Transplantation of endothelial progenitor cells transfected with VEGF165 to restore erectile function in diabetic rats

Gou, Xin; He, Wei-Yang; Xiao, Mingzhao; Qiu, Ming; Wang, Ming; Deng, Yuan-Zhong; Liu, Chao-Dong; Tang, Zao-Bing; Li, Jie; Chen, Yong

doi:10.1038/aja.2010.116

Cited by 50 publications

(45 citation statements)

References 27 publications

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“…In addition, the co-expression of these markers also characterizes the isolated EPCs at a specific maturation stage (14). EPCs have been reported to ameliorate acute myocardial infarction and diabetic erectile dysfunction by promoting angiogenesis (29)(30). However, few data are available regarding the role of EPCs in other diabetic complications, particularly in DCM.…”

Section: Discussionmentioning

confidence: 99%

Transplantation of bone marrow-derived endothelial progenitor cells attenuates myocardial interstitial fibrosis and cardiac dysfunction in streptozotocin-induced diabetic rats

Cheng¹,

Guo²,

Liu³

et al. 2012

International Journal of Molecular Medicine

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Abstract. Diabetic cardiomyopathy (DCM) is a progressive disease of the heart muscle and the third most common cause of heart failure. In the present study, we evaluated the effects of bone marrow-derived endothelial progenitor cell (EPC) transplantation on the development of DCM in a streptozotocin (STZ)-induced diabetic rat model. Ex vivo generated, characterized and cultivated rat EPCs were identified by flow cytometry of their surface markers. EPCs were transplanted intravenously into rats through the tail vein 6 weeks after they were challenged with STZ and the rats were sacrificed 4 weeks later. Before sacrifice, left ventricular (LV) catheterization was performed to evaluate the cardiac function. Myocardium sections were stained with Masson's trichrome staining to investigate myocardial collagen contents. Fibrosis-, apoptosis-and oxidative stress-related gene expressions were analyzed by western blot analysis. Transplantation of EPCs alleviated the impaired cardiac function associated with diabetes and decreased the collagen volume in diabetic myocardium resulting in improved cardiac function. Furthermore, EPC transplantation decreased the expression of type I collagen, Bax, caspase-3 and p67phox, while increasing the expression of Bcl-2 and manganese superoxide dismutase (MnSOD). Taken together, our results suggest that transplantation of EPCs improved cardiac function in the rat DCM model, likely through inhibition of cardiomyocyte apoptosis and attenuating myocardial fibrosis.

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Section: Discussionmentioning

confidence: 99%

Transplantation of bone marrow-derived endothelial progenitor cells attenuates myocardial interstitial fibrosis and cardiac dysfunction in streptozotocin-induced diabetic rats

Cheng¹,

Guo²,

Liu³

et al. 2012

International Journal of Molecular Medicine

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“…Mesenchymal stem cells (MSCs) have been tested in transplantation therapy for diabetic ED [11][12][13] . Although stem cell transplantation can improve erectile function in animal studies, the effect last only 7-28 d before gradually diminishing [14][15][16] . The main mechanism of these limited effects is assumed to be the apoptotic death of the transplanted stem cells.…”

Section: Introductionmentioning

confidence: 99%

ROS activates JNK-mediated autophagy to counteract apoptosis in mouse mesenchymal stem cells in vitro

et al. 2015

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Aim: Transplantation of mesenchymal stem cells (MSCs) for the treatment of diabetic erectile dysfunction (ED) is hampered by apoptosis of the transplanted cells. In diabetic ED, there is increased oxidative stress and decreased NO in the corpora cavernosa, and reactive oxygen species (ROS) induce apoptosis of the transplanted cells. In this study we examined whether and how autophagy was involved in ROS-induced apoptosis of MSCs. Methods: Mouse C3H10 MSCs were treated with H 2 O 2 to simulate the high oxidative condition in diabetic ED. Cell viability was measured using MTT assay. Apoptosis was analyzed by flow cytometry. Apoptosis-and autophagy-related proteins were detected with Western blot assays. Intracellular autophagosome accumulation was studied using transmission electron microscopy.

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“…40 Improved intracavernous pressure in diabetic animals transfected with the VEGF gene was also observed. 41 In humans specific polymorphisms of VEGF and transforming growth factor-␤1 are related to ED development following radiation therapy for prostate cancer. 42 IGF and its receptors have varied expression in ED.…”

Section: Gene Expression Profilingmentioning

confidence: 99%

Genetics of Erectile Dysfunction

Lopushnyan

Chitaley

2012

Journal of Urology

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Studies investigating the genetics of erectile dysfunction are mostly derived from animal models and candidate gene approaches. Candidate gene studies omit the greater portion of the genome, a problem that can be solved using a genome wide association study approach. The lack of persistently replicated results of candidate gene studies may be related to different patient ethnic backgrounds, variations in erectile dysfunction etiology and small sample sizes. Using strict inclusion/exclusion criteria for erectile dysfunction etiology and ethnicity in human studies may lead to improved understanding of the genetics of erectile dysfunction in specific populations.

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Transplantation of endothelial progenitor cells transfected with VEGF165 to restore erectile function in diabetic rats

Cited by 50 publications

References 27 publications

Transplantation of bone marrow-derived endothelial progenitor cells attenuates myocardial interstitial fibrosis and cardiac dysfunction in streptozotocin-induced diabetic rats

Transplantation of bone marrow-derived endothelial progenitor cells attenuates myocardial interstitial fibrosis and cardiac dysfunction in streptozotocin-induced diabetic rats

ROS activates JNK-mediated autophagy to counteract apoptosis in mouse mesenchymal stem cells in vitro

Genetics of Erectile Dysfunction

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