Role of angiogenesis in patients with cerebral ischemic stroke.

Krupiński, Jerzy; Kałuza, J; Kumar, Patricia; Kumar, Shant; Wang, Ji Min

doi:10.1161/01.str.25.9.1794

Cited by 772 publications

(599 citation statements)

References 23 publications

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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].…”

Section: Tissue Regeneration After Strokementioning

confidence: 99%

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%

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

Carmichael

2016

Neurotherapeutics

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“…In the early 1990s, Krupinski et al [57] analyzed brain tissues from 10 patients, and found that the number of microvessels, particularly in the penumbra, is significantly increased after cerebral ischemic stroke. The microvessel density correlates with the long-term survival of patients.…”

Section: Angiogenesis After Cerebral Ischemiamentioning

confidence: 99%

Axon guidance factor netrin-1 and its receptors regulate angiogenesis after cerebral ischemia

Ding

Liao

2014

Neurosci. Bull.

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Neurogenesis and angiogenesis play important roles in functional recovery after ischemic stroke. When cerebral ischemia occurs, axon regeneration can compensate for the loss of apoptotic neurons in the ischemic area. The formation of new blood vessels ameliorates the local decrease in blood supply, enhancing the supply of oxygen and nutrients to newly-formed neurons. New blood vessels also act as a scaffold for the migration of neuroblasts to the infarct area after ischemic stroke. In light of this, researchers have been actively searching for methods to treat cerebral infarction. Netrins were fi rst identifi ed as a family of proteins that mediate axon guidance and direct axon migration during embryogenesis. Later studies have revealed other functions of this protein family. In this review, we focus on netrin-1, which has been shown to be involved in axon migration and angiogenesis, which are required for recovery after cerebral ischemia. Thus, therapies targeting netrin-1 may be useful for the treatment of ischemic stroke.

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“…New vasculature created by angiogenesis at the ischemic border becomes evident at 2 to 4 days after focal ischemia in rats (Hermann and Zechariah, 2009) and correlates with survival in ischemic stroke patients (Krupinski et al, 1994), suggesting that it is a natural recovery process in periinfarct regions. Chronically, hyperperfusion occurs when vasoactive agents such as nitric oxide or adenosine arise from the endothelium or glia (Iadecola and Nedergaard, 2007) and promote CBF increase to serve cellular processes with high energy demands.…”

Section: Delayed Hyperperfusion Coincides With Angiogenesis In the Thmentioning

confidence: 99%

Chronic Hyperperfusion and Angiogenesis Follow Subacute Hypoperfusion in the Thalamus of Rats with Focal Cerebral Ischemia

Hayward

Yanev

Haapasalo

et al. 2010

J Cereb Blood Flow Metab

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Cerebral blood flow (CBF) is disrupted after focal ischemia in rats. We examined long-term hemodynamic and cerebrovascular changes in the rat thalamus after focal cerebral ischemia. Cerebral blood flow quantified by arterial spin labeling magnetic resonance imaging was decreased in the ipsilateral and contralateral thalamus 2 days after cerebral ischemia. Partial thalamic CBF recovery occurred by day 7, then the ipsilateral thalamus was chronically hyperperfused at 30 days and 3 months compared with its contralateral side. This contrasted with permanent hypoperfusion in the ipsilateral cortex. Angiogenesis was indicated by endothelial cell (RECA-1) immunohistochemistry that showed increased blood vessel branching in the ipsilateral thalamus at the end of the 3-month follow-up. Only transient thalamic IgG extravasation was observed, indicating that the blood-brain barrier was intact after day 2. Angiogenesis was preceded by transiently altered expression levels of cadherin family adhesion molecules, cadherin-7, protocadherin-1, and protocadherin-17. In conclusion, thalamic pathology after focal cerebral ischemia involved longterm hemodynamic changes and angiogenesis preceded by altered expression of vascular adhesion factors. Postischemic angiogenesis in the thalamus represents a novel type of remote plasticity, which may support removal of necrotic brain tissue and aid functional recovery.

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Role of angiogenesis in patients with cerebral ischemic stroke.

Cited by 772 publications

References 23 publications

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

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

Axon guidance factor netrin-1 and its receptors regulate angiogenesis after cerebral ischemia

Chronic Hyperperfusion and Angiogenesis Follow Subacute Hypoperfusion in the Thalamus of Rats with Focal Cerebral Ischemia

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