Localization of Angiopoietin-1 and Tie2 Immunoreactivity in Rodent Ependyma and Adjacent Blood Vessels Suggests Functional Relationships

Horton, Brooke; Solanki, Rajanikant B.; Rajneesh, Kiran; Kulesza, Piotr; Ardelt, Agnieszka

doi:10.1369/jhc.2009.954610

Cited by 10 publications

(3 citation statements)

References 18 publications

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“…This is in accordance with previous reports showing that sources of Ang-1 include perivascular astrocytes, endothelial cells, ependymal cells, and the choroid plexus (Acker et al, 2001;Nourhaghighi et al, 2003;Ward et al, 2005;Ohab et al, 2006;Tonchev et al, 2007;Fukuhara et al, 2008;Horton et al, 2010). Moreover, Ang-1 mRNA was detected in SVZ from adult mice (Liu et al, 2009), and we showed that proliferating DCXpositive neuroblasts and EGFR-positive progenitors express Tie-2.…”

Section: Discussionsupporting

confidence: 93%

The Angiogenic Factor Angiopoietin-1 Is a Proneurogenic Peptide on Subventricular Zone Stem/Progenitor Cells

Rosa¹,

Gonçalves²,

Cortes³

et al. 2010

J. Neurosci.

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Section: Discussionsupporting

confidence: 93%

The Angiogenic Factor Angiopoietin-1 Is a Proneurogenic Peptide on Subventricular Zone Stem/Progenitor Cells

Rosa¹,

Gonçalves²,

Cortes³

et al. 2010

J. Neurosci.

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“…ANGPT1 is expressed in astrocytes, neurons, pericytes and endothelial cells but is predominantly expressed by astrocytes in the brain 43–46 . Angiopoietin-1 has previously been shown to reduce infarct size by stabilizing endothelial cell integrity, reducing blood brain barrier permeability, and promoting angiogenesis 47–49 .…”

Section: Discussionmentioning

confidence: 99%

Integrative Mouse and Human Studies Implicate ANGPT1 and ZBTB7C as Susceptibility Genes to Ischemic Injury

Zhou

Lorenzano

et al. 2015

Stroke

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Background and Purpose The extent of ischemic injury in response to cerebral ischemia is known to be affected by native vasculature. However, the non-vascular and dynamic vascular responses and their genetic basis are not well-understood. Methods We performed a genome-wide association study in 235 mice from 33 inbred strains using the middle cerebral artery occlusion model. Population structure and genetic relatedness were accounted for by using the efficient mixed-model association method. Human orthologs to the genes associated with the significant and suggestive SNPs from the mouse strain survey were examined in patients with M1 occlusions admitted with signs and symptoms of acute ischemic stroke. Results We identified four genome-wide significant and suggestive SNPs to be associated with infarct volume in mice (rs3694965, p=2.17×10−7; rs31924033, p=5.61×10−6; rs32249495, p=2.08×10−7; rs3677406, p=9.56×10−6). Rs32249495, which corresponds to angiopoietin-1 (ANGPT1), was also significant in the recessive model in humans, while rs1944577, which corresponds to ZBTB7C was nominally significant in both the additive and dominant genetic models in humans. ZBTB7C was shown to be upregulated in endothelial cells using both in vitro and in vivo models of ischemia. Conclusions Genetic variations of ANGPT1 and ZBTB7C are associated with increased infarct size in both mice and humans. ZBTB7C may modulate the ischemic response via neuronal apoptosis as well as dynamic collateralization and, in addition to ANGPT1, may serve as potential novel targets for treatments of cerebral ischemia.

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“…This ligand–receptor binding triggers pericyte proliferation and migration along the newly formed vascular sprout which stabilizes the newly formed vessel [ 21 , 22 , 23 ]. Other pathways known to be involved in endothelial-pericyte crosstalk include angiopoietin/Tie2 [ 24 , 25 ] transforming growth factor (TGF) superfamily signaling [ 26 , 27 ] and vascular endothelial growth factor (VEGF) [ 18 , 28 ].…”

Section: Pericytes – Mural Cells Of Capillaries That Play Roles In Anmentioning

confidence: 99%

The role played by perivascular cells in kidney interstitial injury

Rojas¹,

Chang²,

Lin³

et al. 2012

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Fibrosis of the kidney is a disease affecting millions worldwide and is a harbinger of progressive loss of organ function resulting in organ failure. Recent findings suggest that understanding mechanisms of development and progression of fibrosis will lead to new therapies urgently required to counteract loss of organ function. Recently, little-known cells that line the kidney microvasculature, known as pericytes, were identified as the precursor cells which become the scar-forming myofibroblasts. Kidney pericytes are extensively branched cells located in the wall of capillaries, embedded within the microvascular basement membrane, and incompletely envelope endothelial cells with which they establish focal contacts. In response to kidney injuries, pericytes detach from endothelial cells and migrate into the interstitial space where they undergo a transition into myofibroblasts. Detachment leads to fibrosis but also leaves an unstable endothelium, prone to rarefaction. Endothelial-pericyte crosstalk at the vascular endothelial growth factor receptors and platelet derived growth factor receptors in response to injury have been identified as major new targets for therapeutic intervention.

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Localization of Angiopoietin-1 and Tie2 Immunoreactivity in Rodent Ependyma and Adjacent Blood Vessels Suggests Functional Relationships

Cited by 10 publications

References 18 publications

The Angiogenic Factor Angiopoietin-1 Is a Proneurogenic Peptide on Subventricular Zone Stem/Progenitor Cells

The Angiogenic Factor Angiopoietin-1 Is a Proneurogenic Peptide on Subventricular Zone Stem/Progenitor Cells

Integrative Mouse and Human Studies Implicate ANGPT1 and ZBTB7C as Susceptibility Genes to Ischemic Injury

The role played by perivascular cells in kidney interstitial injury

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