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Author Correction: Using Gjd3-CreEGFP mice to examine atrioventricular node morphology and composition.

ABSTRACT: An amendment to this paper has been published and can be accessed via a link at the top of the paper.

SUBMITTER: Bhattacharyya S

PROVIDER: S-EPMC7046679 | biostudies-literature | 2020 Feb

REPOSITORIES: biostudies-literature

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Author Correction: Using Gjd3-CreEGFP mice to examine atrioventricular node morphology and composition.

Bhattacharyya Samadrita S Duan Jialei J Wang Lin L Li Boxun B Bhakta Minoti M Fernandez-Perez Antonio A Hon Gary C GC Munshi Nikhil V NV

Scientific reports 20200228 1

An amendment to this paper has been published and can be accessed via a link at the top of the paper. ...[more]

PMID: 32107454

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Using Gjd3-CreEGFP mice to examine atrioventricular node morphology and composition.

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Using Gjd3-CreEGFP mice to examine atrioventricular node morphology and composition

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Using Gjd3-CreEGFP mice to examine atrioventricular node morphology and composition

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ZO-1 Regulates Intercalated Disc Composition and Atrioventricular Node Conduction.

Project description:RationaleZO-1 (Zona occludens 1), encoded by the tight junction protein 1 (TJP1) gene, is a regulator of paracellular permeability in epithelia and endothelia. ZO-1 interacts with the actin cytoskeleton, gap, and adherens junction proteins and localizes to intercalated discs in cardiomyocytes. However, the contribution of ZO-1 to cardiac physiology remains poorly defined.ObjectiveWe aim to determine the role of ZO-1 in cardiac function.Methods and resultsInducible cardiomyocyte-specific Tjp1 deletion mice (Tjp1fl/fl; Myh6Cre/Esr1*) were generated by crossing the Tjp1 floxed mice and Myh6Cre/Esr1* transgenic mice. Tamoxifen-induced loss of ZO-1 led to atrioventricular (AV) block without changes in heart rate, as measured by ECG and ex vivo optical mapping. Mice with tamoxifen-induced conduction system-specific deletion of Tjp1 (Tjp1fl/fl; Hcn4CreERt2) developed AV block while tamoxifen-induced conduction system deletion of Tjp1 distal to the AV node (Tjp1fl/fl; Kcne1CreERt2) did not demonstrate conduction defects. Western blot and immunostaining analyses of AV nodes showed that ZO-1 loss decreased Cx (connexin) 40 expression and intercalated disc localization. Consistent with the mouse model study, immunohistochemical staining showed that ZO-1 is abundantly expressed in the human AV node and colocalizes with Cx40. Ventricular conduction was not altered despite decreased localization of ZO-1 and Cx43 at the ventricular intercalated disc and modestly decreased left ventricular ejection fraction, suggesting ZO-1 is differentially required for AV node and ventricular conduction.ConclusionsZO-1 is a key protein responsible for maintaining appropriate AV node conduction through maintaining gap junction protein localization.

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