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Toll-like receptor 4-induced ryanodine receptor 2 oxidation and sarcoplasmic reticulum Ca²⁺ leakage promote cardiac contractile dysfunction in sepsis.

ABSTRACT: Studies suggest the potential role of a sarcoplasmic reticulum (SR) Ca²⁺ leak in cardiac contractile dysfunction in sepsis. However, direct supporting evidence is lacking, and the mechanisms underlying this SR leak are poorly understood. Here, we investigated the changes in cardiac Ca²⁺ handling and contraction in LPS-treated rat cardiomyocytes and a mouse model of polymicrobial sepsis produced by cecal ligation and puncture (CLP). LPS decreased the systolic Ca²⁺ transient and myocyte contraction as well as SR Ca²⁺ content. Meanwhile, LPS increased Ca²⁺ spark-mediated SR Ca²⁺ leak. Preventing the SR leak with ryanodine receptor (RyR) blocker tetracaine restored SR load and increased myocyte contraction. Similar alterations i

SUBMITTER: Yang J

PROVIDER: S-EPMC5777254 | biostudies-literature | 2018 Jan

REPOSITORIES: biostudies-literature

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Toll-like receptor 4-induced ryanodine receptor 2 oxidation and sarcoplasmic reticulum Ca²⁺ leakage promote cardiac contractile dysfunction in sepsis.

OmicsDI is part of the ELIXIR infrastructure

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Dataset Information

Toll-like receptor 4-induced ryanodine receptor 2 oxidation and sarcoplasmic reticulum Ca2+ leakage promote cardiac contractile dysfunction in sepsis.

OmicsDI is part of the ELIXIR infrastructure

Tweets

Toll-like receptor 4-induced ryanodine receptor 2 oxidation and sarcoplasmic reticulum Ca²⁺ leakage promote cardiac contractile dysfunction in sepsis.