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Glycine receptors contribute to cytoprotection of glycine in myocardial cells

摘要:

Background The classic glycine receptor (GlyR) in the central nervous system is a ligand-gated membrane-spanning ion channel. Recent studies have provided evidence for the existence of GlyR in endothelial cells, renal proximal tubular cells and most leukocytes. In contrast, no evidence for GlyR in myocardial cells has been found so far. Our recent researches have showed that glycine could protect myocardial cells from the damage induced by lipopolysaccharide (LPS). Further studies suggest that myocardial cells could contain GlyR or binding site of glycine.Methods In isolated rat heart damaged by LPS, the myocardial monophasic action potential (MAP), the heart rate (HR),the myocardial tension and the activities of lactate dehydrogenase (LDH) from the coronary effluent were determined.The concentration of intracellular free calcium ([Ca2+]i) was measured in cardiomyocytes injured by LPS and by hypoxia/reoxygenation (H/R), which excludes the possibility that reduced calcium influx because of LPS neutralized by glycine. Immunohistochemistry was used to detect the GlyR in myocardial tissue. GlyR and its subunit in the purified cultured cardiomyocytes were identified by Western blotting.Results Although significant improvement in the MAP/MAPD20, HR, and reduction in LDH release were observed in glycine + LPS hearts, myocardial tension did not recover. Further studies demonstrated that glycine could prevent rat mycordial cells from LPS and hypoxia/reoxygenation injury (no endotoxin) by attenuating calcium influx.Immunohistochemistry exhibited a positive green-fluorescence signaling along the cardiac muscle fibers. Western blotting shows that the purified cultured cardiomyocytes express GlyR β subunit, but GlyR α1 subunit could not be detected.Conclusions The results suggest that glycine receptor is expressed in cardiomyocytes and participates in cytoprotection from LPS and hypoxia/reoxygenation injury. Glycine could directly activate GlyR on the cardiomyocytes and prevent calcium influx into the cardiomyocytes.

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作者单位: Department of Pathophysiology, Medical College of Jinan University, Guangzhou 510632, China [1] Department of Respiratory Diseases, Children's Hospital of Shanxi Province, Taiyuan 030013, China [2] Department of Physiology, Wannan Medical College, Wuhu 241001, China [3]
期刊: 《中华医学杂志(英文版)》2007年120卷10期 915-921页 SCIMEDLINEISTICCSCDBP
分类号: R3
栏目名称: ORIGINAL ARTICLES
发布时间: 2008-03-03
基金项目:
国家自然科学基金 广东省自然科学基金 and the Foundation from the Bureau of Science and Technology in Guangzhou
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