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首页> 外文期刊>Bone >Microdamage induced calcium efflux from bone matrix activates intracellular calcium signaling in osteoblasts via L-type and T-type voltage-gated calcium channels
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Microdamage induced calcium efflux from bone matrix activates intracellular calcium signaling in osteoblasts via L-type and T-type voltage-gated calcium channels

机译：微损伤诱导的骨基质钙流出通过L型和T型电压门控钙通道激活成骨细胞中的细胞内钙信号传导

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Mechanisms by which bone microdamage triggers repair response are not completely understood. It has been shown that calcium efflux ([Ca2+](E)) occurs from regions of bone undergoing microdamage. Such efflux has also been shown to trigger intracellular calcium signaling ([Ca2+)(I)] in MC3T3-E1 cells local to damaged regions. Voltage-gated calcium channels (VGCCs) are implicated in the entry of [Ca2+](E) to the cytoplasm. We investigated the involvement of VGCC in the extracellular calcium induced intracellular calcium response (ECIICR). MC3T3-E1 cells were subjected to one dimensional calcium efflux from their basal aspect which results in an increase in [Ca2+](I). This increase was concomitant with membrane depolarization and it was significantly reduced in the presence of Bepridil, a non-selective VGCC inhibitor. To identify specific type(s) of VGCC in ECIICR, the cells were treated with selective inhibitors for different types of VGCC. Significant changes in the peak intensity and the number of [Ca2+](I) oscillations were observed when L-type and T-type specific VGCC inhibitors (Verapamil and NNC55-0396, respectively) were used. So as to confirm the involvement of L- and T-type VGCC in the context of microdamage, cells were seeded on devitalized notched bone specimen, which were loaded to induce microdamage in the presence and absence of Verapamil and NNC55-0396. The results showed significant decrease in [Ca2+](I) activity of cells in the microdamaged regions of bone when L- and T-type blockers were applied. This study demonstrated that extracellular calcium increase in association with damage depolarizes the cell membrane and the calcium ions enter the cell cytoplasm by L- and T-type VGCCs. (C) 2015 Elsevier Inc. All rights reserved.
机译：骨骼微损伤触发修复反应的机制尚未完全了解。已经显示钙流出（[Ca 2+]（E））发生在遭受微损伤的骨骼区域。还显示出这种流出可在受损区域局部的MC3T3-E1细胞中触发细胞内钙信号传导（[Ca2 +]（I）]。电压门控钙通道（VGCC）涉及[Ca2 +]（E）进入细胞质。我们调查了VGCC参与细胞外钙诱导的细胞内钙反应（ECIICR）。从其基础方面对MC3T3-E1细胞进行一维钙外排，这导致[Ca2 +]（I）增加。这种增加与膜去极化同时发生，并且在非选择性VGCC抑制剂Bepridil的存在下明显减少。为了鉴定ECIICR中VGCC的特定类型，用针对不同类型VGCC的选择性抑制剂处理细胞。当使用L型和T型特异性VGCC抑制剂（分别为维拉帕米和NNC55-0396）时，观察到峰强度和[Ca2 +]（I）振荡数的显着变化。为了证实L型和T型VGCC参与微损伤，将细胞接种在失活的带槽骨标本上，在存在和不存在维拉帕米和NNC55-0396的情况下，将细胞加载以诱导微损伤。结果表明，当使用L型和T型阻滞剂时，骨骼微损伤区域中细胞的[Ca2 +]（I）活性显着降低。这项研究表明，细胞外钙的增加与损伤相关，使细胞膜去极化，钙离子通过L型和T型VGCC进入细胞质。 （C）2015 Elsevier Inc.保留所有权利。

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