肌纤维细胞通过异细胞连接43间隙结合通过微孔损害心肌脉冲的传播
Yumika Tsuji1,2, Takehiro Ogata1, Kentaro Mochizuki1
1Department of Pathology and Cell Regulation and, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Frontiers in physiology
|March 11, 2024
概括
肌纤维细胞 (MFs) 通过连接素43 (Cx43) 与心肌细胞 (CMs) 的间隙连接改变心脏脉冲的传播. 这种异细胞合,即使没有直接的结构干扰,也可以促进心脏中的亲节律失常的电活动.
科学领域:
- 心血管生理学心血管生理学
- 心脏电生理学 心脏电生理学
- 细胞生物学 细胞生物学
背景情况:
- 已知心肌组织中的肌纤维细胞 (MFs) 影响脉冲传播,并导致心律失常.
- 在没有复杂的结构整合的情况下,直接肌纤维细胞-心肌细胞 (CM) 接触对冲动传播的具体影响仍然不太清楚.
研究的目的:
- 研究MF和CM之间的单面异细胞连接如何影响CM单层中的冲动传播.
- 确定差距连接合在调节这些效应中的作用,独立于空间或机械干扰.
主要方法:
- 新生小鼠CM单层被培养在微孔膜上,背面有MF或CM (CM-MF和CM-CM模型).
- 基于Fluo8的成像评估了1Hz和2Hz节奏期间的时空脉冲传播模式.
- 在MF中,使用间隙结抑制剂 (heptanol) 和选择性Cx43敲击,检查了Connexin 43 (Cx43) 的参与.
主要成果:
- 与CM-CM模型相比,CM-MF模型显示导电速度明显减慢,脉冲传播的方向变化更大,特别是2Hz.
- 局部化的MF集群诱导了冲动传播的细分抑制,导致非统一的模式.
- 染料转移和Cx43免疫细胞化学证实了CMs和MFs之间的异细胞间隙连接合,该合被赫普坦醇抑制,并通过Cx43敲击改善.
结论:
- 异细胞Cx43间隙连接CMs和MFs之间的合改变心肌脉冲传播模式,即使没有直接的空间或机械相互作用.
- 在与心肌密切接触时,MFs可以促进亲心律失常的脉冲传播,这与诸如治愈心脏梗塞边界区域等情况有关.
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