title: Comparing the effects of MSCs and CD34+ cell therapy in a rat model of myocardial infarction.
abstract: Stem cell therapy is considered as a promising approach in the treatment of myocardial infarction (MI). This study was designed as a comparison of human umbilical cord blood (HUCB)-derived CD34+ and HUCB-derived MSCs for the repair of cardiac tissue by induction of the angiogenesis. Forty-eight male rats were randomized into four groups: sham-operated group, MI group, MSCs-treated group, and CD34+ cells-treated group. After 4 weeks, the rats were sacrificed. All sections from left ventricles of all groups were subjected to hematoxylin & eosin, Masson's trichrome, and immunohistochemical stains (CD133, CD44, and α-smooth muscle actin). RNA was extracted for gene expression of the angiogenic markers. A significant reduction of the infarct size and the amplitude of T-wave in the CD34+ cells-treated group when compared with the MSCs-treated group were determined. Histologically, the MI group showed scar tissue, congested blood capillaries around the infarcted area, some necrotic cells, and inflammatory cells. Administration of either MSCs or CD34+ cells had a therapeutic potential to induce regenerative changes in the myocardium with better results in CD34+cells-treated group. Quantitative RT-PCR analysis revealed a significant increase in the expression of vascular endothelial growth factor (VEGF), VEGFR-2, Ang-1, and Tie-2 and a significant decreased expression of Ang-2 in stem cells transplanted groups when compared with the noncell transplanted hearts. A significant increase of VEGF, VEGFR-2, Ang-1, and Tie-2 expression in the group receiving CD34+ cells than those receiving MSCs was found. Finally, there was an upregulation of both human VEGF and human hypoxia-inducible factor 1α in the infarcted hearts treated by CD34+ cells than that treated by MSCs. We first revealed a superior efficacy of CD34+ cells when compared with MSCs in induction of regenerative changes in the MI model. Both cell therapies may repair the damaged heart tissue primarily by secretion of proangiogenic factors that induce the angiogenesis and activate the angiogenesis signaling pathway. © 2016 IUBMB Life, 68(5):343-354, 2016.
authors.affiliation: Medical Biochemistry Department, Faculty of Medicine, Zagazig University, Zagazig, Egypt.
authors.forename: Sally M
authors.initials: SM
authors.lastname: Shalaby
authors.affiliation: Medical Biochemistry Department, Faculty of Medicine, Zagazig University, Zagazig, Egypt.
authors.forename: Amal S
authors.initials: AS
authors.lastname: El-Shal
authors.affiliation: Medical Biochemistry Department, Faculty of Medicine, Zagazig University, Zagazig, Egypt.
authors.forename: Haidy E
authors.initials: HE
authors.lastname: Zidan
authors.affiliation: Histology and Cell Biology Department, Faculty of Medicine, Zagazig University, Zagazig, Egypt.
authors.forename: Nehad F
authors.initials: NF
authors.lastname: Mazen
authors.affiliation: Histology and Cell Biology Department, Faculty of Medicine, Zagazig University, Zagazig, Egypt.
authors.forename: Manal R
authors.initials: MR
authors.lastname: Abd El-Haleem
authors.affiliation: Clinical Pharmacology Department, Faculty of Medicine, Zagazig University, Zagazig, Egypt.
authors.forename: Dalia M
authors.initials: DM
authors.lastname: Abd El Motteleb
mesh_terms: D042501:Angiogenic Proteins / Q000378:metabolism; D000818:Animals; D018952:Antigens, CD34 / Q000378:metabolism; D004195:Disease Models, Animal; D005312:Fetal Blood / Q000166:cytology; D006801:Humans; D008297:Male; D045164:Mesenchymal Stem Cell Transplantation; D059630:Mesenchymal Stem Cells / Q000502:physiology*; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D018919:Neovascularization, Physiologic; D017208:Rats, Wistar
chemical_list: D042501:Angiogenic Proteins; D018952:Antigens, CD34
keywords: CD34+ cells; MSCs; animal models; human umbilical cord blood; myocardial infarction