title: Adenovirus-mediated stromal cell-derived- factor-1alpha gene transfer induces cardiac preservation after infarction via angiogenesis of CD133+ stem cells and anti-apoptosis.
abstract: In our study, we found cardiocytes expressed CXCR4, and the number of cardiocytes apoptosis with SDF-1 treatment decreased obviously through SDF-1 induced the up-regulation of phosphorylated Akt. On day 7 after myocardial infarction, marked expression of SDF-1alpha, and the number of CD133(+) cells was the highest in the AdV-SDF-1 injection hearts. On day 28 post-treatment, blood vessel density in the AdV. SDF-1 group was higher in infracted zones. Infarct size and collagen accumulation in the infracted area decreased significantly, thickness of LV wall, vessels and cardiocytes' density increased obviously in the AdV-SDF-1 group than in control or Adv-LacZ group, and hemodynamics showed the improvement of left ventricle heart function in the AdV.SDF-1 group. Therefore, SDF-1alpha could improve cardiac structure and function through the combined effects of angiogenesis and anti-apoptosis.
authors.affiliation: Institute of Clinical Medicine, Renmin Hospital, Yunyang Medical College, Shiyan, Hubei 442000, People's Republic of China.
authors.forename: Junming
authors.initials: J
authors.lastname: Tang
authors.forename: Jianing
authors.initials: J
authors.lastname: Wang
authors.forename: Jianye
authors.initials: J
authors.lastname: Yang
authors.forename: Xia
authors.initials: X
authors.lastname: Kong
mesh_terms: D000071916:AC133 Antigen; D000256:Adenoviridae / Q000235:genetics*; D000818:Animals; D015703:Antigens, CD / Q000378:metabolism; D017209:Apoptosis; D002465:Cell Movement; D002470:Cell Survival; D054377:Chemokine CXCL12 / Q000235:genetics / Q000378:metabolism*; D003094:Collagen / Q000378:metabolism; D004195:Disease Models, Animal; D042783:Endothelial Cells / Q000378:metabolism / Q000473:pathology; D015316:Genetic Therapy / Q000379:methods*; D005822:Genetic Vectors; D006023:Glycoproteins / Q000378:metabolism; D006801:Humans; D009203:Myocardial Infarction / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy*; D009206:Myocardium / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology; D018919:Neovascularization, Physiologic; D010455:Peptides / Q000378:metabolism; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D051381:Rats; D019718:Receptors, CXCR4 / Q000378:metabolism; D013234:Stem Cells / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D013997:Time Factors; D016277:Ventricular Function, Left
chemical_list: D000071916:AC133 Antigen; D015703:Antigens, CD; C515255:CXCL12 protein, human; D054377:Chemokine CXCL12; C486264:Cxcr4 protein, rat; D006023:Glycoproteins; C000606023:PROM1 protein, human; D010455:Peptides; C000606025:Prom1 protein, rat; D019718:Receptors, CXCR4; D003094:Collagen; D051057:Proto-Oncogene Proteins c-akt