Dedifferentiation of atrial myocytes during atrial fibrillation: role of fibroblast proliferation in vitro

Rücker‐Martin, Catherine; Pecker, Françoise; Godreau, David; Hatem, Stéphane N.

doi:10.1016/s0008-6363(02)00338-3

Cited by 90 publications

(65 citation statements)

References 34 publications

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“…Cells were isolated from the right atrial appendage, collected from 3-month-old patients during surgery required to relieve congenital diseases, and cultured as previously described (60). Approval of human tissue collection, care, and use was given by the ethics committee of Hospital Kremlin Bicêtre (AP-HP), Kremlin Bicêtre, France (Committee, protocol 04-26).…”

Section: Methodsmentioning

confidence: 99%

A purified population of multipotent cardiovascular progenitors derived from primate pluripotent stem cells engrafts in postmyocardial infarcted nonhuman primates

et al. 2010

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Cell therapy holds promise for tissue regeneration, including in individuals with advanced heart failure. However, treatment of heart disease with bone marrow cells and skeletal muscle progenitors has had only marginal positive benefits in clinical trials, perhaps because adult stem cells have limited plasticity. The identification, among human pluripotent stem cells, of early cardiovascular cell progenitors required for the development of the first cardiac lineage would shed light on human cardiogenesis and might pave the way for cell therapy for cardiac degenerative diseases. Here, we report the isolation of an early population of cardiovascular progenitors, characterized by expression of OCT4, stage-specific embryonic antigen 1 (SSEA-1), and mesoderm posterior 1 (MESP1), derived from human pluripotent stem cells treated with the cardiogenic morphogen BMP2. This progenitor population was multipotential and able to generate cardiomyocytes as well as smooth muscle and endothelial cells. When transplanted into the infarcted myocardium of immunosuppressed nonhuman primates, an SSEA-1 + progenitor population derived from Rhesus embryonic stem cells differentiated into ventricular myocytes and reconstituted 20% of the scar tissue. Notably, primates transplanted with an unpurified population of cardiac-committed cells, which included SSEA-1 -cells, developed teratomas in the scar tissue, whereas those transplanted with purified SSEA-1 + cells did not. We therefore believe that the SSEA-1 + progenitors that we have described here have the potential to be used in cardiac regenerative medicine.

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Section: Methodsmentioning

confidence: 99%

A purified population of multipotent cardiovascular progenitors derived from primate pluripotent stem cells engrafts in postmyocardial infarcted nonhuman primates

et al. 2010

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“…One study found that SAP97 is localized also to the t-tubule system in isolated ventricular myocytes (232). Further evidence that cardiac SAP97 is targeted to specialized membrane domains was obtained through the use of a model of cultured adult cardiac myocytes, in which the in vitro formation of specialized myocyte-myocyte contacts such as adherens and gap junctions can be followed (142,210,363). In this model, both endogenous and exogenous SAP97 localizes exclusively at newly formed myocyte-myocyte contacts containing cadherins and connexin channels (1).…”

Section: Figurementioning

confidence: 99%

Dynamic of Ion Channel Expression at the Plasma Membrane of Cardiomyocytes

Balse

Steele

Abriel

et al. 2012

Physiological Reviews

109

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Cardiac myocytes are characterized by distinct structural and functional entities involved in the generation and transmission of the action potential and the excitation-contraction coupling process. Key to their function is the specific organization of ion channels and transporters to and within distinct membrane domains, which supports the anisotropic propagation of the depolarization wave. This review addresses the current knowledge on the molecular actors regulating the distinct trafficking and targeting mechanisms of ion channels in the highly polarized cardiac myocyte. In addition to ubiquitous mechanisms shared by other excitable cells, cardiac myocytes show unique specialization, illustrated by the molecular organization of myocyte-myocyte contacts, e.g., the intercalated disc and the gap junction. Many factors contribute to the specialization of the cardiac sarcolemma and the functional expression of cardiac ion channels, including various anchoring proteins, motors, small GTPases, membrane lipids, and cholesterol. The discovery of genetic defects in some of these actors, leading to complex cardiac disorders, emphasizes the importance of trafficking and targeting of ion channels to cardiac function. A major challenge in the field is to understand how these and other actors work together in intact myocytes to fine-tune ion channel expression and control cardiac excitability.

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“…29 Heterocellular electrotonic coupling of myofibroblasts and myocytes has been shown in native atrial tissue 30 and is thought to increase heterogeneity in excitability, refractoriness, and electrical load, 31 potentially inducing heterogeneous slowing of conduction. 32 These mechanisms may also contribute to microscopic zigzag conduction, allowing re-entry to occur in regions as small as 1 to 2 mm 2 , 13,16 largely facilitating reentrant arrhythmias.…”

Section: Anisotropy Of CVmentioning

confidence: 99%

Rearrangement of Atrial Bundle Architecture and Consequent Changes in Anisotropy of Conduction Constitute the 3-Dimensional Substrate for Atrial Fibrillation

Maesen

Zeemering

Afonso

et al. 2013

Circ: Arrhythmia and Electrophysiology

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Background— Anisotropy of conduction facilitates re-entry and is, therefore, a key determinant of the stability of atrial fibrillation (AF). Little is known about the effect of AF on atrial bundle architecture and consequent changes in anisotropy of conduction and maintenance of AF. Methods and Results— Direct contact mapping was performed in left atria of goats with acute AF (n=6) or persistent AF (n=5). The degree and direction of anisotropic conduction were analyzed. Mapped tissue regions were imaged by high-resolution MRI for identification of endocardial and epicardial bundle directions. Correlation between endocardial and epicardial bundle directions and between bundle directions and anisotropic conduction was quantified. In persistent AF, epicardial bundles were oriented more perpendicularly to endocardial bundles than in acute AF (% angles <20° between epicardial and endocardial bundle directions were 7.63% and 21.25%, respectively; P <0.01). In acute AF, the direction of epicardially mapped anisotropic conduction correlated with endocardial but not with epicardial bundles. In persistent AF, the direction of anisotropic conduction correlated better with epicardial than with endocardial bundles (% angles <20° between direction of anisotropic conduction and bundle direction were 28.77% and 18.45%, respectively; P <0.01). Conclusions— During AF, atrial bundle rearrangement manifests itself in more perpendicular orientation of epicardial to endocardial bundles. Propagation of fibrillation waves is dominated by endocardial bundles in acute AF and by epicardial bundles in persistent AF. Together with the loss of endo-epicardial electrical connections, rearrangement of atrial bundles underlies endo-epicardial dissociation of electrical activity and the development of a 3-dimensional AF substrate.

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Dedifferentiation of atrial myocytes during atrial fibrillation: role of fibroblast proliferation in vitro

Abstract: In diseased atria, myolytic myocytes are in a dedifferentiated state resembling that of immature muscle cells. In vitro, fibroblast proliferation prevents the reversibility of this cellular alteration.

Cited by 90 publications

References 34 publications

A purified population of multipotent cardiovascular progenitors derived from primate pluripotent stem cells engrafts in postmyocardial infarcted nonhuman primates

A purified population of multipotent cardiovascular progenitors derived from primate pluripotent stem cells engrafts in postmyocardial infarcted nonhuman primates

Dynamic of Ion Channel Expression at the Plasma Membrane of Cardiomyocytes

Rearrangement of Atrial Bundle Architecture and Consequent Changes in Anisotropy of Conduction Constitute the 3-Dimensional Substrate for Atrial Fibrillation

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