What question did this study set out to answer?

To determine the inotropic and hypertrophic effects of chronic endothelin-1 exposure on cardiac trabeculae and delineate the downstream signaling pathways involved.

August 17, 2012PLoS ONEOpen Access

Role of Endothelin in the Induction of Cardiac Hypertrophy In Vitro

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Population

rabbit cardiac trabeculae in a novel in vitro multicellular culture system

Comparison

1 nM Endothelin for 24 hours, with or without… vs non-ET-1 treated muscles

Design

Preclinical

Follow-up

24 hours

Authors

TBTepmanas Bupha‐IntrMahidol University KHKaylan M. HaizlipUniversity of Colorado Boulder PJPaul M.L. JanssenHeart Failure & Transplant

Discussion

Member takes

Implication

Animal ET-1 effects on force and size are hypothesis-generating; leaves open relevance to human myocardial remodeling.

Key Points

To determine the inotropic and hypertrophic effects of chronic endothelin-1 exposure on cardiac trabeculae and delineate the downstream signaling pathways involved.
Cultured rabbit cardiac trabeculae in a multicellular in vitro system exposed to 1 nM endothelin-1 (ET-1) for 24 hours.
Assessed contractile force, contraction kinetics (time to peak contraction and time to 90% relaxation), and muscle diameter.
Evaluated mechanistic pathways using pharmacological antagonists against NCX, CaMKII, MAPKK, IP3 receptors, and calcineurin-NFAT.
ET-1 treatment produced a ~2.5-fold increase in developed force at 24 hours without altering contraction or relaxation kinetics, alongside a 12.5 ± 3.2% increase in muscle diameter.
Inhibition of NCX, CaMKII, and MAPKK attenuated both force development and muscle hypertrophy, whereas IP3 receptor antagonism attenuated force development but failed to prevent hypertrophy.
Calcineurin-NFAT pathway inhibition prevented ET-1-mediated muscle hypertrophy without altering developed contractile force.

Structured PICO

Population

rabbit cardiac trabeculae in a novel in vitro multicellular culture system

Intervention

1 nM Endothelin (ET-1) for 24 hours, with or without specific signaling antagonists (NCX, CaMKII, MAPKK, IP3, calcineurin-NFAT inhibitors)

Comparator

non-ET-1 treated muscles

Outcome

changes in contractile force and kineticssurrogate

In vitro, ET-1 provokes both inotropic and hypertrophic activations on myocardium sharing the same signaling pathway through MAPK and CaMKII associated with NCX activity.

Cite This Study

Bupha‐Intr et al. (2012) studied this question.

synapsesocial.com/papers/6a853274f2bb7ee68cf23eb9 https://doi.org/10.1371/journal.pone.0043179

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Role of Endothelin in the Induction of Cardiac Hypertrophy In Vitro

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Role of Endothelin in the Induction of Cardiac Hypertrophy In Vitro

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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