Time course of arteriogenesis following femoral artery occlusion in the rabbit

Hoefer, Imo E.; Royen, Niels van; Buschmann, Ivo; Piek, Jan J.; Schäper, Wolfgang

doi:10.1016/s0008-6363(00)00243-1

Cited by 204 publications

(177 citation statements)

References 22 publications

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“…This morphology, identified in our experiments exclusively after MCP-1 treatment, is typical for arteries induced by arteriogenesis. 22,24 The concomitant increase in the number and diameter of induced collateral arteries are in good agreement with the pronounced increase in peripheral conductance between control-and MCP1_genomic-treated pigs. In addition, other enlarged or induced blood vessels not visualized by angiography may additionally contribute to the peripheral conductance.…”

Section: Mcp-1 Gene Transfer-mediated Arteriogenesis a Muhs Et Alsupporting

confidence: 78%

“…This is comparable to improvements of conductance mediated by continuous infusion of MCP-1 protein in rabbit and pig. 22,23 The present study showed for the first time that a nonviral gene therapeutic approach was equipotent to a protein perfusion therapy. Transfection of 2 mg MCP-1_genomic led to significant improvements of conductance and to an increase in peripheral blood pressure.…”

Section: Mcp-1 Gene Transfer-mediated Arteriogenesis a Muhs Et Almentioning

confidence: 61%

“…This is in contrast to the time course and magnitude seen in the rabbit model, in which natural collateralization is pronounced enough to virtually restore peripheral blood pressure to preocclusion level after 4 weeks. 22 Thus, the pig hindlimb model reveals significant advantages for testing effects of therapeutic interventions on collateralization and may therefore be of higher predictive value for a clinical setting than, for example, the rabbit model. MCP-1 protein has been shown to be a potent arteriogenic stimulant when infused in the rabbit femoral artery ligation model over 8 days and in pigs over a 2-week treatment period.…”

Section: Mcp-1 Gene Transfer-mediated Arteriogenesismentioning

confidence: 99%

“…MCP-1 protein has been shown to be a potent arteriogenic stimulant when infused in the rabbit femoral artery ligation model over 8 days and in pigs over a 2-week treatment period. 17,18,22,23 Since prolonged administration of MCP-1 in a clinical setting via intraarterial application appears undesirable, a liposomebased nonviral gene transfer to achieve local MCP-1 overexpression and production was developed and …”

Section: Mcp-1 Gene Transfer-mediated Arteriogenesismentioning

confidence: 99%

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Nonviral monocyte chemoattractant protein-1 gene transfer improves arteriogenesis after femoral artery occlusion

et al. 2004

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Local infusion of recombinant monocyte chemoattractant protein-1 (MCP-1) has been shown to enhance collateral artery formation in rabbit and pig hindlimb models. Owing to clinical disadvantages of protein infusion, a nonviral, liposome-based MCP-1 gene transfer was developed. Collateralization in a porcine hindlimb model served to provide a proof-of-principle for the functional benefit of MCP-1 overexpression. Development of arterial conductance as a measure of functionally relevant collateralization was evaluated in occluded as well as untreated hindlimbs in each animal. At the time of occlusion, MCP-1 and control DNA/DC-30 lipoplexes were transferred to femoral arteries of Goettingen minipigs (two therapeutic MCP-1 groups: 2 and 4 mg and one control group), using the Infiltrator s local drug-delivery device. At 2 weeks following occlusion, collateralization was determined as changes in peripheral haemodynamic conductance, peripheral over aortic blood pressure ratio and angiographically visible morphology of the peripheral vessel tree. Nonviral MCP-1 gene transfer significantly improved peripheral conductance (control 11.6972.78%, 2 mg 23.8172.81%, Po0.05 and 4 mg 23.3673.1%, Po0.05; n ¼ 12 per group) as well as the ratio of peripheral over aortic blood pressure (control 0.6470.03%, 2 mg 0.7570.02%, Po0.05 and 4 mg 0.7570.02%, Po0.05; n ¼ 12 per group) when compared to the untreated controls 2 weeks after occlusion. Thus, it could be demonstrated for the first time that in situ overexpression of MCP-1 following local nonviral gene transfer is a potential approach to improve peripheral collateralization.

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Section: Mcp-1 Gene Transfer-mediated Arteriogenesis a Muhs Et Alsupporting

confidence: 78%

Section: Mcp-1 Gene Transfer-mediated Arteriogenesis a Muhs Et Almentioning

confidence: 61%

Section: Mcp-1 Gene Transfer-mediated Arteriogenesismentioning

confidence: 99%

Section: Mcp-1 Gene Transfer-mediated Arteriogenesismentioning

confidence: 99%

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Nonviral monocyte chemoattractant protein-1 gene transfer improves arteriogenesis after femoral artery occlusion

et al. 2004

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“…8 Experimental therapy with growth factors can improve on that by not more than several percentage points. 9 Increased FSS is thought to be responsible for triggering arteriogenesis, 10,11 because the sudden decrease in peripheral pressure after an arterial occlusion increases the velocity of flow in pre-existent collateral arterioles that interconnect the prestenotic high-pressure bed with the poststenotic lowpressure bed.…”

Section: Discussionmentioning

confidence: 99%

Elevated Fluid Shear Stress Enhances Postocclusive Collateral Artery Growth and Gene Expression in the Pig Hind Limb

Pipp

Boehm

Cai

et al. 2004

ATVB

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217

205

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Objective-The role of fluid shear stress (FSS) in collateral vessel growth remains disputed and prospective in vivo experiments to test its morphogenic power are rare. Therefore, we studied the influence of FSS on arteriogenesis in a new model with extremely high levels of collateral flow and FSS in pig and rabbit hind limbs. Methods and Results-A side-to-side anastomosis was created between the distal stump of one of the bilaterally occluded femoral arteries with the accompanying vein. This clamps the collateral reentry pressure at venous levels and increases collateral flow, which is directed to a large part into the venous system. This decreases circumferential wall stress and markedly increases FSS. One week after anastomosis, angiographic number and size of collaterals were significantly increased. Maximal collateral flow exceeded by 2.3-fold that obtained in the ligature-only hind limb. Capillary density increased in lower leg muscles. Immunohistochemistry revealed augmented proliferative activity of endothelial and smooth muscle cells. Intercellular adhesion molecule-1 and vascular cell adhesion molecule (VCAM)-1 were upregulated, and monocyte invasion was markedly increased. In 2-dimensional gels, actin-regulating cofilin1 and cofilin2, destrin, and transgelin2 showed the highest degree of differential regulation. Conclusions-High levels of FSS cause a strong arteriogenic response, reinstate cellular proliferation, stimulate cytoskeletal rearrangement, and normalize maximal conductance. FSS is the initiating molding force in arteriogenesis. Key Words: fluid shear stress Ⅲ shunt Ⅲ arteriogenesis Ⅲ proteomics Ⅲ cytoskeletal proteins N umerous studies have documented the influence of fluid shear stress (FSS) as an arterial molding force, 1-3 but information on the actions of markedly increased in vivo FSS on the development of arterial collateral vessels after occlusion of a conduit artery is lacking. Such studies are needed because attempts at changing FSS often also alter the circumferential wall stress, another acknowledged molding force of growing collateral vessels. The formation of a collateral circulation after an arterial occlusion correlates well with the calculated increase in FSS because of the increased collateral flow caused by the pressure decrease along pre-existent collaterals. However, because of the fast increase in collateral diameter by cellular proliferation, FSS decreases quickly again, and the early termination of the growth process at an incomplete stage of adaptation is believed to be caused by the only transient action of FSS. One of the hypotheses to be tested was, therefore, whether prolonged action of FSS would also improve the final adaptation by continued growth. The present experiments were therefore undertaken to prospectively study the causal relations between arteriogenesis and FSS by a stepwise and lasting increase of collateral flow brought about by the creation of a side-to-side anastomosis between the distal stump of the occluded femoral artery and its accompanying vei...

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Vascular Networks

Kannan

Seifalian

2006

Wiley Encyclopedia of Biomedical Engineering

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The holy grail of artificial tissue is currently limited by the absence of a viable vascular network to sustain it. Although a growing amount of interest exists in engineering such a construct, they are essentially in their infancy. In this chapter, the basic concepts of microcirculation are laid down, along with current state‐of‐the‐art technology used to develop an artificial capillary bed. A major limitation is the poor patency rates, especially at low‐flow states, of contemporary microvascular grafts. Newer options for microvessels including the use of nano‐engineered materials are explored and tissue engineering biological microvessels are also discussed. At the lower end of the spectrum, biomedical researchers have also used angiogenic factors to stimulate capillary development. More recently, stem cell technology has also come into vogue with the potential to promote arteriogenesis. In the future, it is foreseen that all these factors would be synergized to bridge the “missing link” between the arterial system and tissue‐engineered scaffolds.

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Time course of arteriogenesis following femoral artery occlusion in the rabbit

Cited by 204 publications

References 22 publications

Nonviral monocyte chemoattractant protein-1 gene transfer improves arteriogenesis after femoral artery occlusion

Nonviral monocyte chemoattractant protein-1 gene transfer improves arteriogenesis after femoral artery occlusion

Elevated Fluid Shear Stress Enhances Postocclusive Collateral Artery Growth and Gene Expression in the Pig Hind Limb

Vascular Networks

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