Conference Calendar
J Vasc Res 2016;53:372 (Source: Journal of Vascular Research)
Source: Journal of Vascular Research - January 31, 2017 Category: Research Source Type: research
Thanks to the Reviewers
J Vasc Res 2016;53:370-371 (Source: Journal of Vascular Research)
Source: Journal of Vascular Research - January 31, 2017 Category: Research Source Type: research
Erratum
J Vasc Res 2016;53:308 (Source: Journal of Vascular Research)
Source: Journal of Vascular Research - January 31, 2017 Category: Research Source Type: research
Contents Vol. 53, 2016
J Vasc Res 2016;53:I-IV (Source: Journal of Vascular Research)
Source: Journal of Vascular Research - January 31, 2017 Category: Research Source Type: research
Dysregulation of Vascular Endothelial Growth Factor Receptor-2 by Multiple miRNAs in Endothelial Colony-Forming Cells of Coronary Artery Disease
Conclusions: This modulation could help develop new therapeutic modalities for cardiovascular diseases and other vascular dysregulated diseases, especially tumor angiogenesis.J Vasc Res 2017;54:22-32 (Source: Journal of Vascular Research)
Source: Journal of Vascular Research - January 25, 2017 Category: Research Source Type: research
Cables1 Inhibits Proliferation and Induces Senescence by Angiotensin II via a p21-Dependent Pathway in Human Umbilical Vein Endothelial Cells
Cables1 (Cdk5 and Abl enzyme substrate 1) is a vital cell cycle regulator and a candidate tumor suppressor that negatively regulates cell growth by inhibiting cyclin-dependent kinases. Here, we report on the critical role of the Cables1/p21 pathway, which inhibits cell proliferation and induces cell senescence in human umbilical vein endothelial cells. Moreover, we confirmed that silencing of Cables1 promoted cell proliferation as well as increased resistance to angiotensin II-induced senescence, at least in part, by altering Cables1 activation. We further demonstrated that knockdown of p21 reverses Cables1-mediated cell g...
Source: Journal of Vascular Research - January 24, 2017 Category: Research Source Type: research
Advancing Age Decreases Pressure-Sensitive Modulation of Calcium Signaling in the Endothelium of Intact and Pressurized Arteries
Aging is the summation of many subtle changes which result in altered cardiovascular function. Impaired endothelial function underlies several of these changes and precipitates plaque development in larger arteries. The endothelium transduces chemical and mechanical signals into changes in the cytoplasmic calcium concentration to control vascular function. However, studying endothelial calcium signaling in larger arteries in a physiological configuration is challenging because of the requirement to focus through the artery wall. Here, pressure- and agonist-sensitive endothelial calcium signaling was studied in pressurized ...
Source: Journal of Vascular Research - January 18, 2017 Category: Research Source Type: research
Impaired Mitochondrial Respiration in Large Cerebral Arteries of Rats with Type 2 Diabetes
In this study, we extend our investigations into the mitochondrial dynamics of the cerebral vasculature of 14-week-old Zucker diabetic fatty obese (ZDFO) rats with early T2DM. Body weight and blood glucose levels were significantly higher in the ZDFO group, and basal mitochondrial respiration and proton leak were significantly decreased in the large cerebral arteries of the ZDFO rats compared with the lean controls (ZDFL). The expression of the mitochondrial proteins total manganese superoxide dismutase (MnSOD) and voltage-dependent anion channel (VDAC) were significantly lower in the cerebral microvessels, and acetylated ...
Source: Journal of Vascular Research - January 17, 2017 Category: Research Source Type: research
Notch4 Signaling Pathway of Endothelial Progenitor Cells in a Kawasaki Disease Model Induced by Lactobacillus casei Cell Wall Extract
In conclusion, the BM EPC functions and bioactivities in the KD models were impaired, and the Notch4 signaling pathway is associated with KD.J Vasc Res 2016;53:340-348 (Source: Journal of Vascular Research)
Source: Journal of Vascular Research - December 27, 2016 Category: Research Source Type: research
Notch4 Signaling Pathway of Endothelial Progenitor Cells in a Kawasaki Disease Model Induced by < b > < i > Lactobacillus casei < /i > < /b > Cell Wall Extract
In conclusion, the BM EPC functions and bioactivities in the KD models were impaired, and the Notch4 signaling pathway is associated with KD.J Vasc Res 2016;53:340-348 (Source: Journal of Vascular Research)
Source: Journal of Vascular Research - December 23, 2016 Category: Research Source Type: research
The Role of HMGB1 in Pial Arteriole Dilating Reactivity following Subarachnoid Hemorrhage in Rats
High-mobility group box 1 protein (HMGB1) has been implicated in inflammatory responses, and is also associated with cerebral vasospasm after subarachnoid hemorrhage (SAH). However, there are no direct evident links between HMGB1 and cerebral vasospasm. We therefore investigated the effects of HMGB1 on pial arteriole reactivity following SAH in rats. We initially found that SAH induced a significant decrease in pial arteriole dilating responses to sciatic nerve stimulation (SNS), hypercapnia (CO2), and the topical suffusion of acetylcholine (ACh), adenosine (ADO), and s-nitroso-N-acetylpenicillamine (SNAP) over a 7-day per...
Source: Journal of Vascular Research - December 21, 2016 Category: Research Source Type: research
Nobiletin Relaxes Isolated Mesenteric Arteries by Activating the Endothelial Ca2+-eNOS Pathway in Rats
Conclusion: Our study showed that nobiletin elicited a dose-dependent vasodilation in phenylephrine precontracted MA rings, but it did not elicit the same response in pulmonary artery rings. Vasodilation was related to endothelium and activated partly by eNOS. Vasodilation was inhibited by denudation of the endothelium or inhibition of eNOS activity. Nobiletin increased NO production by promoting the phosphorylation of eNOS at Ser-1177 without changing the level of eNOS expression in rat mesenteric artery endothelial cells (RMAECs). Nobiletin increased the concentration of endothelial [Ca2+]i, which enhances eNOS activity ...
Source: Journal of Vascular Research - December 19, 2016 Category: Research Source Type: research
Nobiletin Relaxes Isolated Mesenteric Arteries by Activating the Endothelial Ca < sup > 2+ < /sup > -eNOS Pathway in Rats
Conclusion: Our study showed that nobiletin elicited a dose-dependent vasodilation in phenylephrine precontracted MA rings, but it did not elicit the same response in pulmonary artery rings. Vasodilation was related to endothelium and activated partly by eNOS. Vasodilation was inhibited by denudation of the endothelium or inhibition of eNOS activity. Nobiletin increased NO production by promoting the phosphorylation of eNOS at Ser-1177 without changing the level of eNOS expression in rat mesenteric artery endothelial cells (RMAECs). Nobiletin increased the concentration of endothelial [Ca2+]i, which enhances eNOS activity ...
Source: Journal of Vascular Research - December 16, 2016 Category: Research Source Type: research
Alveolar Hypoxia-Induced Pulmonary Inflammation: From Local Initiation to Secondary Promotion by Activated Systemic Inflammation
Pulmonary hypertension (PH) is a pathological condition with high mortality and morbidity. Hypoxic PH (HPH) is a common form of PH occurring mainly due to lung disease and/or hypoxia. Most causes of HPH are associated with persistent or intermittent alveolar hypoxia, including exposure to high altitude and chronic obstructive respiratory disease. Recent evidence suggests that inflammation is a critical step for HPH initiation and development. A detailed understanding of the initiation and progression of pulmonary inflammation would help in exploring potential clinical treatments for HPH. In this review, the mechanism for a...
Source: Journal of Vascular Research - December 15, 2016 Category: Research Source Type: research
Adenovirus-Mediated Overexpression of Septin 2 Attenuates α-Smooth Muscle Actin Expression and Adventitial Myofibroblast Migration Induced by Angiotensin II
In this study, we investigate whether septin 2 contributes to the adventitial MF phenotypic modulation caused by Ang II. The decreased level of septin 2 and the increased expression of α-smooth muscle actin (α-SMA), a marker of MFs, were readily observed in Ang II-stimulated MF differentiation. After gene transfer of septin 2, the expression of α-SMA was markedly decreased and the MF migration response to Ang II was inhibited. Furthermore, the inhibition of RhoA, another molecu le involved in MF phenotypic modulation, decreased the motility of MFs and the expression of septin 2 triggered in Ang II. Finally, transfection...
Source: Journal of Vascular Research - December 15, 2016 Category: Research Source Type: research
