP和贵宾。重要的是,PACAP /贵宾以及forskolin显著抑制碱性的感应在分化和磷酸酶mRNA预处理2 ',5 ' -dideoxyadenosine,营地抑制剂,其抑制作用的恢复PACAP。刺激器刺激释放il - 6的骨头吸收,VPAC2-R沉默抑制il - 6的分泌生产。腺苷酸环化酶反应和调节il - 6通过VPAC2受体与深远的功能抑制的影响在MC3T3-E1细胞成骨细胞的分化。

著录项

相似文献

  • 外文文献
  • 中文文献
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