Sphingosine 1-phosphate receptor regulation of N-cadherin mediates vascular stabilization

Paik, Jihye; Skoura, Athanasia; Chae, Sung-Suk; Cowan, Ann E.; Han, David K.; Proia, Richard L.; Hla, Timothy

doi:10.1101/gad.1227804

Cited by 248 publications

(202 citation statements)

References 64 publications

(65 reference statements)

Supporting

Mentioning

190

Contrasting

Order By: Relevance

“…PP protrusions S1pr1 in MKs controls PPF. As reported previously for endothelial cells (Paik et al, 2004), we found that S1P, and also the S1pr1-specific agonist SEW2871, enhances Rac GTPase activity via S1pr1 in megakaryocytic cell lines (Fig. 4,E and F).…”

Section: S1pr1 Is Essential For Intravascular Pp Formation (Ppf)supporting

confidence: 65%

A novel role of sphingosine 1-phosphate receptor S1pr1 in mouse thrombopoiesis

Zhang¹,

Orban²,

Lorenz³

et al. 2012

J Cell Biol

Self Cite

View full text Add to dashboard Cite

Section: S1pr1 Is Essential For Intravascular Pp Formation (Ppf)supporting

confidence: 65%

A novel role of sphingosine 1-phosphate receptor S1pr1 in mouse thrombopoiesis

Zhang¹,

Orban²,

Lorenz³

et al. 2012

J Cell Biol

Self Cite

View full text Add to dashboard Cite

“…The intermediary pathways that allow SphK2 to regulate the expression and localization of the junctional proteins at the BBB have yet to be clarified, but it would not be unexpected if SphK2-derived S1P signaling proceeded via mediators and pathways already known to regulate BBB tight junctions and/or BBB permeability, such as nitric oxide, vascular endothelial growth factor, proteases, and reactive oxygen species, as well as the actin cytoskeleton, caveolae, and pericytes (Sandoval and Witt, 2008). Indeed, there is evidence from studies in the peripheral vasculature that S1P activates endothelial nitric oxide synthase via PI3K/ Akt, counteracts the deleterious effects of reactive oxygen species on vascular endothelium via ERK1/2 and endothelial nitric oxide synthase (Igarashi and Michel, 2008), and regulates pericyte recruitment via N-cadherin signaling (Paik et al, 2004). Sphingosine-1-phosphate R1 receptor activation also induces intracellular calcium release from the endoplasmic reticulum and Rac-1 activation, promoting adherens junction formation at the endothelial cell periphery that can block vascular endothelial growth factorinduced vascular permeability (Hoang et al, 2011;Mehta et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Junctional Protein Regulation by Sphingosine Kinase 2 Contributes to Blood–Brain Barrier Protection in Hypoxic Preconditioning-Induced Cerebral Ischemic Tolerance

Wacker

Freie

Perfater

et al. 2012

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

Protection of the blood-brain barrier (BBB) is correlated with improved outcome in stroke. Sphingosine kinase (SphK)-directed production of sphingosine-1-phosphate, which we previously documented as being vital to preconditioning-induced stroke protection, mediates peripheral vascular integrity via junctional protein regulation. We used a hypoxic preconditioning (HPC) model in adult wild-type and SphK2-null mice to examine the isoform-specific role of SphK2 signaling for ischemic tolerance to transient middle cerebral artery occlusion and attendant BBB protection. Reductions in infarct volume and BBB permeability in HPC-treated mice were completely lost in SphK2-null mice. Hypoxic preconditioning-induced attenuation of postischemic BBB disruption in wild types, evidenced by reduced extravascular immunoglobulin G intensity, suggests direct protection of BBB integrity. Measurement of BBB junctional protein status in response to HPC revealed SphK2-dependent increases in triton-insoluble claudin-5 and VE-cadherin, which may serve to strengthen the BBB before stroke. Postischemic loss of VE-cadherin, occludin, and zona occludens-1 in SphK2-null mice with prior HPC suggests that SphK2-dependent protection of these adherens and tight junction proteins is compulsory for HPC to establish a vasculoprotective phenotype. Further elucidation of the mediators of this endogenous, HPC-activated lipid signaling pathway, and their role in protecting the ischemic BBB, may provide new therapeutic targets for cerebrovascular protection in stroke patients.

show abstract

“…S1P 1 activation enhances the recruitment of pericytes to remodeling vessels (6,34). Recent evidence by Stark et al identifies interactions between arterial pericytes and CX3CR1 + monocytes during inflammation (32), which may suggest that pericytes play multiple roles in regulation of vascular and inflammatory modulation.…”

Section: Discussionmentioning

confidence: 99%

Sphingosine 1-phosphate receptor 3 regulates recruitment of anti-inflammatory monocytes to microvessels during implant arteriogenesis

Awojoodu

Ogle

Sefcik

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

135

229

View full text Add to dashboard Cite

Endothelial cells play significant roles in conditioning tissues after injury by the production and secretion of angiocrine factors. At least two distinct subsets of monocytes, CD45 + CD11b + Gr1 + Ly6C + inflammatory and CD45 + CD11b + Gr1 − Ly6C − anti-inflammatory monocytes, respond differentially to these angiocrine factors and promote pathogen/debris clearance and arteriogenesis/tissue regeneration, respectively. We demonstrate here that local sphingosine 1-phosphate receptor 3 (S1P 3 ) agonism recruits anti-inflammatory monocytes to remodeling vessels. Poly(lactic-co-glycolic acid) thin films were used to deliver FTY720, an S1P 1/3 agonist, to inflamed and ischemic tissues, which resulted in a reduction in proinflammatory cytokine secretion and an increase in regenerative cytokine secretion. The altered balance of cytokine secretion results in preferential recruitment of antiinflammatory monocytes from circulation. The chemotaxis of these cells, which express more S1P 3 than inflammatory monocytes, toward SDF-1α was also enhanced with FTY720 treatment, but not in S1P 3 knockout cells. FTY720 delivery enhanced arteriolar diameter expansion and increased length density of the local vasculature. This work establishes a role for S1P receptor signaling in the local conditioning of tissues by angiocrine factors that preferentially recruit regenerative monocytes that can enhance healing outcomes, tissue regeneration, and biomaterial implant functionality.sphingolipid | microvascular remodeling | biomaterials | immunomodulation | tissue engineering

show abstract

Sphingosine 1-phosphate receptor regulation of N-cadherin mediates vascular stabilization

Abstract: [Keywords: sphingosine 1-phosphate; cadherin; angiogenesis; vascular stabilization; endothelial cells; pericytes] Supplemental material is available at http://www.genesdev.org.

Cited by 248 publications

References 64 publications

A novel role of sphingosine 1-phosphate receptor S1pr1 in mouse thrombopoiesis

A novel role of sphingosine 1-phosphate receptor S1pr1 in mouse thrombopoiesis

Junctional Protein Regulation by Sphingosine Kinase 2 Contributes to Blood–Brain Barrier Protection in Hypoxic Preconditioning-Induced Cerebral Ischemic Tolerance

Sphingosine 1-phosphate receptor 3 regulates recruitment of anti-inflammatory monocytes to microvessels during implant arteriogenesis

Contact Info

Product

Resources

About