ABSTRACT
OBJECTIVE: To study the effects of ephrinB2 gene transfection on the differentiation of bone marrow mesenchymal stem cells (BMSCs) into vascular endothelial cells. METHODS: Wistar rat BMSCs were isolated by density gradient centrifugation and purified on the basis of their adhesion ability. The BMSCs were transfected with a lenti-virus vector encoding a constitutively active form of human ephrinB2 gene, and the cell markers including CD105, CD73, CD44, von Willebrand factor (VWF) and vascular growth factor receptor 2 (KDR) were detected using flow cytometry. The potential of ephrinB2-BMSCs for differentiation into osteoblasts and adipoblasts in vitro were tested, and the differentiation of the cells into endothelial-like cells was induced by culture in the presence of 2% fetal bovine serum and 50 ng/ml vascular endothelial growth factor. RESULTS: EphrinB2-BMSCs were positive for the markers CD105, CD73 and CD44, and negative for the typical endothelial markers like VWF and KDR, and retained high potentials for differentiation into osteoblasts and adipoblasts in vitro after cultivation in respective media. After induced differentiation, ephrinB2-BMSCs expressed VWF and KDR and showed greater ability of differentiation into vascular endothelial cells and formation of capillary structures on matrix gel than the BMSCs without transfection. CONCLUSIONS: EphrinB2 gene transfection efficiently promotes the differentiation of BMSCs into vascular endothelial cells. These genetically engineered cells provide valuable sources for new therapies of coronary heart disease.
Subject(s)
Bone Marrow Cells/cytology , Cell Differentiation/physiology , Endothelial Cells/cytology , Ephrin-B2/physiology , Mesenchymal Stem Cells/cytology , Animals , Bone Marrow Cells/metabolism , Cell Differentiation/genetics , Cells, Cultured , Coronary Disease/therapy , Endothelial Cells/metabolism , Ephrin-B2/genetics , Genetic Therapy/methods , Male , Mesenchymal Stem Cells/metabolism , Rats , Rats, Wistar , TransfectionABSTRACT
OBJECTIVE: To compare the effects of puerarin and granulocyte colony-stimulating factor (G-CSF) in treating acute myocardial infarction (AMI) and on the size of infarcted area and cytokines. METHODS: Seventy-nine patients with anterior AMI were randomly divided into three groups, they were treated with conventional Western medical treatment, but to the puerarin group (PG) and the G-CSF group (GCG) puerarin and G-CSF was given additionally, respectively. The infarcted size, plasma G-CSF, matrix metalloproteinase-9 (MMP-9), serum interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) were detected before and after treatment. RESULTS: The infarcted size was positively correlated to the levels of G-CSF, MMP-9, IL-6 and TNF-alpha before treatment ( r = 0.45, 0.42, 0.44 and 0.42, P<0.01 ). The infarcted size in the PG and the GCG decreased on the 28th day (P<0.01), the level of G-CSF, MMP-9, IL-6 and TNF-alpha in the PG on the 7th day all decreased (P<0.05), but these indexes in the GCG increased (P<0.05), while those in the control group were unchanged (P>0.05). CONCLUSION: Puerarin and G-CSF are effective in decreasing infarcted size, but their effects on cytokines are different entirely.
Subject(s)
Granulocyte-Macrophage Colony-Stimulating Factor/therapeutic use , Isoflavones/therapeutic use , Myocardial Infarction/drug therapy , Phytotherapy , Aged , Antigens, CD34/metabolism , Drug Therapy, Combination , Female , Humans , Interleukin-6/blood , Male , Matrix Metalloproteinase 9/blood , Middle Aged , Recombinant Proteins , Tumor Necrosis Factor-alpha/metabolismABSTRACT
OBJECTIVE: To investigate the effects of carvedilol on neurohormone and magnesium metabolism in patients with chronic heart failure (CHF). METHODS: Fifty-seven patients with CHF were divided into two groups randomly: received conventional treatment alone or combined with carvedilol for 8 weeks, respectively. Urine magnesium excretion (UME), plasma levels of magnesium (PMC), norepinephrine (NE), angiotensin-II (Ang-II), aldosterone (ALD), plasma renin activity (PRA) and peripheral monocyte magnesium content (MMC) were measured before and after treatments. Twenty-six health persons were selected as normal subjects. RESULTS: There was a significant increase in UME and plasma concentrations of NE, ALD, Ang-II and PRA, and a significant decrease in MMC in patients with CHF, compared with the control group (P < 0.01). UME was positively correlated with ALD, Ang-II, PRA r = 0.41, 0.42, 0.38, respectively (P < 0.01). These parameters significantly improved after carvedilol (P < 0.05). CONCLUSION: Carvedilol decreases significantly plasma concentrations of neurohormone and urine magnesium excretion, and increases cell magnesium content in patients with CHF.
