Angiogenesis

Ergul, Adviye; Alhusban, Ahmed; Fagan, Susan C.

doi:10.1161/strokeaha.111.642710

Cited by 232 publications

(115 citation statements)

References 86 publications

(90 reference statements)

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“…In early human studies, the degree of angiogenesis was correlated with the degree of recovery [105]. Angiogenesis and vascular remodeling occur most prominently in peri-infarct tissue [106], although there are changes in vascular structure in cortex contralateral to stroke [107]. Angiogenesis initiates early after stroke, with changes in gene expression that underlie angiogenesis within days of stroke [108].…”

Section: Tissue Regeneration After Strokementioning

confidence: 99%

“…The photothrombotic stroke model, which is used in many optogenetic studies of stroke neural repair, does not produce substantial angiogenesis [65,109]. However, other stroke models with reperfusion and the production of a periinfarct region of partial damage do induce angiogenesis [29,107,110]. Angiogenesis serves to bring new blood flow to peri-infarct tissue, but this occurs too late for an actual survival effect in the evolution of stroke damage.…”

Section: Tissue Regeneration After Strokementioning

confidence: 99%

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The 3 Rs of Stroke Biology: Radial, Relayed, and Regenerative

Carmichael

2016

Neurotherapeutics

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Stroke not only causes initial cell death, but also a limited process of repair and recovery. As an overall biological process, stroke has been most often considered from the perspective of early phases of ischemia, how these inter-relate and lead to expansion of the infarct. However, just as the biology of later stages of stroke becomes better understood, the clinical realities of stroke indicate that it is now more a chronic disease than an acute killer. As an overall biological process, it is now more important to understand how early cell death leads to the later, limited recovery so as develop an integrative view of acute to chronic stroke. This progression from death to repair involves sequential stages of primary cell death, secondary injury events, reactive tissue progenitor responses, and formation of new neuronal circuits. This progression is radial: from the tissue that suffers the infarct secondary injury signals, including free radicals and inflammatory cytokines, radiate out from the stroke core to trigger later regenerative events. Injury and repair processes occur not just in the local stroke site, but are also triggered in the connected networks of neurons that had existed in the stroke center: damage signals are relayed throughout a brain network. From these relayed, distributed damage signals, reactive astrocytosis, inflammatory processes, and the formation of new connections occur in distant brain areas. In short, emerging data in stroke cell death studies and the development of the field of stroke neural repair now indicate a continuum in time and in space of progressive events that can be considered as the 3 Rs of stroke biology: radial, relayed, and regenerative.

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Section: Tissue Regeneration After Strokementioning

confidence: 99%

Section: Tissue Regeneration After Strokementioning

confidence: 99%

The 3 Rs of Stroke Biology: Radial, Relayed, and Regenerative

Carmichael

2016

Neurotherapeutics

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“…88,89 There is now mounting evidence that angiogenesis occurs in concert with neurogenesis and synaptogenesis in experimental models of recovery after ischemic brain injury. 90 These processes take place in response to a disparate range of interventions, from cortical stimulation 91 to antidepressant therapy. 92 Although the time course of angiogenesis and neurogenesis overlaps, many investigators have now concluded that the angiogenesis occurs first and leads to axonal remodeling 93 and neuroblast migration along new blood vessels.…”

Section: Stroke and Neovascularizationmentioning

confidence: 99%

“…98 Most investigators have focused their efforts on quantification of angiogenesis after stroke in the peri-infarct areas, however. 90 Recently, we showed that the angiotensin II type 1 receptor antagonist, candesartan, when administered at reperfusion in a rat model of temporary MCAO, promoted recovery and angiogenesis in the contralesional striatum at 7 days after the stroke. 99 This was confirmed in a more recent investigation where normoglycemic rats showed increased angiogenesis and recovery after stroke compared with diabetic animals, where vascular regression after stroke accompanied a much poorer functional outcome.…”

Section: Stroke and Neovascularizationmentioning

confidence: 99%

Cerebral Neovascularization in Diabetes: Implications for Stroke Recovery and beyond

Ergul

Abdelsaid

Fouda

et al. 2014

J Cereb Blood Flow Metab

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Neovascularization is an innate physiologic response by which tissues respond to various stimuli through collateral remodeling (arteriogenesis) and new vessel formation from existing vessels (angiogenesis) or from endothelial progenitor cells (vasculogenesis). Diabetes has a major impact on the neovascularization process but the response varies between different organ systems. While excessive angiogenesis complicates diabetic retinopathy, impaired neovascularization contributes to coronary and peripheral complications of diabetes. How diabetes influences cerebral neovascularization remained unresolved until recently. Diabetes is also a major risk factor for stroke and poor recovery after stroke. In this review, we discuss the impact of diabetes, stroke, and diabetic stroke on cerebral neovascularization, explore potential mechanisms involved in diabetes-mediated neovascularization as well as the effects of the diabetic milieu on poststroke neovascularization and recovery, and finally discuss the clinical implications of these effects.

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“…(1)(2)(3) All neurotrophins can enhance recovery of ischemic stroke patients through the process of angiogenesis, neurogenesis and plasticity of neurons. (1) Angiogenic genes are upregulated within minutes upon the onset of cerebral ischemia and angiogenic proteins remain increased in the ischemic area for days to weeks.…”

Section: Introductionmentioning

confidence: 99%

Vascular Endothelial Growth Factor and Brain-Derived Neurotropic Factor Levels in Ischemic Stroke Subject

et al. 2016

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BACKGROUND: Vascular endothelial growth factor (VEGF) and brain-derived neurotropic factor (BDNF) present during early neuronal development and play important roles in the process of neurorepairing includes angiogenesis, neurogenesis and neuronal plasticity after ischemic stroke. In this study, we observed VEGF and BDNF levels of subjects with ischemic stroke in different onset time.METHODS: A cross sectional study was designed. Study subjects were 51 ischemic stroke subjects, aged 30-80 years old, recruited from Gatot Subroto Army Central Hospital, Jakarta, Indonesia. Ischemic stroke was diagnosed by neurologist, based on clinical examination and magnetic resonance imaging (MRI) result. Subjects were divided into 3 groups based on onset time of stroke: <7 days (group A), 7-30 days (group B) and >30 days (Group C). VEGF and BDNF levels from serum were measured using lumine Magpix. The data was analyzed for comparison and correlation.RESULTS: VEGF and BDNF levels of group B and C were significantly different with p=0.034 and p=0.007, respectively. Group B had the highest VEGF levels, whereas Group C had the highest BDNF level. VEGF and BDNF levels in each group were not significantly correlated.CONCLUSION: Each stage of time after ischemic stroke has different recovery activities like angiogenesis, neurogenesis and plasticity. Angiogenesis process was optimum in 7-30 days after onset. in more than 30 days onset, Low VEGF with high BDNF have important role in a long period of time after the onset of stroke in the regeneration and repair, such as maintaining neuronal survival and plasticity.KEYWORDS: ischemic stroke, VEGF, BDNF

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Angiogenesis

Cited by 232 publications

References 86 publications

The 3 Rs of Stroke Biology: Radial, Relayed, and Regenerative

The 3 Rs of Stroke Biology: Radial, Relayed, and Regenerative

Cerebral Neovascularization in Diabetes: Implications for Stroke Recovery and beyond

Vascular Endothelial Growth Factor and Brain-Derived Neurotropic Factor Levels in Ischemic Stroke Subject

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