Expression of Angiopoietin-1, Angiopoietin-2, and Tie Receptors after Middle Cerebral Artery Occlusion in the Rat

Beck, Heike; Acker, Till; Wiessner, Christoph; Allegrini, Peter R.; Plate, Karl H.

doi:10.1016/s0002-9440(10)64786-4

Cited by 187 publications

(157 citation statements)

References 41 publications

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“…The abrupt up-regulation of Ang-2 mRNA during non-neoplastic cerebral angiogenesis has been described previously in human arteriovenous malformations (Hashimoto et al, 2001), after systemic hypoxia in rat brain (Mandriota et al, 2000), and in infarcts produced by middle cerebral artery occlusion in the rat (Beck et al, 2000). Unlike the present study, Ang-1 mRNA levels in these models were similar or only slightly increased compared with control brains.…”

Section: Ang-1 and Ang-2 Expression During Cerebral Angiogenesissupporting

confidence: 58%

“…Ang-1 and Ang-2 mRNA were localized in neurons, whereas Ang-1 was also observed in vessels (Stratmann et al, 1998). Subsequent studies reported only Ang-1 mRNA in glia and cerebellar Purkinje cells (Beck et al, 2000;Hashimoto et al, 2001) but not in blood vessels, whereas another study failed to demonstrate Ang-1 or Ang-2 mRNA in normal brain (Zagzag et al, 1999). These inconsistent results may be a result of technical difficulties such as fixation techniques and probe sensitivity.…”

Section: Ang-1 Ang-2 and Tie-2 Mrna Expression In Normal Brainmentioning

confidence: 99%

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Altered Expression of Angiopoietins During Blood-Brain Barrier Breakdown and Angiogenesis

Nourhaghighi

Teichert-Kuliszewska

Davis

et al. 2003

Laboratory Investigation

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SUMMARY:Angiopoietin-1 (Ang-1) and angiopoietin-2 (Ang-2) belong to a novel family of endothelial growth factors that function as ligands for the endothelial-specific receptor tyrosine kinase, Tie-2. Ang-1 reduces endothelial permeability of noncerebral vessels and has a major role in vascular stabilization and maturation, whereas Ang-2 is thought to be an endogenous antagonist of the action of Ang-1 at Tie-2. Expression of these ligands at the mRNA and protein level were studied during both blood-brain barrier (BBB) breakdown and cerebral angiogenesis occurring in the rat cortical cold-injury model by RT-PCR analysis and immunohistochemistry respectively, during a time course of 6 hours to 6 days. In addition, immunohistochemical detection of fibronectin was used to detect BBB breakdown at the lesion site and dual labeling was used to determine whether the vessels demonstrating BBB breakdown expressed endothelial Ang-1 or Ang-2. Endothelial Ang-1 and Tie-2 proteins were present in all cerebral vessels of normal brain including those of the choroid plexuses, whereas both these proteins as well as Ang-2 were present in choroid plexus epithelium and in ependymal cells, suggesting that angiopoietins have an autocrine effect on these cell types as well. In contrast, in the early phase after injury during the known period of BBB breakdown, increased Ang-2 mRNA and protein and decreased endothelial Ang-1 and Tie-2 proteins were observed. Two to 6 days after injury, the progressive increase in Ang-1 mRNA and protein and the decrease in Ang-2 coincided with cerebrovascular angiogenesis. Confocal microscopy showed colocalization of both Ang-1 and Ang-2 in endothelium of lesion vessels, and our observation of colocalization of Ang-1 and Ang-2 in polymorphonuclear leukocytes and macrophages has not been reported previously. This study demonstrates that Ang-1 is an important factor in maintaining normal homeostasis in the brain. Thus Ang-1 therapy may have therapeutic potential in reducing BBB breakdown and the ensuing edema after massive brain injury. (Lab Invest 2003, 83:1211-1222.

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Section: Ang-1 and Ang-2 Expression During Cerebral Angiogenesissupporting

confidence: 58%

Section: Ang-1 Ang-2 and Tie-2 Mrna Expression In Normal Brainmentioning

confidence: 99%

Altered Expression of Angiopoietins During Blood-Brain Barrier Breakdown and Angiogenesis

Nourhaghighi

Teichert-Kuliszewska

Davis

et al. 2003

Laboratory Investigation

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“…It is quite possible that the effect of Ang2 depends on differences in the VEGF levels (Goede et al, 1998;Holash et al, 1999;Beck et al, 2000). Our data provide evidence of a complementary Membrane fractions were collected 72 h after transfection and analysed by western blotting for Tie2 protein levels as described previously (Lee et al, 2006b).…”

mentioning

confidence: 57%

“…Several studies have shown that this contextual behavior of Ang2 is, at least partially, dependent on VEGF levels. Ang2 appears to initiate and stimulate angiogenesis when acting together with VEGF, but to induce vessel regression in the absence of VEGF (Goede et al, 1998;Holash et al, 1999;Beck et al, 2000). Such a coordinated effect implies the existence of certain mechanisms that both temporally and spatially govern the expression of these molecules and hence their concurrent or sequential effect on tumorigenesis.…”

mentioning

confidence: 99%

Angiopoietin-2 decreases vascular endothelial growth factor expression by modulating HIF-1α levels in gliomas

Lee

Fueyo

et al. 2007

Oncogene

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“…Using cDNA analysis, Hayashi et al [59] examined the expression levels of 96 angiogenesis-related genes after transient MCAO (tMCAO) in mice, and found that 42, 29, and 13 genes are upregulated at 1 h, 1 day, and 21 days, respectively, after transient occlusion. Beck et al [60] found that the mRNA expression of angiogenin-2, which promotes angiogenesis, is upregulated after 6 h of occlusion in MCAO rats. These changes lead to the synthesis of pro-angiogenic proteins such as VEGF.…”

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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Expression of Angiopoietin-1, Angiopoietin-2, and Tie Receptors after Middle Cerebral Artery Occlusion in the Rat

Abstract: Experimental models and studies on stroke patients have shown that hypoxia/ischemia induces vascular proliferation in the peri-infarct area.

Cited by 187 publications

References 41 publications

Altered Expression of Angiopoietins During Blood-Brain Barrier Breakdown and Angiogenesis

Altered Expression of Angiopoietins During Blood-Brain Barrier Breakdown and Angiogenesis

Angiopoietin-2 decreases vascular endothelial growth factor expression by modulating HIF-1α levels in gliomas

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

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