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December 3, 2004Circulation Research

Connexin 43 Downregulation and Dephosphorylation in Nonischemic Heart Failure Is Associated With Enhanced Colocalized Protein Phosphatase Type 2A

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Key result

In nonischemic heart failure, there is a decrease in Cx43 expression and an increase in nonphosphorylated Cx43 (P<0.05), associated with increased colocalized PP2A.

Why the study?

Does altered Connexin43 expression and phosphorylation, mediated by protein phosphatases, contribute to cellular uncoupling in nonischemic heart failure?

Population

Arrhythmogenic rabbit model of nonischemic heart failure and left ventricular tissue from patients with…

Comparison

Okadaic acid for in vitro coupling assessment vs Healthy controls (rabbit and human)

Design

Preclinical

Authors

XAXun AiRush University Medical CenterSPSteven M. PogwizdUniversity of Alabama at Birmingham

Discussion

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Implication

Hypothesis-generating for PP2A-mediated Cx43 uncoupling in nonischemic HF; human studies needed before targeting arrhythmias.

Structured PICO

Does altered Connexin43 expression and phosphorylation, mediated by protein phosphatases, contribute to cellular uncoupling in nonischemic heart failure?

P
Population
Rabbit model of nonischemic HF and patients with HF attributable to idiopathic dilated cardiomyopathy.
E
Exposure
Okadaic acid (10 nmol/L) for in vitro coupling assessment
C
Comparator
Healthy controls (rabbit and human)
O
Outcome
Connexin43 (Cx43) expression, phosphorylation state, colocalization with protein phosphatases (PP1 and PP2A), and intercellular couplingsurrogate

Main Result

p-value: p=<0.05

In nonischemic heart failure, decreased Connexin43 expression and increased dephosphorylation mediated by PP2A contribute to cellular uncoupling, identifying a potential therapeutic target for arrhythmias.

Cite This Study

Ai et al. (2004) studied Nonischemic heart failure. Nonischemic heart failure vs. Controls was evaluated on Cx43 expression and phosphorylation state (p=<0.05). In nonischemic heart failure, there is a decrease in Cx43 expression and an increase in nonphosphorylated Cx43 (P<0.05), associated with increased colocalized PP2A.

synapsesocial.com/papers/6a6380de3eb69703d1b71d9dhttps://doi.org/10.1161/01.res.0000152325.07495.5a

Topics

Heart failureHFrEF treatmentVentricular arrhythmias
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Renin-Angiotensin System and Cell Communication in the Failing Heart1996 · 96 citations
  2. 2Triggered activity and automaticity in ventricular trabeculae of failing human and rabbit hearts1994 · 218 citations
  3. 3Dephosphorylation and Intracellular Redistribution of Ventricular Connexin43 During Electrical Uncoupling Induced by Ischemia2000 · 510 citations
  4. 4Upregulation of Na+/Ca2+Exchanger Expression and Function in an Arrhythmogenic Rabbit Model of Heart Failure1999 · 399 citations
  5. 5Increased Association of ZO-1 With Connexin43 During Remodeling of Cardiac Gap Junctions2002 · 190 citations