Autologous endothelial progenitor cells transplantation promoting endothelial recovery in mice

Zhao, Xinshu; Huang, Lan; Yin, Yi; Fang, Yuqiang; Zhou, Yifan

doi:10.1111/j.1432-2277.2007.00497.x

Cited by 27 publications

(17 citation statements)

References 23 publications

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“…Immunohistochemical staining, such as that of VWF, takes over 30 min and causes tissue contents such as nucleic acid to degrade (6). UEA I is a glycoprotein that binds to endothelial cells and endothelial progenitor cells (7). In human skin tissue, UEA1 was effective in specifically identifying blood vessels as a structure encircling a lumen.…”

Section: Resultsmentioning

confidence: 99%

Transcriptome-wide analysis of blood vessels laser captured from human skin and chronic wound-edge tissue

Roy

Patel

Khanna

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

103

131

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Chronic wounds represent a substantial public health problem. The development of tools that would enable sophisticated scrutiny of clinical wound tissue material is highly desirable. This work presents evidence enabling rapid specific identification and laser capture of blood vessels from human tissue in a manner which lends itself to successful high-density (U133A) microarray analysis. Such screening of transcriptome followed by real-time PCR and immunohistochemical verification of candidate genes and their corresponding products were performed by using 3 mm biopsies. Of the 18,400 transcripts and variants screened, a focused set of 53 up-regulated and 24 down-regulated genes were noted in woundderived blood vessels compared with blood vessels from intact human skin. The mean abundance of periostin in wound-site blood vessels was 96-fold higher. Periostin is known to be induced in response to vascular injury and its expression is associated with smooth muscle cell differentiation in vitro and promotes cell migration. Forty-fold higher expression of heparan sulfate 6-Oendosulfatase1 (Sulf1) was noted in wound-site vessels. Sulf1 has been recently recognized to be anti-angiogenic. During embryonic vasculogenesis, CD24 expression is down-regulated in human embryonic stem cells. Wound-site vessels had lower CD24 expression. The findings of this work provide a unique opportunity to appreciate the striking contrast in the transcriptome composition in blood vessels collected from the intact skin and from the wound-edge tissue. Sets of genes with known vascular functions but never connected to wound healing were identified to be differentially expressed in wound-derived blood vessels paving the way for innovative clinically relevant hypotheses.angiogenesis ͉ microarray ͉ wound healing

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Section: Resultsmentioning

confidence: 99%

Transcriptome-wide analysis of blood vessels laser captured from human skin and chronic wound-edge tissue

Roy

Patel

Khanna

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

103

131

View full text Add to dashboard Cite

show abstract

“…Several animal testing models have suggested that the transfusion of ex vivo expanded EPCs can accelerate re-endothelialization, prevent neointimal formation, and promote neovascularization. [101][102][103] Clinical follow-up results further demonstrate that the intracoronary infusion of autologous progenitor cells presents favorable safety and feasibility in patients with acute myocardial infarction. 104,105 Besides, functional modification such as magnetic-label of EPCs before transfusion may contribute to the migration of EPCs to the site of injury under the guidance of magnetic field gradient.…”

Section: Cellular Therapymentioning

confidence: 94%

“…Based on the low concentration of circulating EPCs, intravenous or intracoronary infusions of bone marrow‐derived cells may be an effective method to rapidly increase the density of circulating EPCs. Several animal testing models have suggested that the transfusion of ex vivo expanded EPCs can accelerate re‐endothelialization, prevent neointimal formation, and promote neovascularization . Clinical follow‐up results further demonstrate that the intracoronary infusion of autologous progenitor cells presents favorable safety and feasibility in patients with acute myocardial infarction .…”

Section: In Vivo Induced Self‐endothelializationmentioning

confidence: 94%

Endothelialization of implanted cardiovascular biomaterial surfaces: The development from in vitro to in vivo

Liu

Zhang

et al. 2013

J Biomedical Materials Res

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Restenosis and thrombosis formation after cardiovascular devices implantation continue to be problematic. Although various platforms and parameters of cardiovascular devices have been designed and optimized over the years, postoperative complications are hard to avoid. The native vascular endothelium always provide a nonthrombogenic surface as well as prevent intimal overproliferation, thereby, the presence of a confluent endothelial cell layer on material surfaces have been widely accepted as an ideal approach to improve the biocompatibility of implanted cardiovascular materials. Endothelialization on biomaterial surfaces is initially developed by in vitro cell seeding. However, numerous no-perfect parts of this method are existed for clinical use. The emergency of endothelial progenitor cells may provide a promising way for setting these limitations. Over the last decades, countless researches about EPCs-based in vivo induced self-endothelialization have been reported and mainly focused on cellular therapy, pharmacological therapy, materials designing, or surface biofunctional modification. This review details the development of endothelialization on cardiovascular material surfaces from in vitro to in vivo. Endothelialization progress on the basis of molecular biological level and bioinformatics theory is expected to be the key point in the coming decades.

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“…Studies looking at the effects of EPC dysfunction in diabetes on endothelial regrowth and neointimal hyperplasia after vessel injury are very few. One study showed that reendothelialization was significantly reduced in nude nondiabetic mice injected with EPCs from diabetic mice when compared with mice injected with normal EPCs (23,24). However, very little is known about the mechanisms that might lead to the inability of EPCs in an inflammatory, insulin-resistant environment, to induce reendothelialization and decrease neointimal hyperplasia.…”

mentioning

confidence: 99%

Role of Inflammation and Insulin Resistance in Endothelial Progenitor Cell Dysfunction

et al. 2011

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OBJECTIVEEndothelial progenitor cells (EPCs) are decreased in number and function in type 2 diabetes. Mechanisms by which this dysfunction occurs are largely unknown. We tested the hypothesis that a chronic inflammatory environment leads to insulin signaling defects in EPCs and thereby reduces their survival. Modifying EPCs by a knockdown of nuclear factor-κB (NF-κB) can reverse the insulin signaling defects, improve EPC survival, and decrease neointimal hyperplasia in Zucker fatty rats postangioplasty.RESEARCH DESIGN AND METHODSEPCs from Zucker fatty insulin-resistant rats were cultured and exposed to tumor necrosis factor-α (TNF-α). Insulin signaling defects and apoptosis were measured in the presence and absence of an NF-κB inhibitor, BAY11. Then, EPCs were modified by a knockdown of NF-κB (RelA) and exposed to TNF-α. For in vivo experiments, Zucker fatty rats were given modified EPCs post–carotid angioplasty. Tracking of EPCs was done at various time points, and neointimal hyperplasia was measured 3 weeks later.RESULTSInsulin signaling as measured by the phosphorylated–to–total AKT ratio was reduced by 56% in EPCs exposed to TNF-α. Apoptosis was increased by 71%. These defects were reversed by pretreatment with an NF-κB inhibitor, BAY11. Modified EPCs exposed to TNF-α showed a lesser reduction (RelA 20%) in insulin-stimulated AKT phosphorylation versus a 55% reduction in unmodified EPCs. Apoptosis was 41% decreased for RelA knockdown EPCs. Noeintimal hyperplasia postangioplasty was significantly less in rats receiving modified EPCs than in controls (intima-to-media ratio 0.58 vs. 1.62).CONCLUSIONSIn conclusion, we have shown that insulin signaling and EPC survival is impaired in Zucker fatty insulin resistant rats. For the first time, we have shown that this defect can be significantly ameliorated by a knockdown of NF-κB and that these EPCs given to Zucker fatty rats decrease neointimal hyperplasia post–carotid angioplasty.

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Autologous endothelial progenitor cells transplantation promoting endothelial recovery in mice

Cited by 27 publications

References 23 publications

Transcriptome-wide analysis of blood vessels laser captured from human skin and chronic wound-edge tissue

Transcriptome-wide analysis of blood vessels laser captured from human skin and chronic wound-edge tissue

Endothelialization of implanted cardiovascular biomaterial surfaces: The development from in vitro to in vivo

Role of Inflammation and Insulin Resistance in Endothelial Progenitor Cell Dysfunction

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