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

Rosa, Agostinho; Gonçalves, Joana; Cortes, Luísa; Bernardino, Liliana; Malva, João O.; Agasse, Fabienne

doi:10.1523/jneurosci.5597-09.2010

Cited by 61 publications

(48 citation statements)

References 76 publications

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“…In addition to its role in regulating vessel growth, a growing body of evidence shows that Ang 1 is a survival factor that can enhance endothelial cell [14,43], cardiomyocyte [44,45], and neuronal cell survival [28,46]. The ability of HSYA to increase Ang 1 expression may be a mechanism by which HSYA protects cells from the effects of various injuries, such as ischemia [35,47], hypoxia [18,24], and methylglyoxal exposure [48], by inhibiting apoptosis.…”

Section: Discussionmentioning

confidence: 99%

“…HUVEC (3 × 10 4 ) were added to the upper chambers and treated with HSYA (0, 1, 10, and 50 μ M ). In some experiments, the cells were exposed to HSYA (10 μ M ) with or without the anti-Tie-2 neutralizing antibody (10 μg/mL) [27,28]. After 24 h of incubation at 37°C in a humidified chamber with 5% CO 2 , the porous membranes were rinsed and the cells remaining in the upper chamber were removed using a cotton swab.…”

Section: Methodsmentioning

confidence: 99%

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Hydroxysafflor Yellow A Promotes Angiogenesis via the Angiopoietin 1/ Tie-2 Signaling Pathway

Chen¹,

Chen

Pang

et al. 2016

J Vasc Res

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Background: The flowers of Carthamus tinctorius L. are widely used in traditional Chinese medicine to treat cerebrovascular and cardiovascular diseases. Hydroxysafflor yellow A (HSYA), the main constituent of C. tinctorius L. flowers, is known for its multiple biological activities. The present study investigated the effects of HSYA on angiogenesis in vitro and in a mouse hindlimb ischemia model. Methods: Using human umbilical vein endothelial cells (HUVEC) in vitro and a mouse hindlimb ischemia model in vivo, the angiogenic role of HSYA was evaluated. Results: HSYA significantly increased the capillary-like tube formation and migration of HUVEC. HSYA not only induced a rise in the expression of angiopoietin 1 and Tie-2 but it also increased phosphorylation of Tie-2, Akt, and extracellular signal-regulated kinase 1/2. Furthermore, an anti-Tie-2 neutralizing antibody significantly inhibited HSYA-induced HUVEC tube formation and migration. In vivo, the recovery of perfusion of ischemic hindlimb tissue after femoral artery interruption was significantly increased in HSYA-treated mice compared to vehicle controls. Consistent with these results, the arteriole and capillary densities in ischemic gastrocnemius muscles were significantly increased in HSYA-treated mice. Conclusions: These results indicate the potential utility of HSYA for the treatment of ischemic diseases.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Hydroxysafflor Yellow A Promotes Angiogenesis via the Angiopoietin 1/ Tie-2 Signaling Pathway

Chen¹,

Chen

Pang

et al. 2016

J Vasc Res

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“…In these conditions, SVZ cells grow in suspension and generate neurospheres that are rich in neural and progenitor stem cells at distinct stages of differentiation and with proliferative and selfrenewing abilities, as previously shown by us [7,24,[27][28][29][30]. Five to six-day-old neurospheres were seeded onto 0.1 mg/mL poly-D-lysine-(PDL; Sigma-Aldrich Co. Zeiss, Jena, Germany).…”

Section: Svz Cell Cultures and Experimental Treatmentsmentioning

confidence: 99%

MicroRNA-124 loaded nanoparticles enhance brain repair in Parkinson's disease

Saraiva

Paiva

Santos

et al. 2016

Journal of Controlled Release

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143

128

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Modulation of the subventricular zone (SVZ) neurogenic niche can enhance brain repair in several disorders including Parkinson's disease (PD). Herein, we used biocompatible and traceable polymeric nanoparticles (NPs) containing perfluoro-1,5-crown ether (PFCE) and coated with protamine sulfate to complex microRNA-124 (miR-124), a neuronal fate determinant. The ability of NPs to efficiently deliver miR-124 and prompt SVZ neurogenesis and brain repair in PD was evaluated. In vitro, miR-124 NPs were efficiently internalized by neural stem/progenitors cells and neuroblasts and promoted their neuronal commitment and maturation. The expression of Sox9 and Jagged1, two miR-124 targets and stemness-related genes, were also decreased upon miR-124 NP treatment. In vivo, the intracerebral administration of miR-124 NPs increased the number of migrating neuroblasts that reached the granule cell layer of the olfactory bulb, both in healthy and in a 6-hydroxydopamine (6-OHDA) mouse model for PD.MiR-124 NPs were also able to induce migration of neurons into the lesioned striatum of 6-OHDA-treated mice. Most importantly, miR-124 NPs proved to ameliorate motor symptoms of 6-OHDA mice, monitored by the apomorphine-induced rotation test.Altogether, we provide clear evidences to support the use of miR-124 NPs as a new therapeutic approach to boost endogenous brain repair mechanisms in a setting of neurodegeneration.

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“…After focal stroke, endothelial cells express Ang-1, which acts on Tie-2 receptors on neuroblasts to promote emigration (89). A recent study found that Ang-1 also promotes SVZ proliferation constitutively (96). In addition, extracellular matrix proteins associated with blood vessels such as laminin are important for the maintenance of neural precursor cells (79,102).…”

Section: Role Of Angiogenic Vasculature As Substrate For Migrationmentioning

confidence: 99%

Cellular and Molecular Determinants of Stroke-Induced Changes in Subventricular Zone Cell Migration

Young

Brooks

Buchan

et al. 2011

Antioxidants & Redox Signaling

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A remarkable aspect of adult neurogenesis is that the tight regulation of subventricular zone (SVZ) neuroblast migration is altered after ischemic stroke and newborn neurons emigrate towards the injury. This phenomenon is an essential component of endogenous repair and also serves to illuminate normal mechanisms and rules that govern SVZ migration. Stroke causes inflammation that leads to cytokine and chemokine release, and SVZ neuroblasts that express their receptors are recruited. Metalloproteinases create pathways and new blood vessels provide a scaffold to facilitate neuroblast migration between the SVZ and the infarct. Most experiments have studied the peri-lesion parenchyma and relatively little is known about SVZ remodeling after stroke. Migration in the SVZ is tightly regulated by cellular interactions and molecular signaling; how are these altered after stroke to allow emigration? Do ependymal cells contribute to this process, given their reported neurogenic potential? How does stroke affect ependymal cell regulation of cerebrospinal fluid flow? Given the heterogeneity of SVZ progenitors, do all types of neuroblasts migrate out, or is this confined to specific subtypes of cells? We discuss these and other questions in our review and propose experiments to address them.

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

Cited by 61 publications

References 76 publications

Hydroxysafflor Yellow A Promotes Angiogenesis via the Angiopoietin 1/ Tie-2 Signaling Pathway

Hydroxysafflor Yellow A Promotes Angiogenesis via the Angiopoietin 1/ Tie-2 Signaling Pathway

MicroRNA-124 loaded nanoparticles enhance brain repair in Parkinson's disease

Cellular and Molecular Determinants of Stroke-Induced Changes in Subventricular Zone Cell Migration

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