Gap junction reduction in cardiomyocytes following transforming growth factor-β treatment and Trypanosoma cruzi infection

Waghabi, Mariana Caldas; Coutinho‐Silva, Robson; Feige, Jean‐Jacques; Higuchi, Maria de Lourdes; Becker, David L.; Burnstock, Geoffrey; Araújo-Jorge, Tânia C.

doi:10.1590/s0074-02762009000800004

Cited by 33 publications

(39 citation statements)

References 46 publications

(46 reference statements)

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“…As such, the classical swine fever virus [177], the Borna disease virus [178] and the human cytomegalovirus [179] have been found to downregulate connexin expression. Similar findings were reported for the protozoan parasites Trypanosoma cruzi [180,181] and Toxoplasma gondii [181]. As specifically addressed in the current paper, bacterial pathogens and their toxins also typically modify connexin production in host cells.…”

Section: Discussionsupporting

confidence: 82%

Modulation of connexin signaling by bacterial pathogens and their toxins

Ceelen

Haesebrouck

Vanhaecke

et al. 2011

Cell. Mol. Life Sci.

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Inherent to their pivotal tasks in the maintenance of cellular homeostasis, gap junctions, connexin hemichannels, and pannexin hemichannels are frequently involved in the dysregulation of this critical balance. The present paper specifically focuses on their roles in bacterial infection and disease. In particular, the reported biological outcome of clinically important bacteria including Escherichia coli, Shigella flexneri, Yersinia enterocolitica, Helicobacter pylori, Bordetella pertussis, Aggregatibacter actinomycetemcomitans, Pseudomonas aeruginosa, Citrobacter rodentium, Clostridium species, Streptococcus pneumoniae, and Staphylococcus aureus and their toxic products on connexin- and pannexin-related signaling in host cells is reviewed. Particular attention is paid to the underlying molecular mechanisms of these effects as well as to the actual biological relevance of these findings.

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Section: Discussionsupporting

confidence: 82%

Modulation of connexin signaling by bacterial pathogens and their toxins

Ceelen

Haesebrouck

Vanhaecke

et al. 2011

Cell. Mol. Life Sci.

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“…First, although in some experimental groups heart rates during 1 to 2 h following peptide treatment were statistically different from controls (Supplementary material, Table 1), these variations were not abnormal and remained within the normal range of the adult rat heart rate. On the other hand, while downregulation of Cx43 channels in general is known to be arrhythmogenic [30][31][32], we noticed only sporadic ventricular fibrillations occurring during the ischemic period while the animals were still under surgery. A total of 5 rats died during ischemia following a ventricular fibrillation (Supplementary material, Table 2).…”

Section: Safety Remarksmentioning

confidence: 87%

Single intravenous low-dose injections of connexin 43 mimetic peptides protect ischemic heart in vivo against myocardial infarction

Hawat

Hélie

Baroudi

2012

Journal of Molecular and Cellular Cardiology

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“…ATP prevents the run-down of gap junctional communication between ventricular myocytes in newborn rats by promoting protein phosphorylation [704]. In a later paper, P2X1R were shown to be closely associated with connexin 43 in gap junctions in the human ventricular myocardium [286] and the possibility that decreased expression of P2X1R is related to arrhythmias in the heart in Chagas disease and diabetes was considered [705]. In the perfused mouse heart, the addition of ATP to the perfusate induced ventricular tachycardia; this effect was mediated by P2R and increased diastolic level of [Ca 2+ ] i [706].…”

Section: Ventricular Arrhythmiasmentioning

confidence: 99%

Cardiac purinergic signalling in health and disease

Burnstock

Pelleg

2014

Purinergic Signalling

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113

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This review is a historical account about purinergic signalling in the heart, for readers to see how ideas and understanding have changed as new experimental results were published. Initially, the focus is on the nervous control of the heart by ATP as a cotransmitter in sympathetic, parasympathetic, and sensory nerves, as well as in intracardiac neurons. Control of the heart by centers in the brain and vagal cardiovascular reflexes involving purines are also discussed. The actions of adenine nucleotides and nucleosides on cardiomyocytes, atrioventricular and sinoatrial nodes, cardiac fibroblasts, and coronary blood vessels are described. Cardiac release and degradation of ATP are also described. Finally, the involvement of purinergic signalling and its therapeutic potential in cardiac pathophysiology is reviewed, including acute and chronic heart failure, ischemia, infarction, arrhythmias, cardiomyopathy, syncope, hypertrophy, coronary artery disease, angina, diabetic cardiomyopathy, as well as heart transplantation and coronary bypass grafts.

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Gap junction reduction in cardiomyocytes following transforming growth factor-β treatment and Trypanosoma cruzi infection

Abstract: Gap junction

Cited by 33 publications

References 46 publications

Modulation of connexin signaling by bacterial pathogens and their toxins

Modulation of connexin signaling by bacterial pathogens and their toxins

Single intravenous low-dose injections of connexin 43 mimetic peptides protect ischemic heart in vivo against myocardial infarction

Cardiac purinergic signalling in health and disease

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