Changes in gap junction proteins Connexin30.2 and Connexin40 expression in the sinoatrial node of rats with dexmedetomidine-induced sinus bradycardia

Yin, Yongqiang; Yi, Zhong; Zhu, Yu; Tian, Lei

doi:10.1016/j.bjane.2022.05.004

Cited by 1 publication

(2 citation statements)

References 23 publications

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“…Cx30 contributes to the slowing of impulse propagation from the AV node and limits the maximum heart rate carried from the atria to the ventricles, thereby preventing rapid conduction of potentially worsening hemodynamics to the ventricles [ 26 , 28 ]. In addition to this, Cx30 also integrates all cardiac pacemaker cells with different intrinsic frequencies [ 29 ].…”

Section: Discussionmentioning

confidence: 99%

“…The Ca 2+ ions play a role in the regulation, flexibility, and contractility of the heart. The entry of Ca 2+ ions through the channel not only plays a role in initiating cardiac excitation and contraction but also affects several crossing pathways that can change the membrane potential [ 29 ]. KCNN is an ion channel that plays an important role in Ca 2+ exchange and the regulation of cardiac excitability [ 32 ].…”

Section: Discussionmentioning

confidence: 99%

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TBX3 transfection and nodal signal pathway inhibition promote differentiation of adipose mesenchymal stem cell to cardiac pacemaker-like cells

Basalamah,

Dilogo,

Raharjo

et al. 2024

Stem Cell Res Ther

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Background Mesenchymal stem cells (MSCs) are known as one of the best candidate cells to produce cardiac pacemaker-like cells (CPLCs). Upregulation of TBX3 transcription factor and inhibition of the nodal signal pathway have a significant role in the formation of cardiac pacemaker cells such as sinoatrial and atrioventricular nodes, which initiate the heartbeat and control the rhythm of heart contractions. This study aimed to confirm the effects of transfection of TBX3 transcription factor and inhibition of the nodal signal pathway on differentiating adipose-derived MSCs (AD-MSCs) to CPLCs. AD-MSCs were characterized using flow cytometry and three-lineage differentiation staining. Methods The transfection of TBX3 plasmid was carried out using lipofectamine, and inhibition of the nodal signal pathway was done using the small-molecule SB431542. The morphology of the cells was observed using a light microscope. Pacemaker-specific markers, including TBX3, Cx30, HCN4, HCN1, HCN3, and KCNN4, were evaluated using the qRT-PCR method. For protein level, TBX3 and Cx30 were evaluated using ELISA and immunofluorescence staining. The electrophysiology of cells was evaluated using a patch clamp. Results The TBX3 expression in the TBX3, SM, and TBX + SM groups significantly higher (p < 0.05) compared to the control group and cardiomyocytes. The expression of Cx40 and Cx43 genes were lower in TBX3, SM, TBX + SM groups. In contrast, Cx30 gene showed higher expression in TBX3 group. The expression HCN1, HCN3, and HCN4 genes are higher in TBX3 group. Conclusion The transfection of TBX3 and inhibition of the nodal signal pathway by small-molecule SB431542 enhanced differentiation of AD-MSCs to CPLCs.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%