Synergistic effect of shear stress and streptavidin‐biotin on the expression of endothelial vasodilator and cytoskeleton genes

Chan, Bernard P.L.; Reichert, William M.; Truskey, George A.

doi:10.1002/bit.20263

Cited by 5 publications

(7 citation statements)

References 51 publications

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“…The genes chosen had all been shown to be sensitive to shear stress in vitro at the mRNA and/or protein level in a variety of endothelial cell types. 2,8,15,16,18,19,22,23,26 Consistent with the global tendencies revealed by microarray analysis, qPCR also showed that positive and negative deviations from moderate levels of shear stress were associated with similar gene expression responses. Among the seven genes studied by qPCR, the expression levels of four of them (b-catenin, c-jun, VCAM-1, and MCP-1) were altered in both the low shear and high shear environments relative to the medium shear environment (Fig.…”

Section: Discussionsupporting

confidence: 75%

Endothelial Gene Expression in Regions of Defined Shear Exposure in the Porcine Iliac Arteries

et al. 2010

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The effect of hemodynamic shear stress on endothelial gene expression was investigated in the porcine iliac arteries. A novel statistical approach was applied to computational fluid dynamics simulations of the iliac artery flow field to identify three anatomical regions likely to experience high, medium, and low levels of time average shear stress magnitude. Subsequently, endothelial cell mRNA was collected from these regions in the iliac arteries of six swine and analyzed by DNA microarray. Gene set enrichment analysis demonstrated a strong tendency for genes upregulated or downregulated in one of the extreme shear environments (low or high, relative to medium) to be regulated in the same direction in the other extreme shear environment. This tendency was confirmed for specific genes by real-time quantitative PCR. Specifically, beta-catenin, c-jun, VCAM-1, and MCP-1 were all upregulated in low and high shear stress regions relative to the medium shear stress region. eNOS expression was not significantly different in any of the regions. These results are consistent with the notion that endothelial cells chronically exposed to abnormally low or high shear levels in vivo exhibit similar genetic responses. Alternative explanations of this outcome are proposed, and its implications for the role of shear stress in atherogenesis are examined.

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Section: Discussionsupporting

confidence: 75%

Endothelial Gene Expression in Regions of Defined Shear Exposure in the Porcine Iliac Arteries

et al. 2010

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“…Thus the capacity of endothelial cells to sustain NO production is severely limited not only by the downregulation of eNOS (2,4,36) but also by the availability of arginine provided by AS via the citrulline-NO cycle. Coordinate upregulation of AS and eNOS expression has been identified previously in a number of systems (10,30). For example, AS and eNOS are coordinately induced in the aorta of diabetic rats after streptozotocin treatment (30).…”

Section: Discussionmentioning

confidence: 95%

“…NO is utilized in signaling, whereas citrulline is recycled back to arginine by two enzymes, argininosuccinate synthase (AS) and argininosuccinate lyase, to complete the cycle. AS catalyzes the rate-limiting step in the arginine regeneration side of the citrulline-NO cycle (42) and appears to be coordinately regulated with eNOS activity (10,30).…”

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confidence: 99%

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Tumor necrosis factor-α reduces argininosuccinate synthase expression and nitric oxide production in aortic endothelial cells

Goodwin¹,

Pendleton²,

Levy³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Endothelial dysfunction associated with elevated serum levels of TNF-alpha observed in diabetes, obesity, and congenital heart disease results, in part, from the impaired production of endothelial nitric oxide (NO). Cellular NO production depends absolutely on the availability of arginine, substrate of endothelial nitric oxide synthase (eNOS). In this report, evidence is provided demonstrating that treatment with TNF-alpha (10 ng/ml) suppresses not only eNOS expression but also the availability of arginine via the coordinate suppression of argininosuccinate synthase (AS) expression in aortic endothelial cells. Western blot and real-time RT-PCR demonstrated a significant and dose-dependent reduction of AS protein and mRNA when treated with TNF-alpha with a corresponding decrease in NO production. Reporter gene analysis demonstrated that TNF-alpha suppresses the AS proximal promoter, and EMSA analysis showed reduced binding to three essential Sp1 elements. Inhibitor studies suggested that the repression of AS expression by TNF-alpha may be mediated, in part, via the NF-kappaB signaling pathway. These findings demonstrate that TNF-alpha coordinately downregulates eNOS and AS expression, resulting in a severely impaired citrulline-NO cycle. The downregulation of AS by TNF-alpha is an added insult to endothelial function because of its important role in NO production and in endothelial viability.

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“…Biotin and avidin mediated binding has previously been shown to enhance endothelial cell (EC) attachment, spreading, and a quiescent phenotype on synthetic surfaces. [23][24][25][26] These attributes may assist in targeting cells to vascular surfaces exploiting the strong interaction between biotin and avidin. Modification of vascular surfaces with protein-reactive PEG-biotin might thus provide a target for the site-specific delivery of microspheres and cells under physiologic flow conditions following intravascular procedures such as angioplasty or end-arterectomy.…”

Section: Introductionmentioning

confidence: 99%

Targeting microspheres and cells to polyethylene glycol‐modified biological surfaces

Deglau¹,

Johnson²,

Villanueva³

et al. 2006

J Biomedical Materials Res

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It has previously been demonstrated that damaged arterial tissue can be acutely modified with proteinreactive polyethylene glycol (PEG) to block undesirable platelet deposition. This concept might be expanded by employing PEG-biotin and its strong interaction with avidin for site-specific targeted delivery. Toward this end, cultured endothelial cells (ECs) were surface modified with PEG-biotin and the available biotin was quantified with flow cytometry. NeutrAvidin-coated microspheres and PEG-biotin modified ECs with NeutrAvidin as a bridging molecule were delivered under arterial shear stress to PEG-biotin modified ECs on a coverslip as well as scrape-damaged bovine carotid arteries. After incubation with a 10 mM solution for 1 min, 8 × 10 7 PEG-biotin molecules/EC were found and persisted for up to 120 h. Perfused microspheres adhered to NHS-PEG-biotin treated bovine carotid arteries with 60 ± 16 microspheres/mm 2 versus 11 ± 4 microspheres/mm 2 for control arteries (p < 0.015). Similarly, 22 ± 5 targeted ECs/mm 2 adhered to NHS-PEG-biotin treated bovine carotid arteries versus 6 ± 2 ECs/mm 2 for control arteries (p < 0.01). The targeting strategy demonstrated here might ultimately find application for drug delivery, gene therapy, or cell therapy where localization to specific labeled vascular regions is desired following catheter-based or surgical procedures.

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Synergistic effect of shear stress and streptavidin‐biotin on the expression of endothelial vasodilator and cytoskeleton genes

Cited by 5 publications

References 51 publications

Endothelial Gene Expression in Regions of Defined Shear Exposure in the Porcine Iliac Arteries

Endothelial Gene Expression in Regions of Defined Shear Exposure in the Porcine Iliac Arteries

Tumor necrosis factor-α reduces argininosuccinate synthase expression and nitric oxide production in aortic endothelial cells

Targeting microspheres and cells to polyethylene glycol‐modified biological surfaces

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