Immunolocalization of the mNav2.3 Na+ channel in mouse heart: upregulation in myometrium during pregnancy.
Immunolocalization of the mNav2.3 Na+ channel in mouse heart: upregulation in myometrium during pregnancy.
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小鼠心脏中 mNav2.3 Na 通道的免疫定位：妊娠期间子宫肌层的上调。
DOI：
10.1152/ajpcell.1996.270.2.c688
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Tamkun,MM
中科院分区：
文献类型：
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作者：
Knittle,TJ;Doyle,KL;Tamkun,MM
mNav2.3是一种推定的电压依赖性钠通道（NaC）基因，在小鼠心脏和子宫中表达，与基因亚家族1的NaC仅具有45%的氨基酸同一性。使用针对两种不同表位的多克隆抗体的免疫荧光研究揭示，心脏中的mNav2.3蛋白与神经特异性抗体结合共定位。在处女子宫中观察到类似的mNav2.3特异性抗体染色。然而，mNav2.3在子宫神经中的表达在妊娠晚期消失，同时在子宫纵、环形平滑肌中出现，在足月时达到最大值，并在产后2天内迅速下降。在足月子宫中mNav2.3表达通常与连接蛋白43共定位于肌细胞表面。免疫荧光结果得到Western分析的支持，其中217 kDa NaC在妊娠晚期增加，产后2天下降。这些数据可能是NaC调节的最引人注目的例子。妊娠期间子宫肌层的急性和短暂上调表明Nav2.3通道在足月子宫功能中起作用。
mNav2.3 is a putative voltage-dependent sodium channel (NaC) gene expressed in both mouse heart and uterus that shares only 45% amino acid identity with NaCs from gene subfamily 1. Immunofluorescence studies using polyclonal antibodies against two distinct epitopes revealed that mNav2.3 protein in heart colocalized with nerve-specific antibody binding. Similar mNav2.3-specific antibody staining was observed in virgin uterus. However, mNav2.3 expression in uterine nerve disappeared during late pregnancy, concurrent with an appearance in both the longitudinal and circular uterine smooth muscle, which reached a maximum at term and quickly declined within 2 days postpartum. mNav2.3 expression in term uterus often colocalized on the myocyte surface with connexin 43. The immunofluorescence results are supported by Western analysis in which the 217-kDa NaC increased during late pregnancy and declined 2 days postpartum. These data provide perhaps the most dramatic example of NaC regulation. The acute and transient upregulation in myometrium during gestation suggests the Nav2.3 channel plays a role in uterine function at term.