Differential gene and protein expression in abluminal sprouting and intraluminal splitting forms of angiogenesis

Williams, James L.; Weichert, Alexander; Zakrzewicz, Andreas; Silva-Azevedo, Luis Da; Pries, Axel R.; Baum, Oliver; Egginton, Stuart

doi:10.1042/cs20050185

Cited by 59 publications

(80 citation statements)

References 46 publications

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“…Over-expression of VEGF simultaneously with Ang-1 or Ang-2 results in large vessels and small holes in the casts of capillaries [60], a sign of intussusceptive angiogenesis. Molecules specifically associated with cell migration such as neuropilin, restin, and midkine are down-regulated during the phase of intussusceptive angiogenesis [22]. To date, no direct evidence linking a specific molecule to intussusceptive angiogenesis has been adduced.…”

Section: Molecular Controlmentioning

confidence: 99%

“…Such protrusions are followed by endothelial cell contacts, reorganization of endothelial cell junctions and invasions of the pillar core by myofibroblasts and pericytes, which lay down collagen fibrils [2,3]. The most important growth factor in angiogenesis is VEGF and is known to support both sprouting and intussusceptive angiogenesis [18,19,22]. Other endothelial growth factors implicated in IA include bFGF [18,19] and PDGF-B [18].…”

Section: Molecular Controlmentioning

confidence: 99%

“…The pillar is indicated with an arrow while Er denotes an erythrocyte. Obtained from [12], with permission has been given different names such as longitudinal splitting [20], longitudinal division [21], intraluminal splitting angiogenesis [22], or internal division [23]. Notably, the direction taken by pillars in relation to the axis of the remodeling vessels depends on the targeted outcomes.…”

Section: Phases and Phenotypes Of Intussusceptive Angiogenesismentioning

confidence: 99%

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Intussusceptive angiogenesis and its role in vascular morphogenesis, patterning, and remodeling

2009

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New blood vessels arise initially as blood islands in the process known as vasculogenesis or as new capillary segments produced through angiogenesis. Angiogenesis itself encompasses two broad processes, namely sprouting (SA) and intussusceptive (IA) angiogenesis. Primordial capillary plexuses expand through both SA and IA, but subsequent growth and remodeling are achieved through IA. The latter process proceeds through transluminal tissue pillar formation and subsequent vascular splitting, and the direction taken by the pillars delineates IA into overt phases, namely: intussusceptive microvascular growth, intussusceptive arborization, and intussusceptive branching remodeling. Intussusceptive microvascular growth circumscribes the process of initiation of pillar formation and their subsequent expansion with the result that the capillary surface area is greatly enhanced. In contrast, intussusceptive arborization entails formation of serried pillars that remodel the disorganized vascular meshwork into the typical tree-like arrangement. Optimization of local vascular branching geometry occurs through intussusceptive branching remodeling so that the vasculature is remodeled to meet the local demand. In addition, IA is important in creation of the local organspecific angioarchitecture. While hemodynamic forces have proven direct effects on IA, with increase in blood flow resulting in initiation of pillars, the preponderant mechanisms are unclear. Molecular control of IA has so far not been unequivocally elucidated but interplay among several factors is probably involved. Future investigations are strongly encouraged to focus on interactions among angiogenic growth factors, angiopoetins, and related receptors.

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Section: Molecular Controlmentioning

confidence: 99%

Section: Molecular Controlmentioning

confidence: 99%

Section: Phases and Phenotypes Of Intussusceptive Angiogenesismentioning

confidence: 99%

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Intussusceptive angiogenesis and its role in vascular morphogenesis, patterning, and remodeling

2009

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“…2006c) and perhaps eNOS phosphorylation by a glycocalyx‐linked deformation of caveolae (Pahakis et al . 2007).…”

Section: Discussionmentioning

confidence: 99%

“…VEGF is vital in physiological angiogenesis: its blockade results in the absence of capillary growth following chronic hyperaemia or muscle overload (Williams et al . 2006a,c, Uchida et al . 2015).…”

mentioning

confidence: 99%

Shear stress‐induced angiogenesis in mouse muscle is independent of the vasodilator mechanism and quickly reversible

et al. 2016

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AimIs modulation of skeletal muscle capillary supply by altering blood flow due to a presumptive shear stress response per se, or dependent on the vasodilator mechanism?MethodsThe response to four different vasodilators, and cotreatment with blockers of NO and prostaglandin synthesis, was compared. Femoral artery blood flow was correlated with capillary‐to‐fibre ratio (C:F) and protein levels of putative angiogenic compounds.ResultsAll vasodilators induced a similar increase in blood flow after 14 days, with a similar effect on C:F (1.62 ± 0.05, 1.60 ± 0.01, 1.57 ± 0.06, 1.57 ± 0.07, respectively, all P < 0.05 vs. control 1.20 ± 0.01). Concomitant inhibitors revealed differential effects on blood flow and angiogenesis, demonstrating that a similar response may have different signalling origins. The time course of this response with the most commonly used vasodilator, prazosin, showed that blood flow increased from 0.40 mL min−1 to 0.61 mL min−1 by 28 days (P < 0.05), dropped within 1 week after the cessation of treatment (0.54 mL min−1; P < 0.05) and returned to control levels by 6 weeks. In parallel with FBF, capillary rarefaction began within 1 week (P < 0.05), giving C:F values similar to control by 2 weeks. Of the dominant signalling pathways, prazosin decreased muscle VEGF, but increased its cognate receptor Flk‐1 (both P < 0.01); levels of eNOS varied with blood flow (P < 0.05), and Ang‐1 initially increased, while its receptor Tie‐2 was unchanged, with only modest changes in the antiangiogenic factor TSP‐1.ConclusionHyperaemia‐induced angiogenesis, likely in response to elevated shear stress, is independent of the vasodilator involved, with a rapid induction and quick regression following the stimulus withdrawal.

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Exercise Training and Peripheral Arterial Disease

Haas

Lloyd

Yang

et al. 2012

Comprehensive Physiology

121

108

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Peripheral arterial disease (PAD) is a common vascular disease that reduces blood flow capacity to the legs of patients. PAD leads to exercise intolerance that can progress in severity to greatly limit mobility, and in advanced cases leads to frank ischemia with pain at rest. It is estimated that 12–15 million people in the United States are diagnosed with PAD, with a much larger population that is undiagnosed. The presence of PAD predicts a 50–1500% increase in morbidity and mortality, depending on severity. Treatment of patients with PAD is limited to modification of cardiovascular disease risk factors, pharmacological intervention, surgery, and exercise therapy. Extended exercise programs that involve walking ~5 times/wk, at a significant intensity that requires frequent rest periods, are most significant. Pre-clinical studies and virtually all clinical trials demonstrate the benefits of exercise therapy, including: improved walking tolerance, modified inflammatory/hemostatic markers, enhanced vasoresponsiveness, adaptations within the limb (angiogenesis, arteriogenesis, mitochondrial synthesis) that enhance oxygen delivery and metabolic responses, potentially delayed progression of the disease, enhanced quality of life indices, and extended longevity. A synthesis is provided as to how these adaptations can develop in the context of our current state of knowledge and events known to be orchestrated by exercise. The benefits are so compelling that exercise prescription should be an essential option presented to patients with PAD in the absence of contraindications. Obviously, selecting for a life style pattern, that includes enhanced physical activity prior to the advance of PAD limitations, is the most desirable and beneficial.

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Differential gene and protein expression in abluminal sprouting and intraluminal splitting forms of angiogenesis

Cited by 59 publications

References 46 publications

Intussusceptive angiogenesis and its role in vascular morphogenesis, patterning, and remodeling

Intussusceptive angiogenesis and its role in vascular morphogenesis, patterning, and remodeling

Shear stress‐induced angiogenesis in mouse muscle is independent of the vasodilator mechanism and quickly reversible

Exercise Training and Peripheral Arterial Disease

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