Quantifying Sphingosine-1-Phosphate-Dependent Activation of the RhoGTPases

Medlin, Matt D.; Taylor, Joan M.; Mack, Christopher P.

doi:10.1007/978-1-61779-800-9_8

Cited by 2 publications

(1 citation statement)

References 14 publications

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“…Rho GTPase activity was determined by pulldown assay as previous described (28). Cells were washed with ice-cold PBS and incubated with lysis buffer (25mM HEPES, pH 7.5, 150mM NaCl, 1% NP-40, 10% glycerol, 25mM NaF, 10mM MgCl2, 1mM EDTA, 1mM sodium orthovanadate, 10µg/ml leupeptin and 10µg/ml aprotinin) for 30 min.…”

Section: Affinity Pull-down Assaymentioning

confidence: 99%

CREG1 promotes angiogenesis and neovascularization

Cao¹

2014

Front Biosci

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Angiogenesis has long been considered as an important strategy for ischemic injury. It has been reported that cellular repressor of E1A-stimulated genes (CREG1) promotes human umbilical vein endothelial cell (HUVEC) proliferation, migration, and protects endothelial cell (EC) from apoptosis. However, its potential effect on angiogenesis remains undefined. In the present study, we investigated the role and mechanisms of CREG1 in promoting angiogenesis. We found that adenovirus-transduced CREG1 expression in HUVECs increases EC tube formation in matrigel and promotes neovascularization in matrigel plugs grafted into wild type mice. In addition, adenoviral CREG1 expression enhances filopodia formation, which is accompanied by increased expression of integrin-linked kinase (ILK) and activation of its downstream effector Cdc42. Hindlimb perfusion was significantly reduced after femoral artery ligation in CREG1 heterozygous knockout mice. Finally, adenoviral CREG1 was injected intramuscularly in gastrochemius and partially restores ischemic hindlimb perfusion. Our results demonstrated that CREG1 increases EC filopodia formation and vascular assembly via ILK-Cdc42 activation and promotes neovascularization, which might be a therapeutic target for ischemic injury.

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Section: Affinity Pull-down Assaymentioning

confidence: 99%

CREG1 promotes angiogenesis and neovascularization

Cao¹

2014

Front Biosci

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WIP modulates dendritic spine actin cytoskeleton by transcriptional control of lipid metabolic enzymes

Franco-Villanueva

Fernández-López

Gabandé‐Rodríguez

et al. 2014

Human Molecular Genetics

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We identify Wiskott-Aldrich syndrome protein (WASP)-interacting protein (WIP) as a novel component of neuronal synapses whose absence increases dendritic spine size and filamentous actin levels in an N-WASP/Arp2/3-independent, RhoA/ROCK/profilinIIa-dependent manner. These effects depend on the reduction of membrane sphingomyelin (SM) due to transcriptional upregulation of neutral sphingomyelinase (NSM) through active RhoA; this enhances RhoA binding to the membrane, raft partitioning and activation in steady state but prevents RhoA changes in response to stimulus. Inhibition of NSM or SM addition reverses RhoA, filamentous actin and functional anomalies in synapses lacking WIP. Our findings characterize WIP as a link between membrane lipid composition and actin cytoskeleton at dendritic spines. They also contribute to explain cognitive deficits shared by individuals bearing mutations in the region assigned to the gene encoding for WIP.

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Quantifying Sphingosine-1-Phosphate-Dependent Activation of the RhoGTPases

Cited by 2 publications

References 14 publications

CREG1 promotes angiogenesis and neovascularization

CREG1 promotes angiogenesis and neovascularization

WIP modulates dendritic spine actin cytoskeleton by transcriptional control of lipid metabolic enzymes

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