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Peer-reviewedCC BY 4.0International Journal of Molecular Sciences

Nicotinic Acetylcholine Receptors Modulate T-Tubule Architecture Under Sympathetic Overstimulation

  • Cai He1,2
  • Qi Zeng1,2
  • Junwei Zhao1
  • Yang Meng2
  • Yingna Guo2
  • Hongguang Wang2
  • Shi-Qiang Wang1,2
  • Xiang Li1
  • Tingting Hou1,2
  1. 1Beijing Life Science Academy, Beijing 102209, China
  2. 2State Key Laboratory of Membrane Biology, College of Life Sciences, Peking University, Beijing 100871, China
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Abstract

Pathological remodeling of transverse tubules (T-tubules, TTs) is commonly observed in cardiac disease and may be promoted by sustained adrenergic stimulation. Although cholinergic signaling has been associated with cardioprotective effects, it remains unclear whether it directly modulates TT integrity in cardiomyocytes. Here, we examined how cholinergic receptor activation affects TT organization during acute β-adrenergic stimulation in isolated adult rat cardiomyocytes. Cells were exposed to isoproterenol (ISO), alone or in combination with acetylcholine (ACh) or nicotine (Nic). Confocal imaging showed that ISO disrupted TT organization and reduced the cellular length-to-width (L/W) ratio. ACh or Nic alone altered TT architecture, primarily by reducing TT power and increasing longitudinal tubule density; however, co-treatment with either agonist was associated with altered TT remodeling responses to ISO in TT structure and cell morphology. The muscarinic receptor agonist xanomeline (Xano) did not reproduce these effects. These results suggest a cardiomyocyte-autonomous role for nAChR signaling in limiting acute β-adrenergic stimulation-induced TT remodeling. Further studies are required to identify the nAChR subtype and downstream signaling mechanisms involved and to determine the relevance of these findings in vivo.

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Cite

BibTeXRIS
BibTeX
@article{he2026nicotinic,
  title = {{Nicotinic Acetylcholine Receptors Modulate T-Tubule Architecture Under Sympathetic Overstimulation}},
  author = {Cai He and Qi Zeng and Junwei Zhao and Yang Meng and Yingna Guo and Hongguang Wang and Shi-Qiang Wang and Xiang Li and Tingting Hou},
  journal = {International Journal of Molecular Sciences},
  year = {2026},
  month = oct,
  doi = {10.3390/ijms27219597},
  url = {https://www.mdpi.com/1422-0067/27/21/9597},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Nicotinic Acetylcholine Receptors Modulate T-Tubule Architecture Under Sympathetic Overstimulation
AU  - Cai He
AU  - Qi Zeng
AU  - Junwei Zhao
AU  - Yang Meng
AU  - Yingna Guo
AU  - Hongguang Wang
AU  - Shi-Qiang Wang
AU  - Xiang Li
AU  - Tingting Hou
PY  - 2026
DA  - 2026/10/27
JO  - International Journal of Molecular Sciences
DO  - 10.3390/ijms27219597
UR  - https://www.mdpi.com/1422-0067/27/21/9597
AB  - Pathological remodeling of transverse tubules (T-tubules, TTs) is commonly observed in cardiac disease and may be promoted by sustained adrenergic stimulation. Although cholinergic signaling has been associated with cardioprotective effects, it remains unclear whether it directly modulates TT integrity in cardiomyocytes. Here, we examined how cholinergic receptor activation affects TT organization during acute β-adrenergic stimulation in isolated adult rat cardiomyocytes. Cells were exposed to isoproterenol (ISO), alone or in combination with acetylcholine (ACh) or nicotine (Nic). Confocal imaging showed that ISO disrupted TT organization and reduced the cellular length-to-width (L/W) ratio. ACh or Nic alone altered TT architecture, primarily by reducing TT power and increasing longitudinal tubule density; however, co-treatment with either agonist was associated with altered TT remodeling responses to ISO in TT structure and cell morphology. The muscarinic receptor agonist xanomeline (Xano) did not reproduce these effects. These results suggest a cardiomyocyte-autonomous role for nAChR signaling in limiting acute β-adrenergic stimulation-induced TT remodeling. Further studies are required to identify the nAChR subtype and downstream signaling mechanisms involved and to determine the relevance of these findings in vivo.
SN  - 1422-0067
ER  -