ArticleActa pharmacologica Sinica2009
Glycine inhibits the LPS-induced increase in cytosolic Ca2+ concentration and TNFalpha production in cardiomyocytes by activating a glycine receptor.
Article in Acta pharmacologica Sinica, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- Glycine as a Metabolic Regulator of Reproductive Function in Livestock: From Gametes to Early Embryos.Animals : an open access journal from MDPI · 2026Review
- Aqueous Fraction fromNutrients · 2023Article
- Nutraceutical, Dietary, and Lifestyle Options for Prevention and Treatment of Ventricular Hypertrophy and Heart Failure.International journal of molecular sciences · 2021Review
- Cucumis sativus Aqueous Fraction Inhibits Angiotensin II-Induced Inflammation and Oxidative Stress In Vitro.Nutrients · 2018Article
- Dietary Glycine Is Rate-Limiting for Glutathione Synthesis and May Have Broad Potential for Health Protection.Ochsner journal · 2018Review
- The effects of verapamil and its combinations with glutamate and glycine on cardiodynamics, coronary flow and oxidative stress in isolated rat heart.Journal of physiology and biochemistry · 2017Article
- The role of glycine in regulated cell death.Cellular and molecular life sciences : CMLS · 2016Review
- Glycine attenuates myocardial ischemia-reperfusion injury by inhibiting myocardial apoptosis in rats.Journal of biomedical research · 2012Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimPrevious studies have demonstrated that glycine (GLY) markedly reduces lipopolysaccharide (LPS)-induced myocardial injury.However, the mechanism of this effect is still unclear. The present study investigated the effect of GLY on cytosolic calcium concentration([Ca2+]c) and tumor necrosis factor-alpha (TNFalpha) production in cardiomyocytes exposed to LPS, as well as whether the glycine-gated chloride channel is involved in this process.
methodsNeonatal rat cardiomyocytes were isolated, and the [Ca2+]c and TNFalpha levels were determined by using Fura-2 and a Quantikine enzyme-linked immunosorbent assay, respectively. The distribution of the GLY receptor and GLY-induced currents in cardiomyocytes were also investigated using immunocytochemistry and the whole-cell patch-clamp technique, respectively.
resultsLPS at concentrations ranging from 10 ng/mL to 100 microg/mL significantly stimulated TNFalpha production. GLY did not inhibit TNFalpha production induced by LPS at concentrations below 10 ng/mL but did significantly decrease TNFalpha release stimulated by 100 microg/mL LPS and prevented an LPS-induced increase in [Ca2+]c, which was reversed by strychnine, a glycine receptor antagonist. GLY did not block the isoproterenol-induced increase in [Ca2+]c, but did prevent the potassium chloride-induced increase in [Ca2+]c in cardiomyocytes.Strychnine reversed the inhibition of the KCl-stimulated elevation in [Ca2+]c by GLY. In chloride-free buffer, GLY had no effect on the dipotassium hydrogen phosphate-induced increase in [Ca2+]c. Furthermore, GLY receptor alpha1 and beta subunit-immunoreactive spots were observed in cardiomyocytes, and GLY-evoked currents were blocked by strychnine.
conclusionCardiomyocytes possess the glycine-gated chloride channel, through which GLY prevents the increase in [Ca2+]c and inhibits the TNFalpha production induced by LPS at high doses in neonatal rat cardiomyocytes.
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