• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Life sciences >Linoleamide, a brain lipid that induces sleep, increases cytosolic Ca2+ levels in MDCK renal tubular cells.
【24h】

Linoleamide, a brain lipid that induces sleep, increases cytosolic Ca2+ levels in MDCK renal tubular cells.

机译：亚油酰胺是一种诱导睡眠的脑脂质，可增加MDCK肾小管细胞的胞质Ca2 +水平。

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

Linoleamide is an endogenous lipid that has been shown to induce sleep in cats, rats and humans. However, its physiological function remains unclear. In this study the effect of linoleamide on cytosolic free Ca2+ concentrations ([Ca2+]i) in Madin Darby canine kidney (MDCK) tubular cells was examined, by using fura-2 as a Ca2+ probe. In a concentration-dependent manner, linoleamide induced increases in [Ca2+]i between 10-500 microM with an EC50 of 20 microM. The signal comprised a slow rise and a persistent phase, and was a result of internal Ca2+ release and external Ca2+ influx because it was partly inhibited by external Ca2+ removal. In Ca2+-free medium, depletion of the endoplasmic reticulum Ca2+ store with 1 microM thapsigargin abolished 100 microM linoleamide-induced internal Ca2+ release, and conversely, pretreatment with linoleamide prevented thapsigargin from releasing internal Ca2+. This demonstrates that the internal source of linoleamide-induced [Ca2+]i increase is located in the endoplasmic reticulum. This discharge of internal Ca2+ caused capacitative Ca2+ entry because after incubation with 100 microM linoleamide in Ca2+-free medium for 8 min readmission of 3 mM CaCl2 induced increases in [Ca2+]i. After the formation of inositol-1,4,5-trisphosphate (IP3) was blocked by the phospholipase C inhibitor U73122 (1 microM), linoleamide still induced an increase in [Ca2+]i but the shape of the increase was altered. Similar results were found for another sleep-inducing lipid 9,10-octadecenoamide. Together, the present study shows that the endogenous sleep-inducing lipid linoleamide was able to cause significant increases in [Ca2+]i in renal tubular cells, by releasing the endoplasmic reticulum Ca2+ store and triggering capacitative Ca2+ entry in a manner independent of IP3.
机译：亚油酰胺是一种内源性脂质，已显示可诱导猫，大鼠和人类的睡眠。但是，其生理功能仍不清楚。在这项研究中，通过使用fura-2作为Ca2 +探针，研究了亚油酰胺对Madin Darby犬肾（MDCK）肾小管细胞中胞质游离Ca2 +浓度（[Ca2 +] i）的影响。以浓度依赖性方式，亚油酰胺诱导的[Ca2 +] i在10-500 microM之间增加，EC50为20 microM。该信号包括缓慢的上升和持续的相位，并且是内部Ca2 +释放和外部Ca2 +流入的结果，因为它被外部Ca2 +的去除部分抑制。在不含Ca2 +的培养基中，用1 microM thapsigargin耗尽内质网Ca2 +储存消除了100 microM亚油酰胺诱导的内部Ca2 +释放，相反，用亚油酰胺预处理可防止thapsigargin释放内部Ca2 +。这表明亚油酰胺诱导的[Ca2 +] i增加的内部来源位于内质网中。内部Ca2 +的这种释放导致电容性Ca2 +进入，因为在无Ca2 +的培养基中与100 microM亚油酰胺孵育8分钟后，重新吸收3 mM CaCl2诱导了[Ca2 +] i的增加。磷脂酶C抑制剂U73122（1 microM）阻止了1,4,5-三磷酸肌醇（IP3）的形成后，亚油酰胺仍然诱导[Ca2 +] i升高，但是改变了其形状。对于另一种诱导睡眠的脂质9,10-十八烯酰胺也发现了相似的结果。总之，本研究表明，内源性睡眠诱导脂质亚油酰胺能够通过释放内质网Ca2 +存储并以独立于IP3的方式触发电容性Ca2 +进入，从而导致肾小管细胞[Ca2 +] i显着增加。

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