Role of reactive oxygen species in inhibition of endothelial cell migration by oxidized low-density lipoprotein

Aalst, John A. van; Zhang, Dong Mei; Miyazaki, Keiko; Colles, Scott M.; Fox, Paul L.; Graham, Linda M.

doi:10.1016/j.jvs.2004.09.020

Cited by 25 publications

(32 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…LysoPC affects a number of cellular properties, including membrane fluidity, production of reactive oxygen species, intracellular calcium concentration, and other signaling pathways. [5][6][7] LysoPC can activate protein kinase C (PKC) in ECs, 8 but the specific isoforms activated have not been reported.…”

mentioning

confidence: 99%

Protein Kinase Cδ–Dependent Phosphorylation of Syndecan-4 Regulates Cell Migration

Chaudhuri

Colles

Fox

et al. 2005

Circulation Research

Self Cite

View full text Add to dashboard Cite

Abstract-Endothelial cell (EC) migration is a complex process requiring exquisitely coordinated focal adhesion assembly and disassembly. Protein kinase C (PKC) is known to regulate focal adhesion formation. Because lysophosphatidylcholine (lysoPC), a major lipid constituent of oxidized low-density lipoprotein, can activate PKC and inhibit EC migration, we explored the signaling cascade responsible for this inhibition. LysoPC increased PKC␦ activity, measured by in vitro kinase activity assay, and increased PKC␦ phosphorylation. Decreasing PKC␦ activation, using pharmacological inhibitors or antisense oligonucleotides, diminished the antimigratory effect of lysoPC. LysoPC-induced PKC␦ activation was followed by increased phosphorylation of the transmembrane proteoglycan, syndecan-4, and decreased binding of PKC␣ to syndecan-4, with a concomitant decrease in PKC␣ activity. A reciprocal relationship was noted between the interaction of PKC␣ and ␣-actinin with syndecan-4. These changes were temporally related to the observed changes in cell morphology and the inhibition of migration of ECs incubated with lysoPC. The data suggested that generalized activation of PKC␦ by lysoPC initiated a cascade of events, including phosphorylation of syndecan-4, displacement and decreased activity of PKC␣, binding of ␣-actinin to syndecan-4, and disruption of the time-and site-specific regulation of focal adhesion complex assembly and disassembly required for normal cell migration.

show abstract

mentioning

confidence: 99%

Protein Kinase Cδ–Dependent Phosphorylation of Syndecan-4 Regulates Cell Migration

Chaudhuri

Colles

Fox

et al. 2005

Circulation Research

Self Cite

View full text Add to dashboard Cite

show abstract

“…30 However, excess levels of ROS are also detrimental as van Aalst et al showed that incubation of endothelial cells with oxidized lowdensity lipoprotein both increased ROS levels and decreased cell migration compared to cells cultured in a normal medium. 31 Prolonged exposure to ROS does not necessarily decrease CXCR4 expression as prior studies have shown that only very high levels of AGEs (500 lg/mL) decreased receptor expression. 12 Thus, ROS is a common intracellular messenger in the signaling pathways activated by CXCR4 and RAGE.…”

Section: Discussionmentioning

confidence: 91%

Soluble Receptor for Advanced Glycation End Products Improves Stromal Cell–Derived Factor-1 Activity in Model Diabetic Environments

Olekson

Faulknor

Hsia

et al. 2016

Advances in Wound Care

View full text Add to dashboard Cite

Objective: In diabetes, hyperglycemia causes the accumulation of advanced glycation end products (AGEs) that trigger reactive oxygen species (ROS) generation through binding the receptor for AGEs (RAGE). Because exogenous growth factors have had little success in enhancing chronic wound healing, we investigated whether hyperglycemia-induced AGEs interfere with cellular responses to extracellular signals. We used stromal cell-derived factor-1 (SDF-1), an angiogenic chemokine also known to promote stem cell recruitment in skin wounds. Approach: Human leukemia-60 (HL-60) cells and mouse peripheral blood mononuclear cells (PBMCs), which express the SDF-1 receptor CXCR-4, were incubated for 24 h in medium supplemented with 25 mM d-glucose. Soluble RAGE (sRAGE) was used to block RAGE activation. Response to SDF-1 was measured in cellular migration and ROS assays. A diabetic murine excisional wound model measured SDF-1 liposome and sRAGE activity in vivo. Results: Hyperglycemia led to significant accumulation of AGEs, decreased SDF-1-directed migration, and elevated baseline ROS levels; it suppressed the ROS spike normally triggered by SDF-1. sRAGE decreased the ROS baseline and restored both the SDF-1-mediated spike and cell migration. Topically applied sRAGE alone promoted healing and enhanced the effect of exogenous SDF-1 on diabetic murine wounds. Innovation: While there is interest in using growth factors to improve wound healing, this strategy is largely ineffective in diabetic wounds. We show that sRAGE may restore signaling, thus potentiating the effect of exogenously applied growth factors. Conclusion: Blocking RAGE with sRAGE restores SDF-1-mediated cellular responses in hyperglycemic environments and may potentiate the effectiveness of SDF-1 applied in vivo.

show abstract

“…ROS dapat diinkubasi (CO 5%, 37°C, 24 jam) (22). Vitamin E (d-α-2 menghambat migrasi sel endotel, diantaranya melalui tokoferol; Sigma) 22 μM atau 50 μM dengan konsentrasi kerusakan sitoskeleton dan gangguan polimerisasi aktin akhir pelarut etanol <0,5% diberikan bersamaan dengan (15). Pemberian donor NO (16) dan superoxyde dismutase pemaparan glukosa.…”

Section: Diabetes Mellitus (Dm) Merupakan Kelainan Endokrinunclassified

“…Protein fungsional pada menghambat migrasi sel endotel. Selain itu, peroksinitrit membran sel membentuk berbagai macam reseptor dan juga dapat menghambat polimerisasi aktin yang penting struktur penting pada membran, diantaranya caveola yang untuk migrasi sel endotel (15).…”

Section: Dari Data T E Rs E B U T D I Ke T a H U I B A H W A V I T A unclassified

Vitamin E Mempertahankan Kemampuan EPC yang Dipapar Glukosa Tinggi dalam Pelepasan NO dan Induksi Migrasi Sel Endotel

Nugrahenny

Widodo

Permatasari

2013

JKB

View full text Add to dashboard Cite

ABSTRAKPeran sel progenitor endotel (EPC) dalam angiogenesis terganggu pada diabetes. Penelitian dilakukan untuk mengamati efek vitamin E pada kemampuan EPC yang dipapar glukosa tinggi dalam melepaskan NO dan menginduksi migrasi sel endotel. Sel mononuklear diisolasi dari darah perifer subjek sehat. Pada hari ke-7, kultur EPC diberikan glukosa normal (5 mM) dengan atau tanpa pemberian vitamin E 22 µM atau 50 µM sebagai kontrol, atau diberikan glukosa tinggi (22 mM Kata Kunci: EPC, glukosa tinggi, NO, ROS, vitamin E ABSTRACT Role of EPCs on angiogenesis is impaired in diabetes. Study was designed to investigate effect of vitamin E toward ability of high glucose (HG) stimulated EPCs to release NO and inducemigration of endothelial cells. Mononuclear cells were isolated

show abstract

Role of reactive oxygen species in inhibition of endothelial cell migration by oxidized low-density lipoprotein

Cited by 25 publications

References 48 publications

Protein Kinase Cδ–Dependent Phosphorylation of Syndecan-4 Regulates Cell Migration

Protein Kinase Cδ–Dependent Phosphorylation of Syndecan-4 Regulates Cell Migration

Soluble Receptor for Advanced Glycation End Products Improves Stromal Cell–Derived Factor-1 Activity in Model Diabetic Environments

Vitamin E Mempertahankan Kemampuan EPC yang Dipapar Glukosa Tinggi dalam Pelepasan NO dan Induksi Migrasi Sel Endotel

Contact Info

Product

Resources

About