Heterogeneous expression of connexin 43 in the myocardium of rabbit right ventricular outflow tract

Ou, Baiqing; Nakagawa, Mikiko; Kajimoto, Munetaka; Nobe, Seiki; Ooie, Tatsuhiko; Ichinose, Masashi; Yonemochi, Hidetoshi; Ono, Noriaki; Shimada, Toshio; Saikawa, Tetsunori

doi:10.1016/j.lfs.2004.12.030

Cited by 12 publications

(11 citation statements)

References 23 publications

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“…Just before birth, most of the RVOT myocardium acquires a working phenotype except for the subregion that is located just below the pulmonary valves ( Figure 1 ) [ 37 , 39 ]. In the adult mouse heart, this myocardial subregion is marked by the absence of Cx43 expression, while the rest of the adult RVOT expresses Cx43 albeit at a lower level compared to the RV [ 53 , 54 , 55 ]. Despite its confined expression in the OFT and not the ventricular wall, and function as a transcriptional suppressor of the genes encoding the fast-conducting connexins Cx40 and Cx43 [ 50 ], Tbx2 was previously found not to regulate the expression of Cx43 in the RVOT [ 39 ].…”

Section: The Right Ventricular Outflow Tractmentioning

confidence: 99%

Mechanisms of Arrhythmias in the Brugada Syndrome

Blok

Boukens

2020

IJMS

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Arrhythmias in Brugada syndrome patients originate in the right ventricular outflow tract (RVOT). Over the past few decades, the characterization of the unique anatomy and electrophysiology of the RVOT has revealed the arrhythmogenic nature of this region. However, the mechanisms that drive arrhythmias in Brugada syndrome patients remain debated as well as the exact site of their occurrence in the RVOT. Identifying the site of origin and mechanism of Brugada syndrome would greatly benefit the development of mechanism-driven treatment strategies.

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Section: The Right Ventricular Outflow Tractmentioning

confidence: 99%

Mechanisms of Arrhythmias in the Brugada Syndrome

Blok

Boukens

2020

IJMS

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“…90 In rabbit myocardium, Cx43 is less abundant in the RVOT than in the left ventricular free wall. 91 The expression of Cx40 is restricted to the subendocardial Purkinje fibers, the bundle branches, and the atrioventricular bundle. 88 Expression of Cx30.2 is restricted to the nodes of the conduction system.…”

Section: Expression Pattern Of Connexinsmentioning

confidence: 99%

“…Cx43 expression is absent from the fetal OFT ( Figure 4A) but is expressed in the RVOT of adults, albeit to a lesser extent than in the free wall of the right ventricle. 91 This suggests that insufficient upregulation of Cx43 and possibly other genes in the RVOT before birth can result in heterogeneous expression in the right ventricular wall. Tbx2 is gradually downregulated toward the end of gestation, which may contribute to the gradual upregulation of Cx43 in the RVOT myocardium.…”

Section: The Oft: a Slowly Conducting Primitive Structurementioning

confidence: 99%

Developmental Basis for Electrophysiological Heterogeneity in the Ventricular and Outflow Tract Myocardium As a Substrate for Life-Threatening Ventricular Arrhythmias

Boukens

Christoffels

Coronel

et al. 2009

Circulation Research

132

102

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Abstract-Reentry is the main mechanism of life-threatening ventricular arrhythmias, including ventricular fibrillation and tachycardia. Its occurrence depends on the simultaneous presence of an arrhythmogenic substrate (a preexisting condition) and a "trigger," and is favored by electrophysiological heterogeneities. In the adult heart, electrophysiological heterogeneities of the ventricle exist along the apicobasal, left-right, and transmural axes. Also, conduction is preferentially slowed in the right ventricular outflow tract, especially during pharmacological sodium channel blockade. We propose that the origin of electrophysiological heterogeneities of the adult heart lies in early heart development. The heart is formed from several progenitor regions: the first heart field predominantly forms the left ventricle, whereas the second heart field forms the right ventricle and outflow tract. Furthermore, the embryonic outflow tract consists of slowly conducting tissue until it is incorporated into the ventricles and develops rapidly conducting properties. The subepicardial myocytes and subendocardial myocytes run distinctive gene programs from their formation onwards. This review discusses the hypothesis that electrophysiological heterogeneities in the adult heart result from persisting patterns in gene expression and function along the craniocaudal and epicardial-endocardial axes of the developing heart. Understanding the developmental origins of electrophysiological heterogeneity contributing to ventricular arrhythmias may give rise to new therapies.

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“…Whether gene expression in the myocardium of the RVOT is different from that of the right-or left-ventricular myocardium is not known. However, decreased expression of Cx43 in the RVOT myocardium compared with the right-and left-ventricular myocardium has been reported [52].…”

Section: The Rvotmentioning

confidence: 99%

Electrophysiological Patterning of the Heart

Boukens¹,

Christoffels²

2012

Pediatr Cardiol

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In the adult heart, electrophysiological heterogeneity is present to guide activation and contraction. A change in electrophysiological heterogeneity, for example, during disease, can contribute to arrhythmogenesis. During development, spatial and temporal patterns of transcriptional activity regulate the localized expression of ion channels that cause electrophysiological heterogeneity throughout the heart. If we gain insight into the regulating processes that generate the electrophysiological characteristics and factors involved during development, we can use this knowledge in the search for new therapeutic targets. In this review, we discuss which factors guide the electrical patterning of atrioventricular conduction system and ventricles and how this patterning relates to arrhythmogenic disease in patients.

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Heterogeneous expression of connexin 43 in the myocardium of rabbit right ventricular outflow tract

Cited by 12 publications

References 23 publications

Mechanisms of Arrhythmias in the Brugada Syndrome

Mechanisms of Arrhythmias in the Brugada Syndrome

Developmental Basis for Electrophysiological Heterogeneity in the Ventricular and Outflow Tract Myocardium As a Substrate for Life-Threatening Ventricular Arrhythmias

Electrophysiological Patterning of the Heart

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