title: Apelin protects sarcoplasmic reticulum function and cardiac performance in ischaemia-reperfusion by attenuating oxidation of sarcoplasmic reticulum Ca2+-ATPase and ryanodine receptor.
abstract: OBJECTIVE
  Apelin, an endogenous cytokine, has a number of biological effects on the cardiovascular system, including a cardioprotective effect and calcium modulation. Because the intracellular calcium abnormality is considered to play an important role in cardiac dysfunction induced by ischaemia-reperfusion (I/R), the aim of this study was to examine the effects of apelin-13 on I/R-induced changes in cardiac performance and sarcoplasmic reticulum (SR) function.
  
  
  RESULTS
  Isolated rat hearts were subjected to global ischaemia followed by reperfusion in the absence or presence of apelin-13 and inhibitors of some survival kinases. We found that depressed cardiac performance induced by I/R was attenuated by apelin-13. Furthermore, apelin-13 depressed oxidative stress during I/R. SR function depressed during I/R was partly reversed by apelin-13. SR oxidative modification levels were increased in I/R and reversed by apelin. Inhibitors of phosphatidylinositol-3-kinase and protein kinase C abolished the effects of apelin. Apelin-13 maintained the Ca(2+) transient against I/R in cardiomyocytes.
  
  
  CONCLUSIONS
  Apelin protects SR function and cardiac performance during I/R by attenuating oxidation of sarco(endo)plasmic reticulum Ca(2+)-ATPase and RyR.
authors.affiliation: Department of Cardiology, Xijing Hospital, the Fourth Military Medical University, Changlexi Road, Xi'an 710032, China.
authors.forename: Chen
authors.initials: C
authors.lastname: Wang
authors.forename: Nan
authors.initials: N
authors.lastname: Liu
authors.forename: Ronghua
authors.initials: R
authors.lastname: Luan
authors.forename: Yan
authors.initials: Y
authors.lastname: Li
authors.forename: Dongjuan
authors.initials: D
authors.lastname: Wang
authors.forename: Wei
authors.initials: W
authors.lastname: Zou
authors.forename: Ying
authors.initials: Y
authors.lastname: Xing
authors.forename: Ling
authors.initials: L
authors.lastname: Tao
authors.forename: Feng
authors.initials: F
authors.lastname: Cao
authors.forename: Haichang
authors.initials: H
authors.lastname: Wang
mesh_terms: D000818:Animals; D000073861:Apelin; D002118:Calcium / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D036341:Intercellular Signaling Peptides and Proteins / Q000378:metabolism* / Q000502:physiology*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008297:Male; D009200:Myocardial Contraction; D015425:Myocardial Reperfusion; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D019837:Ryanodine Receptor Calcium Release Channel / Q000378:metabolism*; D012519:Sarcoplasmic Reticulum / Q000502:physiology*; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases / Q000378:metabolism*; D015398:Signal Transduction
chemical_list: D000073861:Apelin; C498579:Apln protein, rat; D036341:Intercellular Signaling Peptides and Proteins; D017382:Reactive Oxygen Species; D019837:Ryanodine Receptor Calcium Release Channel; C495199:apelin-13 peptide; D007770:L-Lactate Dehydrogenase; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases; D005978:Glutathione; D002118:Calcium
keywords: Ca2+; Ischaemic contracture; PI3K; PKC; ROS