Preconditioning enhances cell survival and differentiation of stem cells during transplantation in infarcted myocardium

Pasha, Zeeshan; Wang, Yigang; Riazuddin, Sheikh; Zhang, Dongsheng; Zhao, Tiemin; Ashraf, Muhammad

doi:10.1093/cvr/cvm025

Cited by 267 publications

(208 citation statements)

References 36 publications

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“…After myocardial infarction and reperfusion, reactive oxygen species (ROS) are generated in the ischemic myocardium and directly cause apoptosis. The in vivo oxidative stressinduced apoptosis can be simulated in vitro by H 2 O 2 treatment of both isolated adult cardiomyocytes and MSCs (Kumar and Jugdutt, 2003;Pasha et al, 2008). In the present study, we have shown that SDF-1 pretreatment can protect MSCs from H 2 O 2 -induced damages.…”

Section: Discussionsupporting

confidence: 53%

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SDF-1/CXCR4 axis modulates bone marrow mesenchymal stem cell apoptosis, migration and cytokine secretion

et al. 2011

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Bone marrow mesenchymal stem cells (MSCs) are considered as a promising cell source to treat the acute myocardial infarction. However, over 90% of the stem cells usually die in the first three days of transplantation. Survival potential, migration ability and paracrine capacity have been considered as the most important three factors for cell transplantation in the ischemic cardiac treatment. We hypothesized that stromal-derived factor-1 (SDF-1)/CXCR4 axis plays a critical role in the regulation of these processes. In this study, apoptosis was induced by exposure of MSCs to H 2 O 2 for 2 h. After re-oxygenation, the SDF-1 pretreated MSCs demonstrated a significant increase in survival and proliferation. SDF-1 pretreatment also enhanced the migration and increased the secretion of pro-survival and angiogenic cytokines including basic fibroblast growth factor and vascular endothelial growth factor. Western blot and RT-PCR demonstrated that SDF-1 pretreatment significantly activated the pro-survival Akt and Erk signaling pathways and up-regulated Bcl-2/Bax ratio. These protective effects were partially inhibited by AMD3100, an antagonist of CXCR4. We conclude that the SDF-1/CXCR4 axis is critical for MSC survival, migration and cytokine secretion.

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Section: Discussionsupporting

confidence: 53%

“…Although SDF-1 pretreatment improved cell survival and differentiation (Joo et al, 2004;Pasha et al, 2008), the mechanism has not been well elucidated. Previous studies suggested that cell survival and proliferation are mediated through activation of the signaling cascades PI3K/Akt and MAPK/ERK (Choi et al, 2008;Zhang and Cai, 2010).…”

Section: Discussionmentioning

confidence: 99%

SDF-1/CXCR4 axis modulates bone marrow mesenchymal stem cell apoptosis, migration and cytokine secretion

et al. 2011

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“…Vascular smooth muscles were identified immunohistochemically using antibodies against α-smooth muscle actin (M0951, DAKO). Myocytes were identified with α-sarcomeric actin antibody (Sigma) and 4′, 6-diamino-2-phenylindole (DAPI, Sigma) was used to stain nuclei [12]. Fluorescent imaging was performed with an Olympus BX41 microscope (Olympus America Inc., Melville, NY, USA) equipped with epiflouresence attachment and images were recorded using a digital camera with MagnaFire™ 2.1 software.…”

Section: Immunohistochemistry and Fish Analysismentioning

confidence: 99%

Over-expression of CXCR4 on mesenchymal stem cells augments myoangiogenesis in the infarcted myocardium

Zhang

Fan

Zhou

et al. 2008

Journal of Molecular and Cellular Cardiology

257

218

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Bone marrow mesenchymal stem cells (MSCs) participate in myocardial repair following myocardial infarction. However, their in vivo reparative capability is limited due to lack of their survival in the infarcted myocardium. To overcome this limitation, we genetically engineered male rat MSCs overexpressing CXCR4 in order to maximize the effect of stromal cell-derived factor-1α (SDF-1α) for cell migration and regeneration. MSCs were isolated from adult male rats and cultured. Adenoviral transduction was carried out to over-express either CXCR4/green fluorescent protein (Ad-CXCR4/GFP) or Ad-null/GFP alone (control). Flow cytometry was used to identify and isolate GFP/CXCR4 over-expressing MSCs for transplantation. Female rats were assigned to one of four groups (n = 8 each) to receive GFP-transduced male MSCs (2 × 10 6 ) via tail vein injection 3 days after ligation of the left anterior descending (LAD) coronary artery: GFP-transduced MSCs (Ad-null/ GFP-MSCs, group 1) or MSCs over-expressing CXCR4/GFP (Ad-CXCR4/GFP-MSCs, group 2), or Ad-CXCR4/GFP-MSCs plus SDF-1α (50 ng/μl) (Ad-CXCR4/GFP-MSCs/SDF-1α, group 3), or Ad-miRNA targeting CXCR4 plus SDF-1α (Ad-miRNA/GFP-MSCs + SDF-1α treatment, group 4). Cardiodynamic data were obtained 4 weeks after induction of regional myocardial infarction (MI) using echocardiography after which hearts were harvested for immunohistochemical studies. The migration of GFP and Y-chromosome positive cells increased significantly in the peri-and infarct areas of groups 2 and 3 compared to control group (p<0.05), or miRNA-CXCR4 group (p<0.01). The number of CXCR4 positive cells in groups 2, 3 was intimately associated with angiogenesis and myogenesis. MSCs engraftment was blocked by pretreatment with miRNA (group 4). Cardiac function was significantly improved in rats receiving MSCs over-expressing CXCR4 alone or with SDF-1α. The up-regulation of matrix metalloproteinases (MMPs) by CXCR4 overexpressing MSCs perhaps facilitated their engraftment in the collagenous tissue of the infarcted area. CXCR4 overexpression led to enhance in vivo mobilization and engraftment of MSCs into ischemic area where these cells promoted neomyoangiogenesis and alleviated early signs of left ventricular remodeling.

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“…Since H 2 O 2 can affect the analysis of PI3K activity, only hypoxia conditions (95% N 2 , 5% CO 2 ) were used when analyzing PI3K activity. Phosphorylation of Akt was measured by Western-blot as previously described [49]. Briefly, quiescent MSCs (10 6 ) were obtained by culturing cells in DMEM for 12 h. Cells were then treated with or without 250 nM 14S,21R-diHDHA under hypoxia conditions for 10 min, 2 h and 12 h, respectively.…”

Section: Phosphoinositide 3-kinase-akt Signalingmentioning

confidence: 99%

14S,21R-dihydroxy-docosahexaenoic Acid Treatment Enhances Mesenchymal Stem Cell Amelioration of Renal Ischemia/Reperfusion Injury

Tian

Lü

Shah

et al. 2012

Stem Cells and Development

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Preconditioning enhances cell survival and differentiation of stem cells during transplantation in infarcted myocardium

Cited by 267 publications

References 36 publications

SDF-1/CXCR4 axis modulates bone marrow mesenchymal stem cell apoptosis, migration and cytokine secretion

SDF-1/CXCR4 axis modulates bone marrow mesenchymal stem cell apoptosis, migration and cytokine secretion

Over-expression of CXCR4 on mesenchymal stem cells augments myoangiogenesis in the infarcted myocardium

14S,21R-dihydroxy-docosahexaenoic Acid Treatment Enhances Mesenchymal Stem Cell Amelioration of Renal Ischemia/Reperfusion Injury

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