Magnetic nanosphere-guided site-specific delivery of vascular endothelial growth factor gene attenuates restenosis in rabbit balloon-injured artery

Zhang, Tiemin; Qu, Guangjin

doi:10.1016/j.jvs.2014.11.068

Cited by 7 publications

(11 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Sixteen animal model studies [27-32, 34-42, 45] reported change in arterial lumen post-VEGF modulation. Fourteen studies reported change in neointimal area proliferation (mm 2 ) [27-29, 32-37, 39, 42-45].…”

Section: Resultsmentioning

confidence: 99%

“…A total of 22 studies remained all of which were included in this systematic review (Fig. 1 ; Table 1 ) [ 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 ].…”

Section: Resultsmentioning

confidence: 99%

“…388 DOI: 10.1159/000527079 which were examined across studies. Twenty studies effectively analyzed decrease or increase of VEGF-A [36,38] or its isoforms (VEGF 121,164,165 ) [27,28,30,31,33,35,37,[39][40][41][42][43][44][45][46][47][48]. One of them employed membrane-bound, VEGF receptor 2 expression plasmid (binding site of VEGF-A), effectively increasing the action of VEGF-A [40].…”

Section: Vegf Sub-types or Isoform Examinedmentioning

confidence: 99%

See 2 more Smart Citations

What Went Wrong with VEGF-A in Peripheral Arterial Disease? A Systematic Review and Biological Insights on Future Therapeutics

et al. 2022

View full text Add to dashboard Cite

Background: Of the 200 million patients worldwide affected by peripheral arterial disease (PAD), 4% will inevitably require major limb amputation. Previous systematic reviews presented a conflicting body of evidence in terms of vascular endothelial growth factor (VEGF) family member effects upon PAD natural progression. Despite that, modulation of intrinsic angiogenesis mechanisms targeting the VEGF family members still confers an attractive therapeutic target. The aim of the present study was to evaluate current evidence of VEGF modulation in the context of PAD. Methods: This is a systematic literature review conducted according to the PRISMA guidelines and registered under PROSPERO database [CRD42021285988]. Independent literature search was performed up to April 1, 2022, on six databases. A total of 22 eligible studies were identified [N: 3, interventional patient studies; N: 19, animal studies]. Animal studies were appraised by the SYRCLE risk of bias tool, while human participant studies were assessed by the Newcastle Ottawa scale. Overall, quality of evidence was deemed fair for both animal and human studies. Main study outcomes were percentage change of injured vessel lumen stenosis and neointimal area formation upon VEGF modulation (inhibition or activation) in comparison with control group. Findings: Nineteen animal models and three human participant studies were included in the systematic review and assessed separately. Positive modulation of VEGF-A in animal models resulted in a median decrease of 65.58% [95% CI 45.2; 71.87] in lumen stenosis [14 studies]. Furthermore, positive modulation of VEGF-A was found to reduce neointimal area proliferation by a median decrease of 63.41% [95% CI 41.6; 79.59] [14 studies]. Median end of study duration was 28 days [range: 14–84 days]. Data were insufficient to assess these outcomes with respect to VEGF-B or VEGF-C modulation. The limited number of available human studies presented inadequate outcome assessment despite their overall fair NOS grading. Interpretation: VEGF-A-positive modulation decreases lumen stenosis and neointimal hyperplasia in PAD simulation animal models. Previously identified variability among outcomes was found to strongly stem from the variability of experimental designs. Clinical applicability and safety profile of VEGF-A in the context of PAD remain to be defined by a robust and uniformly designed body of further animal model-based experiments.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Vegf Sub-types or Isoform Examinedmentioning

confidence: 99%

See 1 more Smart Citation

What Went Wrong with VEGF-A in Peripheral Arterial Disease? A Systematic Review and Biological Insights on Future Therapeutics

et al. 2022

View full text Add to dashboard Cite

show abstract

“…Mature EC or EC progenitor cell transplantation to the injured vessel lumen [27][28][29][30][31] , or accelerating reendothelialization by VEGF or VEGF gene delivery 32,33 , may be promising to combat restenosis after balloon injury or in-stent stenosis. To compare the effect of ECs and arterial flow on vascular remodeling, we seeded HUVECs in the lumen of rat aortas and human umbilical arteries immediately after injury.…”

Section: Discussionmentioning

confidence: 99%

“…Therapeutic use of ECs, or elements of their secretome, may be an effective biological approach to treat vascular injuries caused by the aforementioned interventions. In animal models, local delivery of endothelial or endothelial progenitor cells to the injury site [27][28][29][30][31] , injection of intra-arterial VEGF 32 or VEGF gene delivery 33 , all result in reduction of intimal hyperplasia after balloon injury in animal models. However, all of these studies employ animal models that are not ideally representative of human physiology.…”

Section: Introductionmentioning

confidence: 99%

An Ex Vivo Vessel Injury Model to Study Remodeling

et al. 2018

View full text Add to dashboard Cite

Objective:Invasive coronary interventions can fail due to intimal hyperplasia and restenosis. Endothelial cell (EC) seeding to the vessel lumen, accelerating re-endothelialization, or local release of mTOR pathway inhibitors have helped reduce intimal hyperplasia after vessel injury. While animal models are powerful tools, they are complex and expensive, and not always reflective of human physiology. Therefore, we developed an in vitro 3D vascular model validating previous in vivo animal models and utilizing isolated human arteries to study vascular remodeling after injury. Approach: We utilized a bioreactor that enables the control of intramural pressure and shear stress in vessel conduits to investigate the vascular response in both rat and human arteries to intraluminal injury.Results:Culturing rat aorta segments in vitro, we show that vigorous removal of luminal ECs results in vessel injury, causing medial proliferation by Day-4 and neointima formation, with the observation of SCA1+ cells (stem cell antigen-1) in the intima by Day-7, in the absence of flow. Conversely, when endothelial-denuded rat aortae and human umbilical arteries were subjected to arterial shear stress, pre-seeding with human umbilical ECs decreased the number and proliferation of smooth muscle cell (SMC) significantly in the media of both rat and human vessels.Conclusion:Our bioreactor system provides a novel platform for correlating ex vivo findings with vascular outcomes in vivo. The present in vitro human arterial injury model can be helpful in the study of EC-SMC interactions and vascular remodeling, by allowing for the separation of mechanical, cellular, and soluble factors.

show abstract

Endothelial Cell Isolation and Manipulation

Brostjan

2019

Fundamentals of Vascular Biology

View full text Add to dashboard Cite

Magnetic nanosphere-guided site-specific delivery of vascular endothelial growth factor gene attenuates restenosis in rabbit balloon-injured artery

Abstract: Intra-arterial VEGF gene delivery by magnetic microspheres significantly increased DNA stability, transfection efficiency, and targeting specificity, resulting in exogenous VEGF overexpression and attenuated intimal hyperplasia in balloon-injured artery.

Cited by 7 publications

References 40 publications

What Went Wrong with VEGF-A in Peripheral Arterial Disease? A Systematic Review and Biological Insights on Future Therapeutics

What Went Wrong with VEGF-A in Peripheral Arterial Disease? A Systematic Review and Biological Insights on Future Therapeutics

An Ex Vivo Vessel Injury Model to Study Remodeling

Endothelial Cell Isolation and Manipulation

Contact Info

Product

Resources

About