Proteomic analysis of vascular endothelial cells in response to laminar shear stress

Wang, Xiao Li; Fu, Alex A.; Raghavakaimal, Sreekumar; Lee, Hon Chi

doi:10.1002/pmic.200600568

Cited by 54 publications

(51 citation statements)

References 67 publications

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“…Proteomics. To determine the abundance of several individual proteins relevant to cellular ATP production, muscle samples from each subject were prepared as previously described, and the relative abundance of single peptides was determined using the iTRAQ approach (27). Samples from YT, YS, OT, and OS subjects were labeled with iTRAQ reagents 114, 115, 116, and 117, separated, and identified using liquid chromatography/tandem mass spectrometry.…”

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confidence: 99%

Endurance Exercise as a Countermeasure for Aging

et al. 2008

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OBJECTIVE-We determined whether reduced insulin sensitivity, mitochondrial dysfunction, and other age-related dysfunctions are inevitable consequences of aging or secondary to physical inactivity.RESEARCH DESIGN AND METHODS-Insulin sensitivity was measured by hyperinsulinemic-euglycemic clamp and ATP production in mitochondria isolated from vastus lateralis biopsies of 42 healthy sedentary and endurance-trained young (18 -30 years old) and older (59 -76 years old) subjects. Expression of proteins involved in fuel metabolism was measured by mass spectrometry. Citrate synthase activity, mitochondrial DNA (mtDNA) abundance, and expression of nuclear-encoded transcription factors for mitochondrial biogenesis were measured. SIRT3, a mitochondrial sirtuin linked to lifespan-enhancing effects of caloric restriction, was measured by immunoblot.RESULTS-Insulin-induced glucose disposal and suppression of endogenous glucose production were higher in the trained young and older subjects, but no age effect was noted. Age-related decline in mitochondrial oxidative capacity was absent in endurance-trained individuals. Although endurance-trained individuals exhibited higher expression of mitochondrial proteins, mtDNA, and mitochondrial transcription factors, there were persisting effects of age. SIRT3 expression was lower with age in sedentary but equally elevated regardless of age in endurance-trained individuals.CONCLUSIONS-The results demonstrate that reduced insulin sensitivity is likely related to changes in adiposity and to physical inactivity rather than being an inevitable consequence of aging. The results also show that regular endurance exercise partly normalizes age-related mitochondrial dysfunction, although there are persisting effects of age on mtDNA abundance and expression of nuclear transcription factors and mitochondrial protein. Furthermore, exercise may promote longevity through pathways common to effects of caloric restriction. Diabetes 57: 2933-2942, 2008 R educed insulin sensitivity is a common factor in the metabolic syndrome, a cluster of clinical conditions that shows increased risk with age (1-3). Mitochondrial dysfunction is also prevalent in the elderly (4,5), with reductions in mitochondrial enzyme activities (6), protein synthesis (7) and expression (5), and DNA (mtDNA) abundance (5,8). A close association between insulin sensitivity and muscle mitochondrial function has been reported in aging (4,5), type 2 diabetes (9), and obesity (10) as well as in offspring of type 2 diabetic individuals (11), prompting a hypothesis that either reduced insulin sensitivity results from muscle mitochondrial dysfunction (4,11) or vice versa (5,12).Endurance exercise increases insulin sensitivity (13,14) and mitochondrial enzyme activities (15,16). Short-term and longitudinal studies have documented that older populations respond favorably to endurance exercise but that there are persisting age effects that cannot be eliminated by short-term exercise programs (8,17). For practical reasons, most training studies ar...

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Endurance Exercise as a Countermeasure for Aging

et al. 2008

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“…Shear stress and cyclic strain, which are high in uterine spiral arterioles and low in uterine veins during pregnancy, offer possible explanations of how Notch signaling is initiated in the arteries. In ECs, these forces rapidly enhance Notch receptor cleavage/activation, increase expression of Notch receptors and ligands, and promote Notchdependent EFNB2 upregulation (Masumura et al, 2009;Morrow et al, 2007;Wang et al, 2007). Interestingly, ligand endocytosis potentiates cleavage and activation of Notch receptors, leading several groups to propose that mechanical forces expose the S2 cleavage site within the Notch receptor (Kopan and Ilagan, 2009).…”

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A role for Notch signaling in trophoblast endovascular invasion and in the pathogenesis of pre-eclampsia

et al. 2011

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SUMMARYPlacental trophoblasts (TBs) invade and remodel uterine vessels with an arterial bias. This process, which involves vascular mimicry, re-routes maternal blood to the placenta, but fails in pre-eclampsia. We investigated Notch family members in both contexts, as they play important roles in arterial differentiation/function. Immunoanalyses of tissue sections showed step-wise modulation of Notch receptors/ligands during human TB invasion. Inhibition of Notch signaling reduced invasion of cultured human TBs and expression of the arterial marker EFNB2. In mouse placentas, Notch activity was highest in endovascular TBs. Conditional deletion of Notch2, the only receptor upregulated during mouse TB invasion, reduced arterial invasion, the size of maternal blood canals by 30-40% and placental perfusion by 23%. By E11.5, there was litter-wide lethality in proportion to the number of mutant offspring. In pre-eclampsia, expression of the Notch ligand JAG1 was absent in perivascular and endovascular TBs. We conclude that Notch signaling is crucial for TB vascular invasion.

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“…8,9 To evaluate the effect of endothelial Notch inhibition in response to ischemia-related vasodilation, we subjected VEtTA-Tet OS -dnMAML and littermate control mice to hind limb ischemia (HLI) using a selective femoral artery ligation model. Figure 1C).…”

Section: Endothelial Notch Activation Is Required For Vasodilation Pomentioning

confidence: 99%

Notch-Dependent Regulation of the Ischemic Vasodilatory Response—Brief Report

Chang

Patenaude

et al. 2013

ATVB

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Objective-We have recently described that Notch activates nitric oxide (NO) signaling in the embryonic endocardium. Both Notch signaling and NO signaling have been shown to be important during adult arteriogenesis. Notch has been shown to be required for remodeling of the collateral vessels, whereas NO is required for the initial vasodilatory response to ischemia. Whether Notch also has an impact on the vasodilatory phase of arteriogenesis after ischemia is not known. We tested the hypothesis that endothelial cell-Notch function is required for NO induction and vasodilation, in response to ischemia in the adult vasculature. Methods and Results-We observed a significant decrease in NO levels in the dorsal aorta using a mouse model where Notch was inhibited in endothelial cell in a Tet-inducible fashion. In a femoral artery ligation model, inhibition of endothelial cell-Notch reduced reperfusion and NO generation, as quantified by laser Doppler perfusion imaging and by phosphoendothelial NO synthase, nitrotyrosine, and phosphovasodilator-stimulated phosphoprotein staining, respectively. Conclusion-Endothelial

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Proteomic analysis of vascular endothelial cells in response to laminar shear stress

Cited by 54 publications

References 67 publications

Endurance Exercise as a Countermeasure for Aging

Endurance Exercise as a Countermeasure for Aging

A role for Notch signaling in trophoblast endovascular invasion and in the pathogenesis of pre-eclampsia

Notch-Dependent Regulation of the Ischemic Vasodilatory Response—Brief Report

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