ArticleMolecular and cellular biochemistry2017
Knockdown of cardiac Kir3.1 gene with siRNA can improve bradycardia in an experimental sinus bradycardia rat model.
Article in Molecular and cellular biochemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 5 citations in OpenAlex.
- The cellular function and molecular mechanism of formaldehyde in cardiovascular disease and heart development.Journal of cellular and molecular medicine · 2021Review
- Gene and Protein Expression Profile of Selected Molecular Targets Mediating Electrophysiological Function inInternational journal of molecular sciences · 2018Article
- Changes in gap junction proteins Connexin30.2 and Connexin40 expression in the sinoatrial node of rats with dexmedetomidine-induced sinus bradycardia.Brazilian journal of anesthesiology (Elsevier)Article
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4 authors at 3 institutions in 1 country.
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Abstract
The objective of this study was to explore whether the inhibition of potassium inwardly rectifying channel (Kir3.1) with short interfering RNA (siRNA) can improve bradycardia in an experimental sinus bradycardia rat model. 54 Sprague Dawley (SD) rats were randomly divided into three groups: experimental group, control group, and sham group. Sinus bradycardia model was established in SD rats through chemical ablation of sinoatrial (SA) node with 20% formaldehyde. Variations of Kir3.1 expression at mRNA and protein level were examined with qPCR and Western blotting. Electrocardiograms (ECG) of rats at 3 days and 1, 2, 3, and 4 weeks after chemical ablation and lentivirus injection were recorded and differences were compared among the three groups. The differences among multiple groups were analyzed by one-way analysis of variance (ANOVA). It was found through RT-PCR and Western blot that the mRNA and protein levels of Kir3.1 at sinoatrial node areas were decreased by 42 ± 7% and 31 ± 7% in comparison with control group, respectively (P < 0.05 in both comparisons) after 4 weeks of chemical ablation/injection. Whole-cell patch clamp data showed that the lentiviral construct could significantly inhibit the potassium current of a muscarinic acetylcholine-sensitive K
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