title: S100A1 transgenic treatment of acute heart failure causes proteomic changes in rats.
abstract: S100 Ca2+-binding protein A1 (S100A1) is an important regulator of myocardial contractility. The aim of the present study was to identify the underlying mechanisms of S100A1 activity via profiling the protein expression in rats administered with an S100A1 adenovirus (Ad‑S100A1‑EGFP) following acute myocardial infarction (AMI). LTQ OrbiTrap mass spectrometry was used to profile the protein expression in the Ad‑S100A1‑EGFP and control groups post‑AMI. Using Protein Analysis Through Evolutionary Relationships (PANTHER) analysis, 134 energy metabolism‑associated proteins, which comprised 20 carbohydrate metabolism‑associated and 27 lipid metabolism associated proteins, were identified as differentially expressed in the Ad‑S100A1‑EGFP hearts compared with controls. The majority of the differentially expressed proteins identified were important enzymes involved in energy metabolism. The present study identified 12 Ca2+‑binding proteins and 22 cytoskeletal proteins. The majority of the proteins expressed in the Ad‑S100A1‑EGFP group were upregulated compared with the control group. These results were further validated using western blot analysis. Following AMI, Ca2+ is crucial for the recovery of myocardial function in S100A1 transgenic rats as indicated by the upregulation of proteins associated with energy metabolism and Ca2+‑binding. Thus, the current study ascertained that energy production and contractile ability were enhanced after AMI in the ventricular myocardium of the Ad‑S100A1‑EGFP group.
authors.affiliation: Department of Cardiology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, P.R. China.
authors.forename: Yichen
authors.initials: Y
authors.lastname: Guo
authors.affiliation: Department of Cardiology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, P.R. China.
authors.forename: Lianqun
authors.initials: L
authors.lastname: Cui
authors.affiliation: Department of Cardiology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, P.R. China.
authors.forename: Shiliang
authors.initials: S
authors.lastname: Jiang
authors.affiliation: Department of Radiology, Shandong Jiao Tong Hospital, Jinan, Shandong 250063, P.R. China.
authors.forename: Dongmei
authors.initials: D
authors.lastname: Wang
authors.affiliation: Department of Cardiology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, P.R. China.
authors.forename: Shu
authors.initials: S
authors.lastname: Jiang
authors.affiliation: Department of Cardiology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, P.R. China.
authors.forename: Chen
authors.initials: C
authors.lastname: Xie
authors.affiliation: Department of Cardiology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, P.R. China.
authors.forename: Yanping
authors.initials: Y
authors.lastname: Jia
mesh_terms: D000818:Animals; D019295:Computational Biology / Q000379:methods; D004195:Disease Models, Animal; D004734:Energy Metabolism; D063990:Gene Ontology; D006333:Heart Failure / Q000235:genetics* / Q000378:metabolism*; D007150:Immunohistochemistry; D008297:Male; D008822:Mice, Transgenic; D020543:Proteome; D040901:Proteomics / Q000379:methods; D051381:Rats; D009418:S100 Proteins / Q000235:genetics*
chemical_list: D020543:Proteome; D009418:S100 Proteins; C110294:S100A1 protein