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1.  Characterization of a novel endothelial biosensor assay reveals increased cumulative serum inflammatory potential in stabilized coronary artery disease patients 
Background
Vascular disease is promoted by systemic inflammation that can arise from sites distal to the affected vessels. We sought to characterize the net inflammatory potential of serum from patients with coronary artery disease (CAD) using cultured endothelial cells as a cumulative biosensor.
Methods and results
Serum samples from CAD patients (N = 45) and healthy control subjects (N = 48) were incubated with primary human coronary artery endothelial cells at a 1:10 dilution for 4 h, followed by isolation of the cellular RNA. Alteration of inflammation-responsive elements (adhesion molecules and cytokines) was assessed by gene expression. Specific indicators included intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and interleukin-8 (IL-8). Additionally, the cytokine levels in serum samples from all subjects were quantified. Serum from CAD subjects induced greater endothelial ICAM-1, VCAM-1, and IL-8 expression compared to healthy control serum (p < 0.001 for each analysis). The three indicators of inflammatory potential (ICAM-1, VCAM-1, and IL-8 mRNA) trended independently of each other and also of serum inflammatory biomarkers. IL-8 expression correlated negatively with serum HDL levels but positively correlated with VLDL, plasminogen activator inhibitor-1 and C-reactive protein. Interestingly, serum levels of cytokines in CAD patients were not statistically different from healthy control subjects. A year of follow-up in a sub-group of CAD subjects revealed relatively stable measures.
Conclusions
As yet unidentified circulating factors in the serum of CAD patients appear to activate endothelial cells, leading to upregulation of adhesion molecules and chemokines. This cumulative assay performed well in terms of discriminating patients with CAD compared to healthy subjects, with greater range and specificity than specific inflammatory markers.
doi:10.1186/s12967-015-0457-5
PMCID: PMC4376347  PMID: 25890092
Coronary artery disease; Biomarker; Inflammatory; Serum; Endothelial
2.  Effects of Nicotine on Cardiovascular Remodeling in a Mouse Model of Systemic Hypertension 
Cardiovascular toxicology  2013;13(4):364-369.
Usage of nicotine-only formulations, such as transdermal patches, nicotine gum, or electronic nicotine delivery systems is increasing, as they are perceived as healthier alternatives to traditional cigarettes. Unfortunately, there is little data available on the effect of isolated nicotine on myocardial and aortic remodeling, especially in the setting of cardiovascular disease risk factors, such as hypertension. We hypothesized that nicotine would exacerbate cardiovascular remodeling induced by angiotensin-II (Ang II) treatment. Subcutaneous osmotic minipumps were implanted to administer Ang II, Nic, nicotine plus ANG II or saline to C57Bl/6 mice for 4 weeks. Heart weights were increased by all treatments, with control < nicotine < Ang II < nicotine + Ang II. Activity levels of matrix metalloproteinase (MMP-2) mirrored these changes and demonstrated clear additivity between nicotine and Ang II. Histopathological analysis of aortas revealed that mice receiving combined nicotine and Ang II treatment induced significant hypertrophy compared to all other groups. This study reveals possible cardiotoxic interactions between nicotine and a common model of systemic hypertension. Safety testing of novel nicotine delivery devices should consider that hypertension is a common impetus to begin smoking cessation therapy, and potential interactions should be more thoroughly studied.
doi:10.1007/s12012-013-9217-z
PMCID: PMC4070620  PMID: 23959951
E-cigarettes; electronic nicotine delivery systems; cardiovascular toxicity; vascular remodeling; angiotensin
3.  ANGIOGENESIS IN MESENTERIC MICROVASCULAR NETWORKS FROM SPONTANEOUSLY HYPERTENSIVE VERSUS NORMOTENSIVE RATS 
Elevated blood pressure during hypertension has been associated with microvascular rarefaction defined by loss of microvessels. However, whether rarefaction is a result of impaired angiogenesis remains unclear. The objective of this study was to compare angiogenesis across the time course of mesenteric microvascular network remodeling in adult spontaneously hypertensive versus normotensive rats. Angiogenic responses in 15–16-week-old SHR and Wistar rats at 0, 3, 5, 10 or 25 days post 20 minute exteriorization of the mesentery were quantified. Consistent with the phenomenon of rarefaction, vascularized area in unstimulated SHR was decreased compared to Wistar. By 25 days, SHR vascular area had increased to the Wistar level and vascular length density and capillary sprouting were comparable. At 3 and 5 days, SHR and Wistar tissues displayed an increase in the capillary sprouting and vascular density relative to their unstimulated controls. At 10 days, capillary sprouting in the SHR remained elevated. The percent change in vascular density was elevated in the SHR compared to the Wistar group at 3 and 5 days and by 25 days the rate of change was more negative. Our results suggest that SHR networks undergo an increased rate of growth followed by an increased rate of pruning.
doi:10.1111/j.1549-8719.2011.00117.x
PMCID: PMC3176994  PMID: 21627712
Hypertension; Angiogenesis; Spontaneously Hypertensive Rat; Microcirculation; Mesentery

Results 1-3 (3)