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  • 1.

    【2hr】Cigarette Smoke Extract Activates Tartrate-Resistant Acid Phosphatase-Positive Macrophage

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    机译 香烟烟雾提取物可激活抗酒石酸的酸性磷酸酶阳性的巨噬细胞
    摘要：Background:It has been reported that smoking is one of the strongest positive risk factors for abdominal aortic aneurysms (AAAs). Although many studies have been directed to decipher the effect of smoking on AAA, its effect on macrophage activation has not yet been explored.
  • 2.

    【2hr】Evaluation of Notch3 deficiency in diabetes-induced pericyte loss in the retina

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    机译 糖尿病诱导的视网膜周细胞丢失中Notch3缺乏症的评估
    摘要：Loss of vascular pericytes has long been associated with the onset of diabetic retinopathy, however mechanisms contributing to pericyte dropout are not understood. Notch3 has been implicated in pericyte stability and survival, and linked to vascular integrity. Notch3 mutant mice exhibit progressive loss of retinal pericytes. Given that diabetic retinopathy is associated with pericyte loss, we sought to determine if perturbation of Notch3 signaling contributes to diabetes-induced pericyte dropout and capillary degeneration. We utilized a pericyte-expressed LacZ transgene (XlacZ4) to examine pericyte loss in retinas of a type I diabetic mouse model (Ins2Akita) and Notch3 deficient mice. Notch3 null animals showed a dramatic loss of the LacZ marker by 8 weeks of age, while Ins2Akita diabetic and Notch3 heterozygous mice exhibited a much slower and subtler loss of LacZ. Although combined Notch3 heterozygosity in Ins2Akita diabetic animals did not show further deficits, trypsin digest method revealed that Notch3 haploinsufficiency increased the formation of acellular capillary in diabetic mice. Our data further indicate that Notch signaling is blunted in diabetic retinas and in cells exposed to hyperglycemia. These results are the first to demonstrate an association between Notch3 signaling, pericyte loss and diabetic retinopathy.
  • 3.

    【2hr】Perfusion Tissue Culture Initiates Differential Remodeling of Internal Thoracic Arteries Radial Arteries and Saphenous Veins

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    机译 灌注组织培养启动内部胸动脉Rad动脉和大隐静脉的差异重塑
    摘要：Adaptive remodeling processes are essential to the maintenance and viability of coronary artery bypass grafts where clinical outcomes depend strongly on the tissue source. In this investigation, we utilized an ex vivo perfusion bioreactor to culture porcine analogs of common human bypass grafts: the internal thoracic artery (ITA), the radial artery (RA), and the great saphenous vein (GSV), and evaluated samples acutely (6 hours) and chronically (7 days) under in situ or coronary-like perfusion conditions. Although morphologically similar, primary cells harvested from ITAs illustrated lower intimal and medial, but not adventitial, cell proliferation rates compared to RAs or GSVs. Basal gene expression levels were similar between all vessels with only COL3A1, SERPINE1, FN1 and TGFB1 differentially expressed prior to culture; however, over half of all genes were affected nominally by the culturing process. When exposed to coronary-like conditions, RAs and GSVs experienced pathological remodeling not present in ITAs or when vessels were studied under their in situ conditions. Many of the remodeling genes perturbed at 6 hours were restored after 7 days (COL3A1, FN1, MMP2, TIMP1) while others (SERPINE1, TGFB1, VCAM1) were not. Findings elucidate potential mechanisms of graft failure and highlight strategies to encourage healthy ex vivo pre-graft conditioning.
  • 4.

    【2hr】Proinflammatory Arterial Stiffness Syndrome: A Signature of Large Arterial Aging

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    机译 促炎性动脉僵硬综合症：大动脉衰老的标志
    摘要：Age-associated structural and functional remodeling of the arterial wall produces a productive environment for the initiation and progression of hypertension and atherosclerosis. Chronic aging stress induces low grade pro-inflammatory signaling and causes cellular proinflammation in arterial walls, which triggers the structural phenotypic shifts characterized by endothelial dysfunction, diffuse intimal-medial thickening, and arterial stiffening. Microscopically, aged arteries exhibit an increase in arterial cell senescence, proliferation, invasion, matrix deposition, elastin fragmentation, calcification, and amyloidosis. These characteristic cellular and matrix alterations not only develop with aging but can also be induced in young animals under experimental proinflammatory stimulation. Interestingly, these changes can also be attenuated in old animals by reducing low grade inflammatory signaling. Thus, mitigating age-associated proinflammation and arterial phenotype shifts is a potential approach to retard arterial aging and prevent the epidemic of hypertension and atherosclerosis in the elderly.
  • 5.

    【2hr】A Simple Method for Normalization of Aortic Contractility

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    机译 主动脉收缩性标准化的简单方法
    摘要：Vascular contractile function changes in proliferative vascular diseases, e.g., atherosclerosis, and is documented using isolated blood vessels, yet, many laboratories differ in their approach to quantification. Some use raw values (e.g., mg, mN); others use a ‘percentage of control agonist’ approach; and, others normalize by blood vessel characteristic, e.g., length, mass, etc. A lack of uniformity limits direct comparison of contractility outcomes. To address this limitation, we developed a simple 2-step normalization method: 1) measure blood vessel segment length (mm), area (mm2) and calculate volume (mm3); and then, 2) normalize isometric contraction (mN) by segment length and volume. Normalized aortic contractions but not raw values were statistically different between normal chow (NC) and high fat diet-fed (HFD) mice supporting the practical utility and general applicability of normalization. It is recommended that aortic contractions be normalized to segment length and/or volume to reduce variability, enhance efficiency and to foster universal comparisons across isometric myograph platforms, laboratories and experimental settings.
  • 6.

    【2hr】Intraoperative Incident Dark Field Imaging of the Human Peritoneal Microcirculation

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    机译 人体腹膜微循环的术中事件暗场成像
    摘要：Background/AimsThis study describes the peritoneal microcirculation, compares quantitative parameters and angioarchitecture to the standard of sublingual microcirculatory assessment, and determines the practical feasibility of this method.
  • 7.

    【2hr】Remodeling of Wall Mechanics and the Myogenic Mechanism of Rat Intramural Coronary Arterioles in Response to a Short-Term Daily Exercise Program: Role of Endothelial Factors

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    机译 壁力学重塑和大鼠壁内冠状小动脉对短期日常锻炼计划的反应的生肌机制：内皮因子的作用。
    摘要：PurposeExercise elicits early adaptation of coronary vessels enabling the coronary circulation to respond adequately to higher flow demands. We hypothesized that short-term daily exercise induces biomechanical and functional remodeling of the coronary resistance arteries related to pressure.
  • 8.

    【2hr】Angiotensin II Infusion Does Not Cause Abdominal Aortic Aneurysms in Apolipoprotein E-Deficient Rats

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    机译 血管紧张素II输注不会引起载脂蛋白E缺乏症大鼠的腹主动脉瘤
    摘要：The apolipoprotein E-deficient mouse model has advanced our understanding of cardiovascular disease mechanisms and experimental therapeutics. This spontaneous model recapitulates aspects of human atherosclerosis and allows for the development of dissecting abdominal aortic aneurysms when combined with angiotensin II. We characterized apolipoprotein E-deficient rats and hypothesized that, similar to mice, they would develop dissecting abdominal aortic aneurysms.We created rats with a 16-basepair deletion of the apolipoprotein E gene using transcription activator-like effector nucleases. We imaged the suprarenal aorta for 28 days after implantation of miniosmotic pumps that infuse angiotensin II (200 ng/kg/min). Blood pressure, serum lipids and lipoproteins, and histology were also analyzed.These rats did not develop pathological aortic dissection, but we did observe a decrease in circumferential cyclic strain, a rise in blood pressure, and microstructural changes in the aortic medial layer. We also measured increased serum lipids with and without high fat diet administration but did not detect atherosclerotic plaques.Chronic infusion of angiotensin II did not lead to formation of dissecting abdominal aortic aneurysms or atherosclerosis in the rats used in this study. While reduced amounts of atherosclerosis may explain this resistance to dissecting aneurysms, further investigation is needed to fully characterize species-specific differences.
  • 9.

    【2hr】VEGF and IGF delivered from alginate hydrogels promotes stable perfusion recovery in ischemic hindlimbs of aged mice and rabbits

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    机译 从藻酸盐水凝胶中输送的VEGF和IGF促进衰老小鼠和兔子缺血后肢的稳定灌注恢复
    摘要：Biomaterial-based delivery of angiogenic growth factors restores perfusion more effectively than bolus delivery methods in rodent models of peripheral vascular disease, but the same success in clinically relevant aged-animal and large-animal studies has not yet been demonstrated. These studies explore, in clinically-relevant models, a therapeutic angiogenesis strategy for the treatment of peripheral vascular disease which overcomes challenges encountered in previous clinical trials. Alginate hydrogels providing sustained release of Vascular Endothelial Growth Factor (VEGF) and Insulin-like Growth Factor-1 (IGF) were injected into ischemic hindlimbs in middle and old age mice, and in young rabbits as a test of the scalability of this local growth factor treatment. Spontaneous perfusion recovery diminished with increasing age, and only the combination of VEGF and IGF delivery from gels significantly rescued perfusion in middle age (13 month) and old age (20 month) mice. In rabbits, delivery of VEGF alone or in combination with IGF from alginate hydrogels, at a dose two orders of magnitude lower than typical doses used in past rabbit studies, enhanced perfusion recovery when given immediately after surgery, or as a treatment for chronic ischemia. Capillary density measurements and angiographic analysis demonstrated the benefit of gel delivery. These data together suggest that alginate hydrogels providing local delivery of low doses of VEGF and IGF constitutes a safe and effective treatment for hindlimb ischemia in clinically relevant animal models, supporting the potential clinical translation of this concept.
  • 10.

    【2hr】Measurement of aortic cell fluid-phase pinocytosis in vivo by flow cytometry

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    机译 流式细胞术在体内测量主动脉细胞液相胞吞作用
    摘要：ObjectiveFluid-phase pinocytosis is a receptor-independent mechanism of endocytosis that occurs in all mammalian cells and may be a mechanism for macrophage uptake of LDL. As there are currently no methods for the measurement of fluid-phase pinocytosis by individual aortic cells in vivo, we sought to identify a suitable method.
  • 11.

    【2hr】Advancing Age Decreases Pressure-Sensitive Modulation of Calcium Signaling in the Endothelium of Intact and Pressurized Arteries

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    机译 年龄的增长降低了完整动脉和加压动脉内皮细胞中钙信号的压力敏感性调节。
    摘要：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 carotid arteries from young (3-month-old) and aged (18-month-old) rats by imaging from within the artery using gradient index fluorescence microendoscopy. Endothelial sensitivity to acetylcholine increased with age. The number of cells exhibiting oscillatory calcium signals and the frequency of oscillations were unchanged with age. However, the latency of calcium responses was significantly increased with age. Acetylcholine-evoked endothelial calcium signals were suppressed by increased intraluminal pressure. However, pressure-dependent inhibition of calcium signaling was substantially reduced with age. While each of these changes will increase endothelial calcium signaling with increasing age, decreases in endothelial pressure sensitivity may manifest as a loss of functionality and responsiveness in aging.
  • 12.

    【2hr】Transplantation of autologous bone marrow mononuclear cells regulates inflammation in a rabbit model of carotid artery atherosclerosis

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    机译 自体骨髓单个核细胞的移植调节兔颈动脉粥样硬化模型的炎症
    摘要：ObjectiveIt is well known that inflammation plays key roles in the development of atherosclerosis and that bone marrow mononuclear cells (BMMNCs) transplantation can suppress inflammation in rodent models of ischemic diseases. Here, we explored whether transplantation of autologous BMMNCs could prevent the progression of atherosclerosis by alleviation of inflammatory responses in a rabbit model of carotid artery atherosclerosis.
  • 13.

    【2hr】G-Protein-Coupled Receptor 35 Mediates Human Saphenous Vein Vascular Smooth Muscle Cell Migration and Endothelial Cell Proliferation

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    机译 G蛋白偶联受体35介导人大隐静脉血管平滑肌细胞迁移和内皮细胞增殖。
    摘要：Vascular smooth muscle cell (VSMC) migration and proliferation is central to neointima formation in vein graft failure following coronary artery bypass. However, there are currently no pharmacological interventions that prevent vein graft failure through intimal occlusion. It is hence a therapeutic target. Here, we investigated the contribution of GPR35 to human VSMC and endothelial cell (EC) migration, using a scratch-wound assay, and also the contribution to proliferation, using MTS and BrdU assays, in in vitro models using recently characterized human GPR35 ortholog-selective small-molecule agonists and antagonists. Real-time PCR studies showed GPR35 to be robustly expressed in human VSMCs and ECs. Stimulation of GPR35, with either the human-selective agonist pamoic acid or the reference agonist zaprinast, promoted VSMC migration in the scratch-wound assay. These effects were blocked by coincubation with either of the human GPR35-specific antagonists, CID-2745687 or ML-145. These GPR35-mediated effects were produced by inducing alterations in the actin cytoskeleton via the Rho A/Rho kinase signaling axis. Additionally, the agonist ligands stimulated a proliferative response in ECs. These studies highlight the potential that small molecules that stimulate or block GPR35 activity can modulate vascular proliferation and migration. These data propose GPR35 as a translational therapeutic target in vascular remodeling.
  • 14.

    【2hr】Effects of Obesity on Perivascular Adipose Tissue Vasorelaxant Function: Nitric Oxide Inflammation and Elevated Systemic Blood Pressure

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    机译 肥胖对血管周围脂肪组织血管舒张功能的影响：一氧化氮炎症和全身血压升高
    摘要：IntroductionPerivascular adipose tissue (PVAT) surrounds most vessels in the human body. Healthy PVAT has a vasorelaxant effect which is not observed in obesity. We assessed the contribution of nitric oxide (NO), inflammation and endothelium to obesity-induced PVAT damage.
  • 15.

    【2hr】Calreticulin regulates neointima formation and collagen depositionfollowing carotid artery ligation

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    机译 钙网蛋白调节新内膜形成和胶原沉积颈动脉结扎后
    摘要：Background/AIMsThe endoplasmic reticulum (ER) stress protein, calreticulin (CRT), is required for TGF-β stimulated extracellular matrix (ECM) production by fibroblasts. Since TGF-β regulates vascular fibroproliferative responses and collagen deposition, we investigated the effects of CRT knockdown on vascular smooth muscle cell (VSMCs) fibroproliferative responses and collagen deposition.
  • 16.

    【2hr】PREVENTION OF VENOUS NEOINTIMAL HYPERPLASIA BY A MULTI-TARGET RECEPTOR TYROSINE KINASE INHIBITOR

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    机译 多目标受体酪氨酸激酶抑制剂预防静脉新膜增生
    摘要：Background/AimsVenous neointimal hyperplasia (NH) is the predominant cause of stenosis in hemodialysis arteriovenous grafts (AVG) but currently there is no clinically used therapies to prevent NH.
  • 17.

    【2hr】Pioglitazone Identifies a New Target for Aneurysm Treatment: Role of Egr1 in an Experimental Murine Model of Aortic Aneurysm

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    机译 吡格列酮确定了动脉瘤治疗的新目标：Egr1在实验性主动脉瘤小鼠模型中的作用。
    摘要：Peroxisome proliferator-activated receptor γ agonists have been shown to inhibit angiotensin II (AngII)-induced experimental abdominal aortic aneurysms. Macrophage infiltration to the vascular wall is an early event in this pathology, and therefore we explored the effects of the peroxisome proliferator-activated receptor γ agonist pioglitazone on AngII-treated macrophages. Using microarray-based expression profiling of phorbol ester-stimulated THP-1 cells, we found that a number of aneurysm-related gene changes effected by AngII were modulated following the addition of pioglitazone. Among those genes, polycystic kidney disease 1 (PKD1) was significantly up-regulated (multiple testing corrected p < 0.05). The analysis of the PKD1 proximal promoter revealed a putative early growth response 1 (EGR1) binding site, which was confirmed by chromatin immunoprecipitation (ChIP) and quantitative PCR. Further analysis of publicly available ChIP-sequencing data revealed that this putative binding site overlapped with a conserved EGR1 binding peak present in 5 other cell lines. Quantitative real-time PCR showed that EGR1 suppressed PKD1, while AngII significantly up-regulated PKD1, an effect counteracted by pioglitazone. Conversely, in EGR1 short hairpin RNA lentivirally transduced THP-1 cells, reduced EGR1 led to a significant up-regulation of PKD1, especially after treatment with pioglitazone. In vivo, deficiency of Egr1 in the haematopoietic compartment of mice completely abolished the incidence of CaCl2-induced aneurysm formation.
  • 18.

    【2hr】Transglutaminase 2 Promotes PDGF-Mediated Activation of PDGFR/Akt1 and β-catenin Signaling in Vascular Smooth Muscle Cells and Supports Neointima Formation

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    机译 转谷氨酰胺酶2促进PDGF介导的PDGFR / Akt1和β-catenin信号在血管平滑肌细胞中的激活并支持新内膜形成。
    摘要：BackgroundPhenotypic switch of vascular smooth muscle cells (VSMCs) accompanies neointima formation and associates with vascular diseases. Platelet derived growth factor (PDGF)-induced activation of PDGFR/Akt1 and β-catenin signaling pathways in VSMCs has been implicated in vessel occlusion. Transglutaminase 2 (TG2) regulates these pathways and its levels are increased in the neointima.
  • 19.

    【2hr】Integration and Modulation of Intercellular Signaling Underlying Blood Flow Control

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    机译 整合和调节基础血流控制的细胞间信号传导。
    • 作者：Steven S. Segal
    • 刊名：Journal of Vascular Research
    • -1年第2期
    摘要：Vascular resistance networks control tissue blood flow in concert with regulating arterial perfusion pressure. In response to increased metabolic demand, vasodilation arising in arteriolar networks ascends to encompass proximal feed arteries. By reducing resistance upstream, ascending vasodilation (AVD) increases blood flow into the microcirculation. Once initiated [e.g., through local activation of K+ channels in endothelial cells (ECs)], hyperpolarization is conducted through gap junctions along the endothelium. Via EC projections through the internal elastic lamina, hyperpolarization spreads into the surrounding smooth muscle cells (SMCs) through myoendothelial gap junctions (MEGJs) to promote their relaxation. Intercellular signaling through electrical signal transmission (i.e., cell-to-cell conduction) can thereby coordinate vasodilation along and among the branches of microvascular resistance networks. Perivascular sympathetic nerve fibers course through the adventitia and release norepinephrine to stimulate SMCs via α-adrenoreceptors to produce contraction. In turn, SMCs can signal ECs through MEGJs to activate K+ channels and attenuate sympathetic vasoconstriction. Activation of K+ channels along the endothelium will dissipate electrical signal transmission and inhibit AVD, thereby restricting blood flow into the microcirculation while maintaining peripheral resistance and perfusion pressure. This review explores the origins and nature of intercellular signaling governing blood flow control in skeletal muscle with respect to the interplay between AVD and sympathetic innervation. Whereas these interactions are integral to physical daily activity and athletic performance, resolving the interplay between respective signaling events provides insight into how selective interventions can improve tissue perfusion and oxygen delivery during vascular disease.
  • 20.

    【2hr】From Structure to Function: Mitochondrial Morphology Motion and Shaping in Vascular Smooth Muscle

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    机译 从结构到功能：血管平滑肌的线粒体形态运动和形态
    摘要：The diversity of mitochondrial arrangements, which arise from the organelle being static or moving, or fusing and dividing in a dynamically reshaping network, is only beginning to be appreciated. While significant progress has been made in understanding the proteins that reorganise mitochondria, the physiological significance of the various arrangements is poorly understood. The lack of understanding may occur partly because mitochondrial morphology is studied most often in cultured cells. The simple anatomy of cultured cells presents an attractive model for visualizing mitochondrial behaviour but contrasts with the complexity of native cells in which elaborate mitochondrial movements and morphologies may not occur. Mitochondrial changes may take place in native cells (in response to stress and proliferation), but over a slow time-course and the cellular function contributed is unclear. To determine the role mitochondrial arrangements play in cell function, a crucial first step is characterisation of the interactions among mitochondrial components. Three aspects of mitochondrial behaviour are described in this review: (1) morphology, (2) motion and (3) rapid shape changes. The proposed physiological roles to which various mitochondrial arrangements contribute and difficulties in interpreting some of the physiological conclusions are also outlined.
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