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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】Digoxin Attenuates Receptor Activation of NF-κB Ligand-Induced Osteoclastogenesis in Macrophages

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    机译 地高辛减弱巨噬细胞中NF-κB配体诱导的破骨细胞生成的受体活化。
    摘要：Background:Even though hypoxia-inducible factor-1α (HIF-1α) is among the transcriptional factors demonstrated to contribute to the formation of abdominal aortic aneurysms (AAAs), the precise mechanism has been unclear. Digoxin is known as an inhibitor of HIF-1α, and shows a protective effect against the progression of AAAs.
  • 3.

    【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.
  • 4.

    【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.
  • 5.

    【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.
  • 6.

    【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.
  • 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】A Novel Ex Vivo Mouse Mesometrium Culture Model for Investigating Angiogenesis in Microvascular Networks

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    机译 在微血管网络中调查血管生成的新型离体小鼠中膜培养模型。
    摘要：Background:Development of models that incorporate intact microvascular networks enables the investigation of multicellular dynamics during angiogenesis. Our laboratory introduced the rat mesentery culture model as such tool, which would be enhanced with mouse tissue. Since mouse mesentery is avascular, an alternative is mouse mesometrium, connective tissue of uterine horns. The study’s objective was to demonstrate that mouse mesometrium contains microvascular networks that can be cultured to investigate multicellular dynamics during angiogenesis.
  • 9.

    【2hr】RANKL Inhibits the Production of Osteoprotegerin from Smooth Muscle Cells under Basal Conditions and following Exposure to Cyclic Strain

    包量

    机译 RANKL抑制碱性条件下和暴露于循环菌株后平滑肌细胞中骨保护素的产生
    摘要：Receptor activator of nuclear factor-κB ligand (RANKL) promotes vascular calcification, while osteoprotegerin (OPG) opposes it by blocking RANKL activity. It remains unclear which vascular cell populations produce and secrete OPG/RANKL. This study characterizes the production of OPG/RANKL from human aortic endothelial and smooth muscle cells (HAECs and HASMCs) under various conditions. HAECs and HASMCs were exposed to inflammatory stimuli (tumor necrosis factor-α or hyperglycemia) or physiological levels of hemodynamic (cyclic) strain. After 72 h, both cells and super-natant media were harvested for assessment of OPG/RANKL production. Based on initial findings, the experiments involving HASMCs were then repeated in the presence of exogenous RANKL. OPG was produced and secreted by HASMCs and (to a considerably lesser degree) HAECs under basal conditions. Inflammatory stimuli upregulated OPG production in both cell populations. Cyclic strain significantly upregulated OPG production in HASMCs. Neither cell population produced RANKL. Exposing HASMCs to exogenous RANKL inhibited basal OPG production and completely abrogated the strain-mediated upregulation of OPG. These data suggest that HASMCs are a significant source of OPG within the vasculature but that RANKL, once present, down-regulates this production and appears capable of preventing the “protective” upregulation of OPG seen with HASMCs exposed to physiological levels of cyclic strain.
  • 10.

    【2hr】Absence of Nicotinamide Nucleotide Transhydrogenase in C57BL/6J Mice Exacerbates Experimental Atherosclerosis

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    机译 C57BL / 6J小鼠中烟酰胺核苷酸转氢酶的缺乏加剧了实验性动脉粥样硬化。
    摘要：Background:Mitochondrial reactive oxygen species (ROS) contribute to inflammation and vascular remodeling during atherosclerotic plaque formation. C57BL/6N (6N) and C57BL/6J (6J) mice display distinct mitochondrial redox balance due to the absence of nicotinamide nucleotide transhydrogenase (NNT) in 6J mice. We hypothesize that differential NNT expression between these animals alters plaque development.
  • 11.

    【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.
  • 12.

    【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.
  • 13.

    【2hr】Effect of Calcium-infiltrated Hydroxyapatite Scaffolds on Hematopoietic Fate of Human Umbilical Vein Endothelial Cells

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    机译 钙渗透性羟基磷灰石支架对人脐静脉内皮细胞造血命运的影响
    摘要：Foamed hydroxyapatite offers a three-dimensional scaffold for the development of bone constructs, mimicking perfectly the in vivo bone structure. In vivo, calcium release at the surface is assumed to provide a locally increased gradient supporting the maintenance of the hematopoietic stem cells niche. We fabricated hydroxyapatite scaffolds with high surface calcium concentration by infiltration, and used Human Umbilical Vein Endothelial Cells (HUVECs) as a model to study the effects on hematopoietic lineage direction. HUVECs are umbilical vein-derived and thus possess progenitor characteristics, with a prospective potential to give rise to hematopoietic lineages. HUVECs were cultured for long-term on three-dimensional porous hydroxyapatite scaffolds, which were either infiltrated bi-phasic foams or untreated. Controls were cultured in two-dimensional dishes. The release of calcium into culture medium was determined, and cells were analysed for typical hematopoietic and endothelial gene expressions, surface markers by flow cytometry, and hematopoietic potential using Colony Forming Unit assays. Our results indicate that the biphasic foams promoted a hematopoietic lineage direction of HUVECs, suggesting an improved in vivo-like scaffold for hematopoietic bone tissue engineering.
  • 14.

    【2hr】Toll-Like Receptor 4 Regulates Occludin and Zonula Occludens 1 to Reduce Retinal Permeability Both in vitro and in vivo

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    机译 Toll样受体4调节Occludin和Zonula Occludens 1降低体内和体外的视网膜通透性
    摘要：We reported that β-adrenergic receptors regulate toll-like receptor 4 (TLR4) signaling in the retina of diabetic mice and in retinal endothelial cells (REC) and Müller cells. We hypothesized that TLR4 regulates retinal permeability both in vitro and in vivo in the retinal vasculature. We used REC cultured in normal and high-glucose conditions and TLR4 siRNA treatments for cell culture studies of permeability and protein analyses of tumor necrosis factor a, occludin, and zonula occludens 1 (ZO-1). We used endothelial cell (EC)-specific Cre-Lox TLR4 knockout mice to study retinal permeability and neuronal and vascular changes following exposure to ocular ischemia/reperfusion (I/R) used as a retinal stressor. We found that the loss of TLR4 in the EC led to the reduced permeability following I/R and fewer degenerate capillaries. Retinal permeability was increased in REC grown in high-glucose conditions but was inhibited by TLR4 siRNA treatment. High-glucose culture conditions significantly reduced occludin and ZO-1 levels in REC, and TLR4 siRNA treatment restored levels to baseline. In conclusion, these studies demonstrate that TLR4 in EC strongly regulates retinal permeability and neuronal and vascular changes following exposure to stressors such as I/R.
  • 15.

    【2hr】Impaired mitochondrial respiration in large cerebral arteries of rats with type 2 diabetes

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    机译 2型糖尿病大鼠大脑动脉线粒体呼吸功能受损
    摘要：Mitochondrial dysfunction has been suggested as a potential underlying cause of pathological conditions associated with type 2 diabetes (T2DM). We have previously shown that mitochondrial respiration and mitochondrial protein levels were similar between the large cerebral arteries of insulin resistant Zucker obese rats and their lean controls. In the present study we extended our investigations into mitochondrial dynamics of the cerebral vasculature of 14 week old Zucker diabetic fatty obese rats (ZDFO) 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 lean controls (ZDFL). The expression of mitochondrial proteins total MnSOD and VDAC were significantly lower in the cerebral microvessels, and the acetylated MnSOD levels were significantly reduced in large arteries of ZDFO group. Additionally, superoxide production was significantly increased in the microvessels of the ZDFO group. Despite evidence of increased oxidative stress in ZDFO, exogenous superoxide dismutase was not able to restore mitochondrial respiration in ZDFO rats. Our results show for the first time that mitochondrial respiration and proteins levels are compromised during the early stages of T2DM.
  • 16.

    【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.
  • 17.

    【2hr】Differential Regulation of BMAL1, CLOCK, and Endothelial Signaling in the Aortic Arch and Ligated Common Carotid Artery

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    机译 在主动脉弓和结扎的颈总动脉中BMAL1，时钟和内皮信号的差异调节。
    摘要：The circadian clock is rhythmically expressed in blood vessels, but the interaction between the circadian clock and disturbed blood flow remains unclear. We examined the relationships between BMAL1 and CLOCK and 2 regulators of endothelial function, AKT1 and endothelial nitric oxide synthase (eNOS), in vascular regions of altered blood flow. We found that the aortic arch from WT mice exhibited reduced sensitivity to acetylcholine (Ach)-mediated relaxation relative to the thoracic aorta. In Clock-mutant (mut) mice the aorta exhibited a reduced sensitivity to Ach. In WT mice, the phosphorylated forms of eNOS and AKT were decreased in the aortic arch, while BMAL1 and CLOCK expression followed a similar pattern of reduction in the arch. In conditions of surgically induced flow reduction, phosphorylated-eNOS (serine 1177) increased, as did p-AKT in the ipsilateral left common carotid artery (LC) of WT mice. Similarly, BMAL1 and CLOCK exhibited increased expression after 5 days in the remodeled LC. eNOS expression was increased at 8 p.m. versus 8 a.m. in WT mice, and this pattern was abolished in mut and Bmal1-KO mice. These data suggest that the circadian clock may be a biomechanical and temporal sensor that acts to coordinate timing, flow dynamics, and endothelial function.
  • 18.

    【2hr】Gram-Negative Pneumonia Alters Large-Vein Cell-Adhesion Molecule Profile and Potentiates Experimental Stasis Venous Thrombosis

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    机译 革兰氏阴性肺炎改变大静脉细胞粘附分子的分布并增强实验性静脉血栓形成
    摘要：Background/AimsPneumonia is a significant risk factor for the development of venous thrombosis (VT). Cell-adhesion molecules (CAMs) are linked to the pathogenesis of both pneumonia and VT. We hypothesized that remote infection would confer a prothrombogenic milieu via systemic elevation of CAMs.
  • 19.

    【2hr】Direct Evidence for P2Y2 Receptor Involvement in Vascular Response to Injury

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    机译 P2Y2受体参与血管损伤反应的直接证据。
    摘要：ObjectivesExtracellular nucleotide release at the site of arterial injury mediates proliferation and migration of vascular smooth muscle cells (SMC). Our aim was to investigate the role of the P2Y2 nucleotide receptor (P2Y2R) in neointimal hyperplasia.
  • 20.

    【2hr】Kcne4 deletion sex-dependently alters vascular reactivity

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    机译 Kcne4缺失性别依赖性改变血管反应性
    摘要：Voltage-gated potassium (Kv) channels formed by Kv7 (KCNQ) α-subunits are recognized as crucial for vascular smooth muscle function, in addition to their established roles in the heart (Kv7.1) and the brain (Kv7.2-5). In vivo, Kv7 α-subunits are often regulated by KCNE subfamily ancillary (β) subunits. We investigated the effects of targeted germline Kcne4 deletion on mesenteric artery reactivity in adult male and female mice. Kcne4 deletion increased mesenteric artery contractility in response to α-adrenoceptor agonist methoxamine, and decreased responses to Kv7.2-7.5 channel activator ML213, in male but not female mice. In contrast, Kcne4 deletion markedly decreased vasorelaxation in response to isoprenaline in both male and female mice. Kcne4 expression was two-fold lower in female versus male mouse mesenteric artery, and Kcne4 deletion elicited only moderate changes of other Kcne transcripts, with no striking sex-specific differences. However, Kv7.4 protein expression in females was twice that in males, and reduced in both sexes by Kcne4 deletion. Our findings confirm a crucial role for KCNE4 in the vasculature, and provide the first known molecular mechanism for sex-specificity of this modulation that has important implications on vascular reactivity and may underlie sex-differences in susceptibility to cardiovascular diseases.
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