• Nanion Technologies: イオンチャネル研究のスマートツール

    Nanion Technologies: イオンチャネル研究のスマートツール

  • CardioExcyte 96 SOL: 心筋の光ペーシング

    CardioExcyte 96 SOL: 心筋の光ペーシング

  • SURFE²R 96SE: ラベルフリーのトランスポーターHTS

    SURFE²R 96SE: ラベルフリーのトランスポーターHTS

  • 脂質二分子膜実験: Orbitシリーズ

    脂質二分子膜実験: Orbitシリーズ

Our Product Portfolio

SyncroPatch 384/768PE

SyncroPatch 384/768PE

Patchliner

Patchliner

Port-a-Patch

Port-a-Patch

CardioExcyte 96

CardioExcyte 96

SURFE²R 96SE

SURFE²R 96SE

SURFE²R N1

SURFE²R N1

Orbit 16

Orbit 16

Orbit Mini

Orbit Mini

Vesicle Prep Pro

Vesicle Prep Pro

2017 - Structural and electrophysiological dysfunctions due to increased endoplasmic reticulum stress in a long-term pacing model using human induced pluripotent stem cell-derived ventricular cardiomyocytes

Icon CE  CardioExcyte 96 publication in Stem Cell Research and Therapy (2017)

Authors: 
Cui C., Geng L., Shi J., Zhu Y., Yang G., Wang Z., Wang J., Chen M.

Journal: 
Stem Cell Research & Therapy (2017) 8:109


Abstract: 

Background:
Long-term ventricular pacing has deleterious effects and becomes more significant when cumulative percent ventricular pacing (Cum%VP) exceeds 40% of time. However, cellular disturbances and pathways by which pacing leads to myocardial disorders are not well understood. Attempts to resolve these questions have been hampered by difficulties in obtaining human cardiac tissue and the inability to build a longer-lasting (lasting longer than weeks) pacing model in vitro.

Methods:
Human induced pluripotent stem cell-derived ventricular cardiomyocytes (VCMs) were cultured in the presence of electrical stimulation for 2 weeks. Quantitative structural and electrophysiological analyses were used to define the functional disturbances of pacing.

Results:
Compared to controls, paced VCMs exhibited a remarkable reduction in the contractile protein expression, an increased apoptosis ratio and electrophysiological remodelling in a Cum%VP-dependent manner. Investigation of the protein expression levels revealed that long-term pacing universally activated both ER stress and downstream calpain. Moreover, the inhibition of calpain attenuated the adverse effects on the structural remodelling and increased the ICa, L in paced VCMs.

Conclusions:
The results demonstrated that pacing VCMs for 2 weeks in vitro led to a series of structural and electrophysiological dysfunctions. The increased ER stress and downstream calpain could be a central mechanism underlying the disease pathogenesis. This finding could represent a new therapeutic target in the management of long-term pacing patients.


Download here

Back

Nanion コーポレートブログ

Cookies make it easier for us to provide you with our services. With the usage of our services you permit us to use cookies.
More information Ok