Mesenchymal stem cell transplantation increases expression of vascular endothelial growth factor in papain-induced emphysematous lungs and inhibits apoptosis of lung cells

Zhen, Guohua; Xue, Zhenyi; Zhao, Jianping; Gu, Naibing; Tang, Zhouping; Xu, Yongjian; Zhang, Zhenxiang

doi:10.3109/14653241003745888

Cited by 82 publications

(73 citation statements)

References 38 publications

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“…More recently it has been shown to confer protection against injury and oxidative stress. This protection may be particularly important in the respiratory alveolus because pharmacological inhibition of VEGF activity and lung-targeted inactivation of the VEGF gene result in emphysematous phenotypes whereas VEGF expression diminishes emphysema in murine modeling systems (11,14,16,(32)(33)(34)49). In accordance with this finding, a number of investigators have reported decreased levels of VEGF expression/ accumulation in biological samples from patients with emphysema (16,33,(35)(36)(37).…”

Section: Discussionsupporting

confidence: 62%

“…It also induces inflammation and tissue remodeling (5), contributes to the pathogenesis of wound healing (7,8), and has a remarkable ability to confer endothelial cell and epithelial cell cytoprotection (9)(10)(11). This may be clearly seen in the lung, where studies from our laboratory and others have demonstrated that VEGF overexpression induces tracheal angiogenesis, tissue edema, parenchymal inflammation, dendritic cell activation, airway fibrosis, mucus metaplasia, enhanced helper T-cell type 2 (Th2)-and IL-13-induced tissue responses and cytoprotection in the setting of oxidant injury (5,12).…”

mentioning

confidence: 99%

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RIG-like Helicase Innate Immunity Inhibits Vascular Endothelial Growth Factor Tissue Responses via a Type I IFN–dependent Mechanism

Cruz²,

Hartl³

et al. 2011

Am J Respir Crit Care Med

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Section: Discussionsupporting

confidence: 62%

mentioning

confidence: 99%

RIG-like Helicase Innate Immunity Inhibits Vascular Endothelial Growth Factor Tissue Responses via a Type I IFN–dependent Mechanism

Cruz²,

Hartl³

et al. 2011

Am J Respir Crit Care Med

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“…Some studies have shown that MSCs could also achieve the biological effects by secreting VEGF. VEGF secreted by MSCs has been used in gastric ulcer and oral ulcer healing (El-Menoufy et al 2010;Hayashi et al 2008), in murine ischemic limbs leading to an increase in vessel density (Hoffmann et al 2010), in inhibiting the apoptosis of lung cells (Zhen et al 2010), in facilitating neurological function (Deng et al 2010), enhancing the repair and regeneration of critical sized bone defects (Kanczler et al 2010) and improving cardiac function in failing rat hearts (Tao et al 2009). Therefore, the VEGF 165 gene is the best target gene in gene therapy for promoting angiogenesis.…”

Section: Discussionmentioning

confidence: 99%

VEGF165 expressing bone marrow mesenchymal stem cells differentiate into hepatocytes under HGF and EGF induction in vitro

Yan

Xiao

et al. 2012

Cytotechnology

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A short half-life and low levels of growth factors in an injured microenvironment necessitates the sustainable delivery of growth factors and stem cells to augment the regeneration of injured tissues. Our aim was to investigate the ability of VEGF 165 expressing bone marrow mesenchymal stem cells (BMMSCs) to differentiate into hepatocytes when cultured with hepatocyte growth factor (HGF) and epidermal growth factor (EGF) in vitro. We isolated, cultured and identified rabbit BMMSCs, then electroporated the BMMSCs with VEGF 165 -pCMV6-AC-GFP plasmid. G418 was used to select transfected cells and the efficiency was up to 70%. The groups were then divided as follows: Group A was electroporated with pCMV6-AC-GFP plasmid ? HGF ? EGF and Group B was electroporated with VEGF 165 -pCMV6-AC-GFP plasmid ?HGF ? EGF. After 14 days, BMMSCs were induced into short spindle and polygonal cells. Alpha-fetoprotein (AFP) was positive and albumin (ALB) was negative in Group A, while both AFP and ALB were positive in group B on day 10. AFP and ALB in both groups were positive on day 20, but the quantity of AFP in group B decreased with prolonged time and was about 43.5% less than group A. The quantity of the ALB gene was increased with prolonged time in both groups. However, there was no significant difference between group A and B on day 10 and 20. Our results demonstrated that VEGF 165 -pCMV6-AC-GFP plasmid modified BMMSCs still had the ability to differentiate into hepatocytes. The VEGF 165 gene promoted BMMSCs to differentiate into hepatocyte-like cells under the induction of HGF and EGF, and reduced the differentiation time. These results have implications for cell therapies.

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“…In the cigarette smoke-induced emphysema model of COPD, MSCs administration and treatment of conditioned media of MSC reduced pulmonary cell apoptosis, attenuated the mean pulmonary arterial pressure, and inhibited muscularization in small pulmonary vessels [71]. In addition, another study showed that the protective effect of MSC transplantation on the rat model of papain-induced pulmonary emphysema may be partly mediated by upregulating VEGF-A expression and inhibiting the apoptosis of lung cells [70]. Therefore, MSCsbased therapies may represent new therapeutic approaches for COPD that currently lacks efficient treatment.…”

Section: Therapy Approaches Of Mscs For Ards and Copdmentioning

confidence: 99%

Protective Effects of Ellagic Acid against UVA-induced Oxidative Stress in Human Dermal Papilla

Kim¹,

Han²,

An³

et al. 2016

Asian J Beauty Cosmetol

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MSCs have become an emerging cell source with their immune modulation, high proliferation rate, and differentiation potential; indeed, they have been challenged in clinical trials. Recently, it has shown that ROS play a dual role as both deleterious and beneficial species depending on their concentration in MSCs. Various environmental stresses-induced excessive production of ROS triggers cellular senescence and abnormal differentiation on MSCs. Moreover, MSCs have been suggested to participate in the treatment of ALI/ARDS and COPD as a major cause of high morbidity and mortality. Therapeutic mechanisms of MSCs in the treatment of ARDS/COPD were focused on cell engraftment and paracrine action. However, ROS-mediated therapeutic mechanisms of MSCs still remain largely unknown. Here, we review the key factors associated with cell cycle and chromatin remodeling to accelerate or delay the MSC aging process. In addition, the enhanced ROS production and its associated pathophysiological pathways will be discussed along with the MSC senescence process. Furthermore, the present review highlights how the excessive amount of ROS-mediated oxidative stress might interfere with homeostasis of lungs and residual lung cells in the pathogenesis of ALI/ARDS and COPD.

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Mesenchymal stem cell transplantation increases expression of vascular endothelial growth factor in papain-induced emphysematous lungs and inhibits apoptosis of lung cells

Cited by 82 publications

References 38 publications

RIG-like Helicase Innate Immunity Inhibits Vascular Endothelial Growth Factor Tissue Responses via a Type I IFN–dependent Mechanism

RIG-like Helicase Innate Immunity Inhibits Vascular Endothelial Growth Factor Tissue Responses via a Type I IFN–dependent Mechanism

VEGF165 expressing bone marrow mesenchymal stem cells differentiate into hepatocytes under HGF and EGF induction in vitro

Protective Effects of Ellagic Acid against UVA-induced Oxidative Stress in Human Dermal Papilla

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