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Related Concept Videos

Feedback Regulation of Calcium Concentration01:27

Feedback Regulation of Calcium Concentration

Calcium is an essential signaling molecule required for various cellular functions. Calcium pumps and ion channels on cell and organellar membranes, such as those on the endoplasmic reticulum (ER), regulate calcium concentrations inside the cell. They remain closed, keeping the cytosolic calcium levels low at a resting state.
Various transmembrane receptors, such as G protein-coupled receptors (GPCRs), elicit a response to extracellular signals by increasing cytosolic calcium. Activated GPCRs...

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Lipopolysaccharides directly decrease Ca2+ oscillations and the hyperpolarization-activated nonselective cation

Robert Wondergem1, Bridget M Graves, Tammy R Ozment-Skelton

  • 1Dept. of Physiology, James H. Quillen College of Medicine, East Tennessee State Univ., P. O. Box 70576, Johnson City, TN 37614-1708, USA. wonderge@etsu.edu

American Journal of Physiology. Cell Physiology
|June 25, 2010
PubMed
Summary
This summary is machine-generated.

Lipopolysaccharide (LPS) disrupts cardiac cell function by altering calcium levels and inhibiting the pacemaker current I(f). These effects occur through Toll-like receptor 4 (TLR-4) and other mechanisms, contributing to heart failure.

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Area of Science:

  • Cardiology
  • Molecular Biology
  • Cell Physiology

Background:

  • Lipopolysaccharide (LPS) is linked to sepsis-induced heart failure and chronic cardiac conditions.
  • Cardiac myocyte function is crucial for overall cardiovascular health.

Purpose of the Study:

  • To investigate the direct effects of LPS on cardiac myocyte function, specifically intracellular calcium ([Ca2+]i) regulation and ion channel activity.
  • To elucidate the role of Toll-like receptors (TLRs), particularly TLR-4, in mediating LPS-induced cardiac effects.

Main Methods:

  • Utilized immortalized HL-1 cardiomyocytes to study LPS effects on [Ca2+]i oscillations and basal levels.
  • Employed whole-cell voltage-clamp techniques to assess LPS impact on the hyperpolarization-activated, nonselective cationic pacemaker current (I(f)).
  • Differentiated LPS effects using ultrapure LPS (TLR-4 ligand) and Pam3CSK4 (TLR-2 ligand).

Main Results:

  • LPS abolished [Ca2+]i oscillations and decreased basal [Ca2+]i in HL-1 cells.
  • Ultrapure LPS reduced the rate of [Ca2+]i oscillations but did not affect basal levels.
  • LPS significantly inhibited I(f) activation and deactivation, particularly at negative potentials, via TLR-4 and non-TLR-4 pathways.

Conclusions:

  • LPS directly impairs cardiac myocyte calcium handling and I(f) function.
  • Both TLR-4-dependent and independent mechanisms contribute to LPS-induced cardiac dysfunction.
  • Findings provide insights into LPS's role in sepsis-mediated cardiac pathology.