What is the clinical evidence from this study?

Study design: Other. Intervention: Taxol (TXL) vs. Untreated cells. Primary outcome: Peak sodium current (I(Na)) amplitude and Na(v)1.5 membrane expression.

What question did this study set out to answer?

The aim was to determine how tubulin polymerization affects cardiac sodium channel (Na(v)1.5) function and expression, particularly through beta1-subunit mediation.

October 26, 2009Cardiovascular ResearchOpen Access

Tubulin polymerization modifies cardiac sodium channel expression and gating

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Key result

Taxol treatment reduced peak sodium current amplitude nearly two-fold and decreased sarcolemmal Na(v)1.5 expression in both HEK293 cells and neonatal rat cardiomyocytes.

Why the study?

Does taxol alter cardiac sodium channel expression and gating in HEK293 cells and neonatal rat cardiomyocytes?

Population

Human embryonic kidney cells transfected with SCN5A cDNA alone or together with SCN1B cDNA, and neonatal rat…

Comparison

Incubation with 100 microM taxol (TXL) vs Absence of taxol (untreated cells)

Design

Preclinical

Authors

SCSimona CasiniAmsterdam Neuroscience HTHanno L. TanElectrophysiology IDIlker DemirayakAmsterdam UMC Location University of Amsterdam

Discussion

Member takes

Implication

No immediate clinical implications from HEK cell data; leaves open tubulin-NaV1.5 links to arrhythmias for in vivo study.

Key Points

The aim was to determine how tubulin polymerization affects cardiac sodium channel (Na(v)1.5) function and expression, particularly through beta1-subunit mediation.
HEK293 cells were transfected with SCN5A or SCN1B cDNA and treated with 100μM taxol (TXL).
Sodium currents were assessed using patch-clamp techniques, and Na(v)1.5 expression was examined through immunocytochemistry and confocal microscopy.
Both treated and untreated conditions were compared in NEK cells and neonatal rat cardiomyocytes.
TXL reduced peak sodium current amplitude by nearly two-fold in both Na(v)1.5 and Na(v)1.5 + beta1 cells.
TXL accelerated I(Na) decay in Na(v)1.5 + beta1, while having no effect on Na(v)1.5 decay rates.
Slow inactivation characteristics of Na(v)1.5 changed significantly under TXL treatment, while those of Na(v)1.5 + beta1 remained stable.

Structured PICO

Does taxol alter cardiac sodium channel expression and gating in HEK293 cells and neonatal rat cardiomyocytes?

Population

Human embryonic kidney (HEK293) cells transfected with SCN5A cDNA alone (Nav1.5) or together with SCN1B cDNA (Nav1.5 + beta1), and neonatal rat cardiomyocytes (NRCs)

Intervention

Incubation with 100 microM taxol (TXL)

Comparator

Absence of taxol (untreated cells)

Outcome

Sodium current (INa) characteristics (amplitude, decay, slow inactivation) and Nav1.5 membrane expressionsurrogate

Taxol-induced tubulin polymerization reduces sarcolemmal Nav1.5 expression and sodium current amplitude, providing a potential mechanism for conduction-slowing-dependent cardiac arrhythmias associated with taxol treatment.

Cite This Study

Casini et al. (2009) studied this question. Taxol (TXL) vs. Untreated cells was evaluated on Peak sodium current (I(Na)) amplitude and Na(v)1.5 membrane expression. Taxol treatment reduced peak sodium current amplitude nearly two-fold and decreased sarcolemmal Na(v)1.5 expression in both HEK293 cells and neonatal rat cardiomyocytes.

synapsesocial.com/papers/6a45aba01413b4119d3b893c https://doi.org/10.1093/cvr/cvp352

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Tubulin polymerization modifies cardiac sodium channel expression and gating

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Tubulin polymerization modifies cardiac sodium channel expression and gating

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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