scholarly journals Mechanisms of Postinfarction Electrophysiological Abnormality: Sympathetic Neural Remodeling, Electrical Remodeling and Gap Junction Remodeling

10.5772/22801 ◽  
2012 ◽  
Author(s):  
Guoqiang Zhong ◽  
Jinyi Li ◽  
Honghong Ke ◽  
Yan He ◽  
Weiyan Xu ◽  
...  
Keyword(s):  
Gap Junction ◽  
Electrical Remodeling ◽  
Neural Remodeling

scholarly journals Electrical Remodeling of Connexin43 Gap‐Junction Protein Expression

2007 ◽  
Vol 21 (6) ◽  
Author(s):  
Satoshi Matsushita ◽  
Van Nam Tran ◽  
Siamak Rassadi ◽  
Andrew S Wechsler ◽  
J.Yasha Kresh
Keyword(s):  
Protein Expression ◽  
Gap Junction ◽  
Electrical Remodeling ◽  
Junction Protein ◽  
Gap Junction Protein

Abstract 16737: Inhibition of Tgf-β1 Signaling Protect Against Cell-Cell Decoupling and Asynchronous Automaticity of Tbx18-ipms

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Jinqi Fan ◽  
Nam Kyun Kim ◽  
Natasha Fernandez ◽  
Minji Shin ◽  
Hee Cho
Keyword(s):  
Gap Junction ◽  
Protein Level ◽  
Electrical Coupling ◽  
Neonatal Rat ◽  
Electrical Remodeling ◽  
Tgfβ Signaling ◽  
Cx43 Expression ◽  
Intramyocardial Injection ◽  
Tgfβ Receptors ◽  
Cell Cell

Background: We have previously demonstrated that TBX18 suffices to reprogram postnatal ventricular cardiomyocytes to induced pacemaker cells (TBX18-iPMs). However, the nascent automaticity appeared to wane over time, characterized by loss of syncytial pacing but preservation of single cell automaticity. Hypothesis: Based on increase in Tgfβ ligands in TBX18-iPMs and the known role of Tgfβ signaling in electrical remodeling, we hypothesized that loss of syncytial automaticity is due to electrical decoupling of the iPMs mediated by Tgfβ signaling. Methods: Adenoviral vectors expressing either human TBX18 or GFP were used for gene transfer into neonatal rat ventricular myocytes (NRVMs) or adult rat ventricular myocardium in vivo. Results: NRVM monolayers transduced with GFP were mostly quiescent, interspersed by paroxysmal contractions. In contrast, TBX18 transduced NRVM monolayers showed spontaneous and rhythmic contractions, but the syncytial pacing wavered over the next 5-7 days although numerous iPMs continued to beat asynchronously. Treatment of TBX18-iPMs with an inhibitor of Tgfβ receptors, A83-01, preserved syncytial pacing, suggesting that electrical remodeling cues from Tgfβ signaling led to loss of iPM-iPM electrical coupling. We examined the molecules that are integral to the function of gap junction in the myocardium, namely Cx43, N-cadherin and β-catenin. Cx43 and N-cadherin were downregulated in TBX18-iPMs compared to control by 77±16% and 43±11% (p<0.01, n=6), respectively. Total β-catenin protein level was unaltered, but its distribution decreased at the sarcolemmal and increased in the nuclei of TBX18-iPMs compared to control. Inhibition of Tgfβ with A83-01 restored Cx43 protein level in TBX18-iPMs (2.2-folds higher) compared to untreated TBX18-iPMs. Similarly, adult rats that received intramyocardial injection of TBX18 showed increased Cx43 expression at the boundary between the iPMs and the host myocardium when the animals were treated with systemic delivery of A83-01 for one week compared to TBX18 animals treated with DMSO. Conclusions: TBX18 activates Tgfβ signaling which suppresses cell-cell electrical coupling. Inhibition of Tgfβ signaling in TBX18-iPMs preserves gap junction components and syncytial pacing.

The Nature of the Intramembrane Particle

1980 ◽  
Vol 38 ◽  
pp. 688-691
Author(s):  
A.J. Verkleij
Keyword(s):  
Escherichia Coli ◽  
Tight Junction ◽  
Gap Junction ◽  
The Other ◽  
Fracture Face ◽  
Band 3 Protein ◽  
Satisfactory Explanation ◽  
Freeze Fracturing ◽  
Intramembrane Particle ◽  
Luminal Membrane

Freeze-fracturing splits membranes into two helves, thus allowing an examination of the membrane interior. The 5-10 rm particles visible on both monolayers are widely assumed to be proteinaceous in nature. Most membranes do not reveal impressions complementary to particles on the opposite fracture face, if the membranes are fractured under conditions without etching. Even if it is considered that shadowing, contamination or fracturing itself might obscure complementary pits', there is no satisfactory explanation why under similar physical circimstances matching halves of other membranes can be visualized. A prominent example of uncomplementarity is found in the erythrocyte manbrane. It is wall established that band 3 protein and possibly glycophorin represents these nonccmplanentary particles. On the other hand a number of membrane types show pits opposite the particles. Scme well known examples are the ";gap junction',"; tight junction, the luminal membrane of the bladder epithelial cells and the outer membrane of Escherichia coli.

304 Fibrosis is an important mechanism of gap junction disorganisation in rat atrial myocardium during heart failure

2003 ◽  
Vol 2 (1) ◽  
pp. 54
Author(s):  
C RUCKERMARTIN ◽  
P MILLIEZ ◽  
N DEANGELIS ◽  
C GOYENVALLE ◽  
J RENAUD ◽  
...  
Keyword(s):  
Heart Failure ◽  
Gap Junction ◽  
Atrial Myocardium

Desipramine prevents from cardiac gap junction uncoupling

2013 ◽  
Vol 61 (S 01) ◽  
Author(s):  
S Dhein ◽  
J Jozwiak ◽  
A Dietze ◽  
R Grover ◽  
A Savtschenko ◽  
...  
Keyword(s):  
Gap Junction

The role of angiotensin in electrophysiological gap junction remodeling in human atrial fibrillation

2004 ◽  
Vol 52 (S 1) ◽  
Author(s):  
S Dhein ◽  
A Boldt ◽  
J Garbade ◽  
L Polontchouk ◽  
U Wetzel ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Gap Junction ◽  
Human Atrial Fibrillation
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