Vascular endothelial growth factor promotes cardiac stem cell migration via the PI3K/Akt pathway

Tang, Jun‐Ming; Wang, Jia‐Ning; Kong, Xiaoni; Yang, Jian-Ye; Guo, Linyun; Zheng, Fei; Zhang, Lei; Huang, Yong-Zhang; Wan, Yu

doi:10.1016/j.yexcr.2009.09.026

Cited by 96 publications

(82 citation statements)

References 34 publications

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“…As an angiogenic factor, VEGF promotes the mobilization and recruitment of endothelial and hematopoietic stem cells into the neo-angiogenic site, thereby accelerating vasculogenesis and angiogenesis (37,38). Tang et al (39) reported that cardiac stem cell (CSC) migration may be induced by multiple signaling pathways such as the VEGFR/PI3K/Akt and p38 mitogen-activated protein kinase (mAPK) cascades but not by platelet-derived growth factor receptor (PDGFR). Therefore, we suggest that the migratory effect of NSCs we observed may involve activated level of VEGF/VEGFR2 signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Additional effects of engineered stem cells expressing a therapeutic gene and interferon-β in a xenograft mouse model of endometrial cancer

Kim

Choi

2015

International Journal of Oncology

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Abstract. Endometrial cancer is the most common gynecologic malignancy in women worldwide. In the present study, we evaluated the effects of neural stem cell-directed enzyme/prodrug therapy (NDEPT) designed to more selectively target endometrial cancer. For this, we employed two different types of neural stem cells (NSCs), HB1.F3.CD and HB1.F3.CD.IFN-β cells. Cytosine deaminase (CD) can convert the non-toxic prodrug, 5-fluorocytosine (5-FC), into a toxic agent, 5-fluorouracil (5-FU), which inhibits DNA synthesis. IFN-β is a powerful cytotoxic cytokine that is released by activated immune cells or lymphocytes. In an animal model xenografted with endometrial Ishikawa cancer cells, the stem cells stained with CM-DiI were injected into nearby tumor masses and 5-FC was delivered by intraperitoneal injection. Co-expression of CD and IFN-β significantly inhibited the growth of cancer (~50-60%) in the presence of 5-FC. Among migration-induced factors, VEGF gene was highly expressed in endometrial cancer cells. Histological analysis showed that the aggressive nature of cancer was inhibited by 5-FC in the mice treated with the therapeutic stem cells. Furthermore, PCNA expression was more decreased in HB1.F3.CD.IFN-β treated mice rather than HB1.F3.CD treated mice. To confirm the in vitro combined effects of 5-FU and IFN-β, 5-FU was treated in Ishikawa cells. 5-FU increased the IFN-β/receptor 2 (IFNAR2) and BXA levels, indicating that 5-FU increased sensitivity of endometrial cancer cells to IFN-β, leading to apoptosis of cancer cells. Taken together, these results provide evidence for the efficacy of therapeutic stem cell-based immune therapy involving the targeted expression of CD and IFN-β genes at endometrial cancer sites.

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Section: Discussionmentioning

confidence: 99%

Additional effects of engineered stem cells expressing a therapeutic gene and interferon-β in a xenograft mouse model of endometrial cancer

Kim

Choi

2015

International Journal of Oncology

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“…Thus intracoronary administration of IGF1 robustly promotes regeneration of the infarcted pig heart (14). Aside from IGF1, the SDF1-mobilized progenitor cells also express abundant VEGF, which is known to stimulate endothelial progenitor cells (17) and promote cardiac stem cell migration (46). FGF2 has also been shown to stimulate cardiac stem cells for myocardial regeneration (45,59).…”

Section: Discussionmentioning

confidence: 99%

Intramuscular VEGF activates an SDF1-dependent progenitor cell cascade and an SDF1-independent muscle paracrine cascade for cardiac repair

Zisa

Shabbir

Mastri

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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“…[14][15][16][17] Vascular endothelial growth factor (VEGF) is a critical factor in the regulation of angiogenesis, 18 and transplantation of VEGF-engineered stem cells promoted angiogenesis and cardiomyocyte regeneration and improved heart function in a rat MI model. 15,19,20 Tissue inhibitor of matrix metalloproteinase-3 (TIMP3) is highly expressed in the normal heart but is reduced in failing hearts in association with maladaptive myocardial remodeling. [21][22][23] A main contributor to the adverse changes in ventricular dimensions and function that follow MI is a shift in the expression or activity of the degradative matrix metalloproteinase (MMP) enzymes relative to that of the TIMPs.…”

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confidence: 99%

Tissue Inhibitor of Matrix Metalloproteinase-3 or Vascular Endothelial Growth Factor Transfection of Aged Human Mesenchymal Stem Cells Enhances Cell Therapy after Myocardial Infarction

Yao

Jiang²,

Liu³

et al. 2012

Rejuvenation Research

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Mesenchymal stem cell (MSC) transplantation has been proposed as a potential therapeutic approach for ischemic heart disease, but the regenerative capacity of these cells decreases with age. In this study, we genetically engineered old human MSCs (O-hMSCs) with tissue inhibitor of matrix metalloproteinase-3 (TIMP3) and vascular endothelial growth factor (VEGF) and evaluated the effects on the efficacy of cell-based gene therapy in a rat myocardial infarction (MI) model. Cultured O-hMSCs were transfected with TIMP3 (O-TIMP3) or VEGF (O-VEGF) and compared with young hMSCs (Y-hMSCs) and non-transfected O-hMSCs for growth, clonogenic capacity, and differentiation potential. In vivo, rats were subjected to left coronary artery ligation with subse-

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Vascular endothelial growth factor promotes cardiac stem cell migration via the PI3K/Akt pathway

Cited by 96 publications

References 34 publications

Additional effects of engineered stem cells expressing a therapeutic gene and interferon-β in a xenograft mouse model of endometrial cancer

Additional effects of engineered stem cells expressing a therapeutic gene and interferon-β in a xenograft mouse model of endometrial cancer

Intramuscular VEGF activates an SDF1-dependent progenitor cell cascade and an SDF1-independent muscle paracrine cascade for cardiac repair

Tissue Inhibitor of Matrix Metalloproteinase-3 or Vascular Endothelial Growth Factor Transfection of Aged Human Mesenchymal Stem Cells Enhances Cell Therapy after Myocardial Infarction

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