Статті в журналах: "Tissu vasculaire"

1

Andreelli, Fabrizio. "Risque cardio-vasculaire et tissu adipeux épicardique." Médecine des Maladies Métaboliques 2, no. 2 (March 2008): 166. http://dx.doi.org/10.1016/s1957-2557(08)70428-0.

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Alessi, Marie-Christine, Corinne Frère, and Irène Juhan-Vague. "Substances produites par le tissu adipeux, obésité et risque vasculaire." La Presse Médicale 34, no. 11 (June 2005): 820–24. http://dx.doi.org/10.1016/s0755-4982(05)84051-5.

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3

Bouloumié, A., M. Lafontan, and D. Langin. "Les cellules de la fraction stroma-vasculaire du tissu adipeux humain: caractérisation et rôles." Obésité 1, no. 2-4 (December 2006): 79–86. http://dx.doi.org/10.1007/s11690-006-0019-3.

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4

Nseir, I., F. Delaunay, C. Latrobe, A. Bonmarchand, D. Coquerel-Beghin, and I. Auquit-Auckbur. "Apport du tissu adipeux et de la fraction vasculaire stromale en chirurgie de la main." Revue de Chirurgie Orthopédique et Traumatologique 103, no. 6 (October 2017): 643–48. http://dx.doi.org/10.1016/j.rcot.2017.06.013.

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5

Nseir, Iad, Isabelle Auquit Auckbur, Dorothée Coquerel Beghin, Albane Bonmarchand, Flore Delaunay, and Charles Latrobe. "Apport du tissu adipeux et de la fraction vasculaire stromale en chirurgie de la main." Hand Surgery and Rehabilitation 35, no. 6 (December 2016): 485–86. http://dx.doi.org/10.1016/j.hansur.2016.10.193.

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6

Thery, A., P. Blery, O. Malard, J. Guicheux, P. Weiss, and F. Espitalier. "Apport de la fraction vasculaire stromale du tissu adipeux associée à un biomatériau dans la reconstruction osseuse en territoire irradié." Annales françaises d'Oto-rhino-laryngologie et de Pathologie Cervico-faciale 130, no. 4 (October 2013): A109. http://dx.doi.org/10.1016/j.aforl.2013.06.343.

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7

Mwamengele, G. L. M., and S. Larsen. "L’ultrastructure de lamicrovasculature cérébrale de chèvres infectées expérimentalement avec Cowdria ruminantium." Revue d’élevage et de médecine vétérinaire des pays tropicaux 46, no. 1-2 (January 1, 1993): 245. http://dx.doi.org/10.19182/remvt.9372.

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Afin d’étudier les lésions de la microvasculature cérébrale dans la cowdriose, 14 chèvres tanzaniennes ont été infectées par inoculation intraveineuse avec le stock Ball-3 de Cowdria ruminantium. Elles ont été suivies sur le plan clinique pendant la période d’incubation et la réaction fébrile, et sacrifiées lorsque les températures ont commencé à baisser. Cinq chèvres saines ont été utilisées pour déterminer la meilleure procédure pour la fixation du cerveau par perfusion et pour servir de témoins. La perfusion a été effectuée par l’artère carotide sous anesthésie générale au pentobarbitone, utilisant du glutaraldehyde de pH 7,4 à 3 p.100, à 500 mOsm. Des prélèvements de tissu cérébral ont été pris pour microscopie classique et électronique. Des signes variables de désordres du système nerveux central et un hydropéricarde peu important se sont développés chez toutes les chèvres infectées. Deux changements neuropathologiques différents ont été observés : des colonies de Cowdria dans des cellules endothéliales vasculaires, sans autres changements, et des petites infiltrations périvasculaires de cellules mononucléaires. Aucun signe de vasculite ou d’une perméabilité vasculaire anormale n’a été observé. Plusieurs phagocytes périvasculaires renfermaient des inclusions cytoplasmiques inhabituelles, se présentant comme des agrégations de particules irrégulièrement arrondies, associées à une membrane, de 0,25 à 0,4 µm de diamètre, ayant dans quelques cas une structure interne évocatrice de mitochondries partiellement dégradées. Néanmoins, ces agrégations ne semblaient pas enfermées de façon convaincante à l’intérieur de membranes, comme il est à à prévoir en cas d’autophagocytose. Une autre interprétation hypothétique est qu’elles représentent des stades abortifs de C. ruminantium qui tentent de se développer en dehors des vaisseaux et qu’une réponse immunitaire cellulaire, développée pendant et après la période d’incubation, limite ce deuxième cycle dans l’hôte et provoque des infiltrations périvasculaires mononucléaires.

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8

Gui, Liqiong, and Laura E. Niklason. "Vascular tissue engineering: building perfusable vasculature for implantation." Current Opinion in Chemical Engineering 3 (February 2014): 68–74. http://dx.doi.org/10.1016/j.coche.2013.11.004.

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9

Meiliana, Anna, and Andi Wijaya. "Perivascular Adipose Tissue and Cardiometabolic Disease." Indonesian Biomedical Journal 5, no. 1 (April 1, 2013): 13. http://dx.doi.org/10.18585/inabj.v5i1.46.

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BACKGROUND: Obesity is associated with insulin resistance, hypertension, and cardiovascular disease, but the mechanisms underlying these associations are incompletely understood. Microvascular dysfunction may play an important role in the pathogenesis of both insulin resistance and hypertension in obesity.CONTENT: Perivascular adipose tissue (PVAT) is a local deposit of adipose tissue surrounding the vasculature. PVAT is present throughout the body and has been shown to have a local effect on blood vessels. The influence of PVAT on the vasculature changes with increasing adiposity. PVAT similarly to other fat depots, is metabolically active, secreting a wide array of bioactive substances, termed ‘adipokines’. Adipokines include cytokines, chemokines and hormones that can act in a paracrine, autocrine or endocrine fashion. Many of the proinflammatory adipokines upregulated in obesity are known to influence vascular function, including endothelial function, oxidative stress, vascular stiffness and smooth muscle migration. Adipokines also stimulate immune cell migration into the vascular wall, potentially contributing to the inflammation found in atherosclerosis. Finally, adipokines modulate the effect of insulin on the vasculature, thereby decreasing insulin-mediated muscle glucose uptake. This leads to alterations in nitric oxide signaling, insulin resistance and potentially atherogenesis.SUMMARY: PVAT surrounds blood vessels. PVAT and the adventitial layer of blood vessels are in direct contact with each other. Healthy PVAT secretes adipokines and regulates vascular function. Obesity is associated with changes in adipokine secretion and the resultant inflammation of PVAT. The dysregulation of adipokines changes the effect of PVAT on the vasculature. Changes in perivascular adipokines secretion in obesity appear to contribute to the development of obesity-mediated vascular disease.KEYWORDS: obesity, perivascular adipose tissue, PVAT, cardiometabolic disease, adipokine

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10

Pommerrenig, Benjamin, Kai Eggert, and Gerd P. Bienert. "Boron Deficiency Effects on Sugar, Ionome, and Phytohormone Profiles of Vascular and Non-Vascular Leaf Tissues of Common Plantain (Plantago major L.)." International Journal of Molecular Sciences 20, no. 16 (August 9, 2019): 3882. http://dx.doi.org/10.3390/ijms20163882.

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Vascular tissues essentially regulate water, nutrient, photo-assimilate, and phytohormone logistics throughout the plant body. Boron (B) is crucial for the development of the vascular tissue in many dicotyledonous plant taxa and B deficiency particularly affects the integrity of phloem and xylem vessels, and, therefore, functionality of long-distance transport. We hypothesize that changes in the plants’ B nutritional status evoke differential responses of the vasculature and the mesophyll. However, direct analyses of the vasculature in response to B deficiency are lacking, due to the experimental inaccessibility of this tissue. Here, we generated biochemical and physiological understanding of B deficiency response reactions in common plantain (Plantago major L.), from which pure and intact vascular bundles can be extracted. Low soil B concentrations affected quantitative distribution patterns of various phytohormones, sugars and macro-, and micronutrients in a tissue-specific manner. Vascular sucrose levels dropped, and sucrose loading into the phloem was reduced under low B supply. Phytohormones responded selectively to B deprivation. While concentrations of abscisic acid and salicylic acid decreased at low B supply, cytokinins and brassinosteroids increased in the vasculature and the mesophyll, respectively. Our results highlight the biological necessity to analyze nutrient deficiency responses in a tissue- rather organ-specific manner.

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11

Liu, Yanzheng, and Albert Deisseroth. "Tumor vascular targeting therapy with viral vectors." Blood 107, no. 8 (April 15, 2006): 3027–33. http://dx.doi.org/10.1182/blood-2005-10-4114.

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AbstractTumor angiogenesis is crucial for the progression and metastasis of cancer. The vasculature of tumor tissue is different from normal vasculature. Therefore, tumor vascular targeting therapy could represent an effective therapeutic strategy with which to suppress both primary tumor growth and tumor metastasis. The use of viral vectors for tumor vascular targeting therapy is a promising strategy based on the unique properties of viral vectors. In order to circumvent the potential problems of antiviral neutralizing antibodies, poor access to extravascular tumor tissue, and toxicities to normal tissue, viral vectors need to be modified to target the tumor endothelial cells. Viral vectors that could be used for tumor vascular targeting therapy include adenoviral vectors, adeno-associated viral vectors, retroviral vectors, lentiviral vectors, measles virus, and herpes simplex viral vectors. In this review, we will summarize the strategies available for targeting viral vectors for tumor vascular targeting therapy.

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12

Witkiewicz, Halina, Phil Oh, and Jan E. Schnitzer. "I. Embryonal vasculature formation recapitulated in transgenic mammary tumor spheroids implanted pseudo-orthotopicly into mouse dorsal skin fold: the organoblasts concept." F1000Research 2 (July 11, 2013): 8. http://dx.doi.org/10.12688/f1000research.2-8.v2.

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Inadequate understanding of cancer biology is a problem. This work focused on cellular mechanisms of tumor vascularization. According to earlier studies, the tumor vasculature derives from host endothelial cells (angiogenesis) or their precursors of bone marrow origin circulating in the blood (neo-vasculogenesis) unlike in embryos. In this study, we observed the neo-vasculature form in multiple ways from local precursor cells. Recapitulation of primitive as well as advanced embryonal stages of vasculature formation followed co-implantation of avascular (in vitro cultured) N202 breast tumor spheroids and homologous tissue grafts into mouse dorsal skin chambers. Ultrastructural and immunocytochemical analysis of tissue sections exposed the interactions between the tumor and the graft tissue stem cells. It revealed details of vasculature morphogenesis not seen before in either tumors or embryos. A gradual increase in complexity of the vascular morphogenesis at the tumor site reflected a range of steps in ontogenic evolution of the differentiating cells. Malignant- and surgical injury repair-related tissue growth prompted local cells to initiate extramedullar erythropoiesis and vascular patterning. The new findings included: interdependence between the extramedullar hematopoiesis and assembly of new vessels (both from the locally differentiating precursors); nucleo-cytoplasmic conversion (karyolysis) as the mechanism of erythroblast enucleation; the role of megakaryocytes and platelets in vascular pattern formation before emergence of endothelial cells; lineage relationships between hematopoietic and endothelial cells; the role of extracellular calmyrin in tissue morphogenesis; and calmyrite, a new ultrastructural entity associated with anaerobic energy metabolism. The central role of the extramedullar erythropoiesis in the formation of new vasculature (blood and vessels) emerged here as part of the tissue building process including the lymphatic system and nerves, and suggests a cellular mechanism for instigating variable properties of endothelial surfaces in different organs. Those findings are consistent with the organoblasts concept, previously discussed in a study on childhood tumors, and have implications for tissue definition.

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13

Shinoka, Toshiharu. "Tissue-Engineered Vascular Grafts in Pediatric Cardiovascular Surgery -Past, Now, and Future." Pediatric Cardiology and Cardiac Surgery 30, no. 5 (2014): 514–22. http://dx.doi.org/10.9794/jspccs.30.514.

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14

Yogi, Alvaro. "Biochemical and Biomechanical Myogenic Differentiation of Adipose-Derived Stem Cells for Tissue Engineering Applications." Journal of Stem Cells Research, Development & Therapy 7, no. 3 (September 10, 2021): 1–7. http://dx.doi.org/10.24966/srdt-2060/100079.

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Tissue engineering has shown great promise in generating vascular grafts with properties similar to that of native blood vessels. Vascular Smooth Muscle Cells (VSMC) are the main component of the vasculature tunica media. Recreation of this layer represents a major challenge in tissue engineering due to difficulties in harvesting and culturing autologous VSMC. The use of stem cells and their inherent ability to differentiate into diverse cell types, including vascular lineages, have been proposed

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15

Born, Gordian, Marina Nikolova, Arnaud Scherberich, Barbara Treutlein, Andrés García-García, and Ivan Martin. "Engineering of fully humanized and vascularized 3D bone marrow niches sustaining undifferentiated human cord blood hematopoietic stem and progenitor cells." Journal of Tissue Engineering 12 (January 2021): 204173142110448. http://dx.doi.org/10.1177/20417314211044855.

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Hematopoietic stem and progenitor cells (HSPCs) are frequently located around the bone marrow (BM) vasculature. These so-called perivascular niches regulate HSC function both in health and disease, but they have been poorly studied in humans due to the scarcity of models integrating complete human vascular structures. Herein, we propose the stromal vascular fraction (SVF) derived from human adipose tissue as a cell source to vascularize 3D osteoblastic BM niches engineered in perfusion bioreactors. We show that SVF cells form self-assembled capillary structures, composed by endothelial and perivascular cells, that add to the osteogenic matrix secreted by BM mesenchymal stromal cells in these engineered niches. In comparison to avascular osteoblastic niches, vascularized BM niches better maintain immunophenotypically-defined cord blood (CB) HSCs without affecting cell proliferation. In contrast, HSPCs cultured in vascularized BM niches showed increased CFU-granulocyte-erythrocyte-monocyte-megakaryocyte (CFU-GEMM) numbers. The vascularization also contributed to better preserve osteogenic gene expression in the niche, demonstrating that niche vascularization has an influence on both hematopoietic and stromal compartments. In summary, we have engineered a fully humanized and vascularized 3D BM tissue to model native human endosteal perivascular niches and revealed functional implications of this vascularization in sustaining undifferentiated CB HSPCs. This system provides a unique modular platform to explore hemato-vascular interactions in human healthy/pathological hematopoiesis.

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Mirzapour-Shafiyi, Fatemeh, Yukinori Kametani, Takao Hikita, Yosuke Hasegawa, and Masanori Nakayama. "Numerical evaluation reveals the effect of branching morphology on vessel transport properties during angiogenesis." PLOS Computational Biology 17, no. 6 (June 16, 2021): e1008398. http://dx.doi.org/10.1371/journal.pcbi.1008398.

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Blood flow governs transport of oxygen and nutrients into tissues. Hypoxic tissues secrete VEGFs to promote angiogenesis during development and in tissue homeostasis. In contrast, tumors enhance pathologic angiogenesis during growth and metastasis, suggesting suppression of tumor angiogenesis could limit tumor growth. In line with these observations, various factors have been identified to control vessel formation in the last decades. However, their impact on the vascular transport properties of oxygen remain elusive. Here, we take a computational approach to examine the effects of vascular branching on blood flow in the growing vasculature. First of all, we reconstruct a 3D vascular model from the 2D confocal images of the growing vasculature at postnatal day 5 (P5) mouse retina, then simulate blood flow in the vasculatures, which are obtained from the gene targeting mouse models causing hypo- or hyper-branching vascular formation. Interestingly, hyper-branching morphology attenuates effective blood flow at the angiogenic front, likely promoting tissue hypoxia. In contrast, vascular hypo-branching enhances blood supply at the angiogenic front of the growing vasculature. Oxygen supply by newly formed blood vessels improves local hypoxia and decreases VEGF expression at the angiogenic front during angiogenesis. Consistent with the simulation results indicating improved blood flow in the hypo-branching vasculature, VEGF expression around the angiogenic front is reduced in those mouse retinas. Conversely, VEGF expression is enhanced in the angiogenic front of hyper-branching vasculature. Our results indicate the importance of detailed flow analysis in evaluating the vascular transport properties of branching morphology of the blood vessels.

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17

Binet, François, Gael Cagnone, Sergio Crespo-Garcia, Masayuki Hata, Mathieu Neault, Agnieszka Dejda, Ariel M. Wilson, et al. "Neutrophil extracellular traps target senescent vasculature for tissue remodeling in retinopathy." Science 369, no. 6506 (August 20, 2020): eaay5356. http://dx.doi.org/10.1126/science.aay5356.

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In developed countries, the leading causes of blindness such as diabetic retinopathy are characterized by disorganized vasculature that can become fibrotic. Although many such pathological vessels often naturally regress and spare sight-threatening complications, the underlying mechanisms remain unknown. Here, we used orthogonal approaches in human patients with proliferative diabetic retinopathy and a mouse model of ischemic retinopathies to identify an unconventional role for neutrophils in vascular remodeling during late-stage sterile inflammation. Senescent vasculature released a secretome that attracted neutrophils and triggered the production of neutrophil extracellular traps (NETs). NETs ultimately cleared diseased endothelial cells and remodeled unhealthy vessels. Genetic or pharmacological inhibition of NETosis prevented the regression of senescent vessels and prolonged disease. Thus, clearance of senescent retinal blood vessels leads to reparative vascular remodeling.

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18

Sekine, Ayumi, Tetsu Nishiwaki, Rintaro Nishimura, Takeshi Kawasaki, Takashi Urushibara, Rika Suda, Toshio Suzuki, et al. "Prominin-1/CD133 expression as potential tissue-resident vascular endothelial progenitor cells in the pulmonary circulation." American Journal of Physiology-Lung Cellular and Molecular Physiology 310, no. 11 (June 1, 2016): L1130—L1142. http://dx.doi.org/10.1152/ajplung.00375.2014.

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Pulmonary vascular endothelial cells could contribute to maintain homeostasis in adult lung vasculature. “Tissue-resident” endothelial progenitor cells (EPCs) play pivotal roles in postnatal vasculogenesis, vascular repair, and tissue regeneration; however, their local pulmonary counterparts remain to be defined. To determine whether prominin-1/CD133 expression can be a marker of tissue-resident vascular EPCs in the pulmonary circulation, we examined the origin and characteristics of prominin-1/CD133-positive (Prom1+) PVECs considering cell cycle status, viability, histological distribution, and association with pulmonary vascular remodeling. Prom1+PVECs exhibited high steady-state transit through the cell cycle compared with Prom1−PVECs and exhibited homeostatic cell division as assessed using the label dilution method and mice expressing green fluorescent protein. In addition, Prom1+PVECs showed more marked expression of putative EPC markers and drug resistance genes as well as highly increased activation of aldehyde dehydrogenase compared with Prom1−PVECs. Bone marrow reconstitution demonstrated that tissue-resident cells were the source of >98% of Prom1+PVECs. Immunofluorescence analyses revealed that Prom1+PVECs preferentially resided in the arterial vasculature, including the resistant vessels of the lung. The number of Prom1+PVECs was higher in developing postnatal lungs. Sorted Prom1+PVECs gave rise to colonies and formed fine vascular networks compared with Prom1−PVECs. Moreover, Prom1+PVECs increased in the monocrotaline and the Su-5416 + hypoxia experimental models of pulmonary vascular remodeling. Our findings indicated that Prom1+PVECs exhibited the phenotype of tissue-resident EPCs. The unique biological characteristics of Prom1+PVECs predominantly contribute to neovasculogenesis and maintenance of homeostasis in pulmonary vascular tissues.

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19

Hossler, Fred E. "Some quantitative applications of vascular corrosion casting." Proceedings, annual meeting, Electron Microscopy Society of America 50, no. 1 (August 1992): 738–39. http://dx.doi.org/10.1017/s0424820100124094.

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Preparation of replicas of the complex arrangement of blood vessels in various organs and tissues has been accomplished by infusing low viscosity resins into the vasculature. Subsequent removal of the surrounding tissue by maceration leaves a model of the intricate three-dimensional anatomy of the blood vessels of the tissue not obtainable by any other procedure. When applied with care, the vascular corrosion casting technique can reveal fine details of the microvasculature including endothelial nuclear orientation and distribution (Fig. 1), locations of arteriolar sphincters (Fig. 2), venous valve anatomy (Fig. 3), and vessel size, density, and branching patterns. Because casts faithfully replicate tissue vasculature, they can be used for quantitative measurements of that vasculature. The purpose of this report is to summarize and highlight some quantitative applications of vascular corrosion casting. In each example, casts were prepared by infusing Mercox, a methyl-methacrylate resin, and macerating the tissue with 20% KOH. Casts were either mounted for conventional scanning electron microscopy, or sliced for viewing with a confocal laser microscope.

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20

Hägerling, René. "Light sheet microscopy-based 3-dimensional histopathology of the lymphatic vasculature in Emberger syndrome." Phlebologie 49, no. 04 (August 2020): 242–48. http://dx.doi.org/10.1055/a-1191-8380.

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Abstract Introduction Lymphovascular diseases represent a heterogenous group of inherited and sporadic disorders and refer to a range of possible underlying pathologies and pathogenesis.Emberger Syndrome, an inherited form of lymphedema, is characterized by bilateral lower limb lymphedema, however, upper limbs do not show any signs of swelling.To identify disease-associated histopathological alterations in patients with Emberger Syndrome and to elucidate potential histological differences between the lymphatic vasculature of upper and lower limbs, a detailed knowledge on the 3-dimensional tissue and vessel architecture is essential. However, the current gold standard in 2-dimensional histology provides only very limited spatial information. Material and methods To elucidate the underlying vascular pathology in Emberger Syndrome on the cellular level, we applied the 3-dimensional visualization and analysis approach VIPAR (volume information-based histopathological analysis by 3D reconstruction and data extraction) to entire wholemount immunofluorescence-stained human tissue samples. VIPAR is a light sheet microscopy-based imaging technique, which allows 3-dimensional reconstruction of entire tissue biopsies followed by automated and semi-automated analysis of vascular parameters in 3-dimensional space. Results Using VIPAR we could show that in Emberger Syndrome the dermal lymphatic vasculature is intact and non-disrupted.However, lower limbs showed an hypoplastic lymphatic vasculature with absence of lymphatic valves in pre-collecting and collecting vessels. In contrast to the lower limbs, the lymphatic vasculature of the upper limbs showed no morphological alterations of lymphatic vessels and lymphatic valves compared to healthy controls. Discussion Based on the 3-dimensional histopathological analysis we were able to perform a detailed phenotyping of lymphatic vessels in the upper and lower limb in Emberger Syndrome and to identify the underlying vascular pathology. In addition, we could show vascular alteration between the upper and lower limbs indicating a vascular heterogeneity of dermal lymph vessels causing the lower limb lymphedema.

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Frey, Carlos, José Luis Acebes, Antonio Encina, and Rafael Álvarez. "Histological Changes Associated with the Graft Union Development in Tomato." Plants 9, no. 11 (November 3, 2020): 1479. http://dx.doi.org/10.3390/plants9111479.

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Despite the importance of grafting in horticultural crops such as tomato (Solanum lycopersicum L.), the structural changes that occur during the graft establishment are little understood. Using histological techniques, the present work examines the time course of changes on the anatomical structure of the graft junction in functional tomato homografts and compares it to that of heterografts and non-functional grafts. No apparent differences were detected between homo- and heterografts, showing similar tissue development. At 10 days after grafting, the cell walls of the scion and rootstock in the area of the graft junction were thicker than usual. Undifferentiated cells and new vascular tissue emerged from the pre-existing vasculature. Adventitious roots appeared mainly on the scion, arising from the pre-existing vasculature. At 20 days, more pronounced vascular tissue was visible, along with large areas showing vascular connection. At 210 days, vestiges of the changes undergone in graft development were still visible. Generally, non-functional grafts presented layers of necrotic remains and deposition of cell wall material in the cut edges, impeding the suitable scion-rootstock connection. Our results show that accurate changes in pre-existing vasculature and the cell walls of the adhesion line are crucial to the development of functional grafts.

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Mancio, Jennifer, Evangelos K. Oikonomou, and Charalambos Antoniades. "Perivascular adipose tissue and coronary atherosclerosis." Heart 104, no. 20 (May 31, 2018): 1654–62. http://dx.doi.org/10.1136/heartjnl-2017-312324.

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Adipose tissue (AT) is no longer viewed as a passive, energy-storing depot, and a growing body of evidence supports the concept that both quantitative and qualitative aspects of AT are critical in determining an individual’s cardiometabolic risk profile. Among all AT sites, perivascular AT (PVAT) has emerged as a depot with a distinctive biological significance in cardiovascular disease given its close anatomical proximity to the vasculature. Recent studies have suggested the presence of complex, bidirectional paracrine and vasocrine signalling pathways between the vascular wall and its PVAT, with far-reaching implications in cardiovascular diagnostics and therapeutics. In this review, we first discuss the biological role of PVAT in both cardiovascular health and disease, highlighting its dual pro-atherogenic and anti-atherogenic roles, as well as potential therapeutic targets in cardiovascular disease. We then review current evidence and promising new modalities on the non-invasive imaging of epicardial AT and PVAT. Specifically, we present how our expanding knowledge on the bidirectional interplay between the vascular wall and its PVAT can be translated into novel clinical diagnostics tools to assess coronary inflammation. To this end, we present the example of a new CT-based method that tracks spatial changes in PVAT phenotype to extract information about the inflammatory status of the adjacent vasculature, highlighting the numerous diagnostic and therapeutic opportunities that arise from our increased understanding of PVAT biology.

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Huang, Xin, Wei-Qun Ding, Joshua L. Vaught, Roman F. Wolf, James H. Morrissey, Roger G. Harrison, and Stuart E. Lind. "A soluble tissue factor-annexin V chimeric protein has both procoagulant and anticoagulant properties." Blood 107, no. 3 (February 1, 2006): 980–86. http://dx.doi.org/10.1182/blood-2005-07-2733.

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AbstractTissue factor (TF) initiates blood coagulation, but its expression in the vascular space requires a finite period of time. We hypothesized that targeting exogenous tissue factor to sites of vascular injury could lead to accelerated hemostasis. Since phosphatidylserine (PS) is exposed on activated cells at sites of vascular injury, we cloned the cDNA for a chimeric protein consisting of the extracellular domain of TF (called soluble TF or sTF) and annexin V, a human PS-binding protein. Both the sTF and annexin V domains had ligand-binding activities consistent with their native counterparts, and the chimera accelerated factor X activation by factor VIIa. The chimera exhibited biphasic effects upon blood coagulation. At low concentrations it accelerated blood coagulation, while at higher concentrations it acted as an anticoagulant. The chimera accelerated coagulation in the presence of either unfractionated or low-molecular-weight heparins more potently than factor VIIa and shortened the bleeding time of mice treated with enoxaparin. The sTF-annexin V chimera is a targeted procoagulant protein that may be useful in accelerating thrombin generation where PS is exposed to the vasculature, such as may occur at sites of vascular injury or within the vasculature of tumors.

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Salehi, Arjang, Amandine Jullienne, Mohsen Baghchechi, Mary Hamer, Mark Walsworth, Virginia Donovan, Jiping Tang, John H. Zhang, William J. Pearce та Andre Obenaus. "Up-regulation of Wnt/β-catenin expression is accompanied with vascular repair after traumatic brain injury". Journal of Cerebral Blood Flow & Metabolism 38, № 2 (21 листопада 2017): 274–89. http://dx.doi.org/10.1177/0271678x17744124.

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Recent data suggest that repairing the cerebral vasculature after traumatic brain injury (TBI) may help to improve functional recovery. The Wnt/β-catenin signaling pathway promotes blood vessel formation during vascular development, but its role in vascular repair after TBI remains elusive. In this study, we examined how the cerebral vasculature responds to TBI and the role of Wnt/β-catenin signaling in vascular repair. We induced a moderate controlled cortical impact in adult mice and performed vessel painting to visualize the vascular alterations in the brain. Brain tissue around the injury site was assessed for β-catenin and vascular markers. A Wnt transgenic mouse line was utilized to evaluate Wnt gene expression. We report that TBI results in vascular loss followed by increases in vascular structure at seven days post injury (dpi). Immature, non-perfusing vessels were evident in the tissue around the injury site. β-catenin protein expression was significantly reduced in the injury site at 7 dpi. However, there was an increase in β-catenin expression in perilesional vessels at 1 and 7 dpi. Similarly, we found increased number of Wnt-GFP-positive vessels after TBI. Our findings suggest that Wnt/β-catenin expression contributes to the vascular repair process after TBI.

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Enbäck, J., and P. Laakkonen. "Tumour-homing peptides: tools for targeting, imaging and destruction." Biochemical Society Transactions 35, no. 4 (July 20, 2007): 780–83. http://dx.doi.org/10.1042/bst0350780.

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Each normal organ and pathological condition contains organ- or disease-specific molecular tags on its vasculature that constitute a vascular ‘zip code’ system. Tissue-selective tumour metastasis may also depend on vascular addresses. We have used phage display peptide libraries to map disease-specific differences in the vasculature. By using this technology, we have isolated several peptides which are targeted specifically to tumour blood vessels, lymphatic vessels and/or tumour cells. Some of the tumour-homing peptides recognize common angiogenesis markers and are capable of binding to several types of tumour, whereas other peptides recognize tumour-type-specific differences. We have also shown that the vasculature of a pre-malignant lesion differs from that of a full-blown tumour and also from the vasculature of the corresponding normal organ. Our peptides have revealed molecules that act as novel biomarkers of this vascular heterogeneity. Interestingly, some of our homing peptides are able to penetrate the target cells. This internalization differs from that of the Tat, penetratins and other related peptides in that our peptides enter the cell in a cell-type-specific manner. These peptides appear to be able to concentrate in the target tissue, making them particularly efficient delivery vectors for the targeting of drugs, other therapeutic moieties and imaging agents.

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Perles-Barbacaru, Adriana T., Boudewijn PJ van der Sanden, Regine Farion, and Hana Lahrech. "How Stereological Analysis of Vascular Morphology Can Quantify the Blood Volume Fraction as a Marker for Tumor Vasculature: Comparison with Magnetic Resonance Imaging." Journal of Cerebral Blood Flow & Metabolism 32, no. 3 (November 9, 2011): 489–501. http://dx.doi.org/10.1038/jcbfm.2011.151.

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To assess angiogenesis noninvasively in a C6 rat brain tumor model, the rapid-steady-state- T1 (RSST1) magnetic resonance imaging (MRI) method was used for microvascular blood volume fraction (BVf) quantification with a novel contrast agent gadolinium per (3,6 anhydro) α-cyclodextrin (Gd-ACX). In brain tissue contralateral to the tumor, equal BVfs were obtained with Gd-ACX and the clinically approved gadoterate meglumine (Gd-DOTA). Contrary to Gd-DOTA, which leaks out of the tumor vasculature, Gd-ACX was shown to remain vascular in the tumor tissue allowing quantification of the tumor BVf. We sought to confirm the obtained tumor BVf using an independent method: instead of using a ‘standard’ two-dimensional histologic method, we study here how vascular morphometry combined with a stereological technique can be used for three-dimensional assessment of the vascular volume fraction ( VV). The VV is calculated from the vascular diameter and length density. First, the technique is evaluated on simulated data and the healthy rat brain vasculature and is then applied to the same C6 tumor vasculature previously quantified by RSST1-MRI with Gd-ACX. The mean perfused VV and the BVf obtained by MRI in tumor regions are practically equal and the technique confirms the spatial heterogeneity revealed by MRI.

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Mace, Maria L., Søren Egstrand, Marya Morevati, Klaus Olgaard, and Ewa Lewin. "New Insights to the Crosstalk between Vascular and Bone Tissue in Chronic Kidney Disease–Mineral and Bone Disorder." Metabolites 11, no. 12 (December 7, 2021): 849. http://dx.doi.org/10.3390/metabo11120849.

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Vasculature plays a key role in bone development and the maintenance of bone tissue throughout life. The two organ systems are not only linked in normal physiology, but also in pathophysiological conditions. The chronic kidney disease–mineral and bone disorder (CKD-MBD) is still the most serious complication to CKD, resulting in increased morbidity and mortality. Current treatment therapies aimed at the phosphate retention and parathyroid hormone disturbances fail to reduce the high cardiovascular mortality in CKD patients, underlining the importance of other factors in the complex syndrome. This review will focus on vascular disease and its interplay with bone disorders in CKD. It will present the very late data showing a direct effect of vascular calcification on bone metabolism, indicating a vascular-bone tissue crosstalk in CKD. The calcified vasculature not only suffers from the systemic effects of CKD but seems to be an active player in the CKD-MBD syndrome impairing bone metabolism and might be a novel target for treatment and prevention.

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Zhu, Chu-hong, Da-jun Ying, and Jian-hong Mi. "Tissue engineering of vascular grafts on xenogenic acellular matrix conduits using endothelial progenitors in human postnatal bone marrow(Cellular & Tissue Engineering)." Proceedings of the Asian Pacific Conference on Biomechanics : emerging science and technology in biomechanics 2004.1 (2004): 79–80. http://dx.doi.org/10.1299/jsmeapbio.2004.1.79.

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29

Arai, Masataka, Shota Hori, Satoshi Miyamoto, Kazuhiro Nakashima, Toshihiro Sera, and Susumu Kudo. "OS18-5 Mechanical Stimulus Effects Diacylglycerol Distribution in Vascular Endothelial Cells(Cell and Tissue mechanics 2,OS18 Cell and tissue mechanics,BIOMECHANICS)." Abstracts of ATEM : International Conference on Advanced Technology in Experimental Mechanics : Asian Conference on Experimental Mechanics 2015.14 (2015): 239. http://dx.doi.org/10.1299/jsmeatem.2015.14.239.

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30

Hossler, Fred E. "Vascular Corrosion Casting Can Provide Quantitative as Well as Morphological Information on the Microvasculature of Organs and Tissues." Microscopy Today 6, no. 7 (September 1998): 14–15. http://dx.doi.org/10.1017/s1551929500068620.

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Complete casts of the vasculature of organs and tissues are obtained by infusing low viscosity resins into the vasculature and allowing the resin to polymerize. Dissolving away the surrounding tissue with alkali leaves a model of the intricate, three-dimensional distribution of vessels in that tissue, which is not easily obtainable by any other means, and which can then be studied with scanning electron microscopy (SEM), Because well prepared casts appear to faithfully replicate the true vascular anatomy of organs including the dimensions of vessels and details of imprints of the endothelial cells lining their lumens, they must also contain quantitative information about that vasculature.

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Dean, Ryan J., Simon J. Clarke, Suzy Y. Rogiers, Timothy Stait-Gardner, and William S. Price. "Solute transport within grape berries inferred from the paramagnetic properties of manganese." Functional Plant Biology 44, no. 10 (2017): 969. http://dx.doi.org/10.1071/fp16406.

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Tracer compounds used for studying solute transport should ideally have identical functions and transport properties to the molecules they are designed to mimic. Unfortunately, the xylem-mobile tracer compounds currently used to infer solute transport mechanisms in botanical specimens such as the fruit of the grapevine, Vitis vinifera L., are typically xenobiotic and have difficulty exiting the xylem during berry ripening. Here it is demonstrated that the transport of paramagnetic Mn ions can be indirectly observed within the grape berry, using relaxation magnetic resonance imaging (MRI). Mn ions from a 10 mM Mn chloride solution were taken up into the grape berry via the pedicel and moved through the peripheral vasculature before exiting into surrounding pericarp tissue. Mn did not exit evenly across the berry, implying that the berry xylem influences which sites Mn exits the vasculature ‘downstream’ of the berry pedicel. It was also found that when the cellular membranes of pericarp tissues were disrupted, the distribution of Mn through the pericarp tissue became noticeably more homogenous. This indicates that the cellular membranes of extra-vascular cells affect the spatial distribution of Mn across the berry extra-vascular pericarp tissue upon exiting the grape berry vasculature.

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Shields, Kelly J., Kostas Verdelis, Michael J. Passineau, Erin M. Faight, Lee Zourelias, Changgong Wu, Rong Chong, and Raymond L. Benza. "Three-Dimensional Micro Computed Tomography Analysis of the Lung Vasculature and Differential Adipose Proteomics in the Sugen/Hypoxia Rat Model of Pulmonary Arterial Hypertension." Pulmonary Circulation 6, no. 4 (December 2016): 586–96. http://dx.doi.org/10.1086/688931.

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Pulmonary arterial hypertension (PAH) is a rare disease characterized by significant vascular remodeling. The obesity epidemic has produced great interest in the relationship between small visceral adipose tissue depots producing localized inflammatory conditions, which may link metabolism, innate immunity, and vascular remodeling. This study used novel micro computed tomography (microCT) three-dimensional modeling to investigate the degree of remodeling of the lung vasculature and differential proteomics to determine small visceral adipose dysfunction in rats with severe PAH. Sprague-Dawley rats were subjected to a subcutaneous injection of vascular endothelial growth factor receptor blocker (Sugen 5416) with subsequent hypoxia exposure for 3 weeks (SU/hyp). At 12 weeks after hypoxia, microCT analysis showed a decrease in the ratio of vascular to total tissue volume within the SU/hyp group (mean ± standard deviation: 0.27 ± 0.066; P = 0.02) with increased vascular separation (0.37 ± 0.062 mm; P = 0.02) when compared with the control (0.34 ± 0.084 and 0.30 ± 0.072 mm). Differential proteomics detected an up-regulation of complement protein 3 (C3; SU/hyp: control ratio = 2.86) and the adipose tissue–specific fatty acid binding protein-4 (FABP4, 2.66) in the heart adipose of the SU/hyp. Significant remodeling of the lung vasculature validates the efficacy of the SU/hyp rat for modeling human PAH. The upregulation of C3 and FABP4 within the heart adipose implicates small visceral adipose dysfunction. C3 has been associated with vascular stiffness, and FABP4 suppresses peroxisome proliferator–activated receptor, which is a major regulator of adipose function and known to be downregulated in PAH. These findings reveal that small visceral adipose tissue within the SU/hyp model provides mechanistic links for vascular remodeling and adipose dysfunction in the pathophysiology of PAH.

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Kugler, Elisabeth, Ryan Snodgrass, George Bowley, Karen Plant, Jovana Serbanovic-Canic, Noémie Hamilton, Paul C. Evans, Timothy Chico, and Paul Armitage. "The effect of absent blood flow on the zebrafish cerebral and trunk vasculature." Vascular Biology 3, no. 1 (August 25, 2021): 1–16. http://dx.doi.org/10.1530/vb-21-0009.

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The role of blood flow in vascular development is complex and context-dependent. In this study, we quantify the effect of the lack of blood flow on embryonic vascular development on two vascular beds, namely the cerebral and trunk vasculature in zebrafish. We perform this by analysing vascular topology, endothelial cell (EC) number, EC distribution, apoptosis, and inflammatory response in animals with normal blood flow or absent blood flow. We find that absent blood flow reduced vascular area and EC number significantly in both examined vascular beds, but the effect is more severe in the cerebral vasculature, and severity increases over time. Absent blood flow leads to an increase in non-EC-specific apoptosis without increasing tissue inflammation, as quantified by cerebral immune cell numbers and nitric oxide. Similarly, while stereotypic vascular patterning in the trunk is maintained, intra-cerebral vessels show altered patterning, which is likely to be due to vessels failing to initiate effective fusion and anastomosis rather than sprouting or path-seeking. In conclusion, blood flow is essential for cellular survival in both the trunk and cerebral vasculature, but particularly intra-cerebral vessels are affected by the lack of blood flow, suggesting that responses to blood flow differ between these two vascular beds.

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Rami, Afifah Zahirah Abd, Adila A. Hamid, Nur Najmi Mohamad Anuar, Amilia Aminuddin, and Azizah Ugusman. "Exploring the Relationship of Perivascular Adipose Tissue Inflammation and the Development of Vascular Pathologies." Mediators of Inflammation 2022 (February 8, 2022): 1–16. http://dx.doi.org/10.1155/2022/2734321.

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Initially thought to only provide mechanical support for the underlying blood vessels, perivascular adipose tissue (PVAT) has now emerged as a regulator of vascular function. A healthy PVAT exerts anticontractile and anti-inflammatory actions on the underlying vasculature via the release of adipocytokines such as adiponectin, nitric oxide, and omentin. However, dysfunctional PVAT produces more proinflammatory adipocytokines such as leptin, resistin, interleukin- (IL-) 6, IL-1β, and tumor necrosis factor-alpha, thus inducing an inflammatory response that contributes to the pathogenesis of vascular diseases. In this review, current knowledge on the role of PVAT inflammation in the development of vascular pathologies such as atherosclerosis and hypertension was discussed.

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Fuseler, John W., Adam Bedenbaugh, Krishna Yekkala, and Troy A. Baudino. "Fractal and Image Analysis of the Microvasculature in Normal Intestinal Submucosa and Intestinal Polyps in ApcMin/+ Mice." Microscopy and Microanalysis 16, no. 1 (December 24, 2009): 73–79. http://dx.doi.org/10.1017/s143192760999119x.

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AbstractTumors are supported by the development of a unique vascular bed. We used fractal dimension (Db) and image analysis to quantify differences in the complexity of the vasculature in normal intestinal submucosa and intestinal polyps. ApcMin/+ mice and wild-type mice were perfused with a curable latex compound, intestines sectioned, and images collected via confocal microscopy. The images were analyzed and area (A), perimeter (P), and integrated optical density (IOD) of the normal and tumor vascular beds were measured. The Db, a quantitative descriptor of morphological complexity, was significantly greater for the polyp vasculature from ApcMin/+ mice than controls. This indicates that the polyp microvasculature is more chaotic than that of the controls, while the IOD and average vascular density values displayed no differences. This suggests the mass of blood volume is equivalent in normal and polyp microvasculature. The lower vascular area-perimeter ratios expressed by the polyp microvasculature suggest it is composed of smaller, more tortuous vessels. These data demonstrate that fractal analysis is applicable for providing a quantitative description of vascular complexity associated with angiogenesis occurring in normal or diseased tissue. Application of Db, IOD, and average density provides a clearer quantification of the complex morphology associated with tissue microvasculature.

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Lee, Hye-Jin, Haifei Shi, Hella S. Brönneke, Bo-Yeong Jin, Sang-Hyun Choi, Randy J. Seeley, and Dong-Hoon Kim. "Vascular reactivity contributes to adipose tissue remodeling in obesity." Journal of Endocrinology 251, no. 3 (December 1, 2021): 195–206. http://dx.doi.org/10.1530/joe-21-0187.

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Vascular reactivity of adipose tissue (AT) is hypothesized to play an important role in the development of obesity. However, the exact role of vascular reactivity in the development of obesity remains unclear. In this study, we investigated the chronological changes in vascular reactivity and the microenvironments of the visceral AT (VAT) and subcutaneous AT (SAT) in lean and obese mice. Changes in blood flow levels induced by a β-adrenoceptor agonist (isoproterenol) were significantly lower in the VAT of the mice fed a high-fat diet (HFD) for 1 and 12 weeks than those in the VAT of the mice fed a low-fat diet (LFD) for the same period; no significant change was observed in the SAT of any mouse group, suggesting depot-specific vascular reactivity of AT. Moreover, the hypoxic area and the expression of genes associated with angiogenesis and macrophage recruitment were increased in the VAT (but not in the SAT) of mice fed an HFD for 1 week compared with mice fed an LFD. These changes occurred with no morphological changes, including those related to adipocyte size, AT vessel density, and the diameter and pericyte coverage of the endothelium, suggesting a determinant role of vascular reactivity in the type of AT remodeling. The suppression of vascular reactivity was accompanied by increased endothelin1 (Edn1) gene expression and extracellular matrix (ECM) stiffness only in the VAT, implying enhanced contractile activities of the vasculature and ECM. The results suggest a depot-specific role of vascular reactivity in AT remodeling during the development of obesity.

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Fernández-Alfonso, Maria S., Marta Gil-Ortega, Concha F. García-Prieto, Isabel Aranguez, Mariano Ruiz-Gayo, and Beatriz Somoza. "Mechanisms of Perivascular Adipose Tissue Dysfunction in Obesity." International Journal of Endocrinology 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/402053.

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Most blood vessels are surrounded by adipose tissue. Similarly to the adventitia, perivascular adipose tissue (PVAT) was considered only as a passive structural support for the vasculature, and it was routinely removed for isolated blood vessel studies. In 1991, Soltis and Cassis demonstrated for the first time that PVAT reduced contractions to noradrenaline in rat aorta. Since then, an important number of adipocyte-derived factors with physiological and pathophysiological paracrine vasoactive effects have been identified. PVAT undergoes structural and functional changes in obesity. During early diet-induced obesity, an adaptative overproduction of vasodilator factors occurs in PVAT, probably aimed at protecting vascular function. However, in established obesity, PVAT loses its anticontractile properties by an increase of contractile, oxidative, and inflammatory factors, leading to endothelial dysfunction and vascular disease. The aim of this review is to focus on PVAT dysfunction mechanisms in obesity.

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Chang, Lin, Minerva T. Garcia-Barrio, and Y. Eugene Chen. "Perivascular Adipose Tissue Regulates Vascular Function by Targeting Vascular Smooth Muscle Cells." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 5 (May 2020): 1094–109. http://dx.doi.org/10.1161/atvbaha.120.312464.

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Adipose tissues are present at multiple locations in the body. Most blood vessels are surrounded with adipose tissue which is referred to as perivascular adipose tissue (PVAT). Similarly to adipose tissues at other locations, PVAT harbors many types of cells which produce and secrete adipokines and other undetermined factors which locally modulate PVAT metabolism and vascular function. Uncoupling protein-1, which is considered as a brown fat marker, is also expressed in PVAT of rodents and humans. Thus, compared with other adipose tissues in the visceral area, PVAT displays brown-like characteristics. PVAT shows a distinct function in the cardiovascular system compared with adipose tissues in other depots which are not adjacent to the vascular tree. Growing and extensive studies have demonstrated that presence of normal PVAT is required to maintain the vasculature in a functional status. However, excessive accumulation of dysfunctional PVAT leads to vascular disorders, partially through alteration of its secretome which, in turn, affects vascular smooth muscle cells and endothelial cells. In this review, we highlight the cross talk between PVAT and vascular smooth muscle cells and its roles in vascular remodeling and blood pressure regulation.

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Maina, Renee M., Maria J. Barahona, Michele Finotti, Taras Lysyy, Peter Geibel, Francesco D’Amico, David Mulligan, and John P. Geibel. "Generating vascular conduits: from tissue engineering to three-dimensional bioprinting." Innovative Surgical Sciences 3, no. 3 (June 27, 2018): 203–13. http://dx.doi.org/10.1515/iss-2018-0016.

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AbstractVascular disease – including coronary artery disease, carotid artery disease, and peripheral vascular disease – is a leading cause of morbidity and mortality worldwide. The standard of care for restoring patency or bypassing occluded vessels involves using autologous grafts, typically the saphenous veins or internal mammary arteries. Yet, many patients who need life- or limb-saving procedures have poor outcomes, and a third of patients who need vascular intervention have multivessel disease and therefore lack appropriate vasculature to harvest autologous grafts from. Given the steady increase in the prevalence of vascular disease, there is great need for grafts with the biological and mechanical properties of native vessels that can be used as vascular conduits. In this review, we present an overview of methods that have been employed to generate suitable vascular conduits, focusing on the advances in tissue engineering methods and current three-dimensional (3D) bioprinting methods. Tissue-engineered vascular grafts have been fabricated using a variety of approaches such as using preexisting scaffolds and acellular organic compounds. We also give an extensive overview of the novel use of 3D bioprinting as means of generating new vascular conduits. Different strategies have been employed in bioprinting, and the use of cell-based inks to create de novo structures offers a promising solution to bridge the gap of paucity of optimal donor grafts. Lastly, we provide a glimpse of our work to create scaffold-free, bioreactor-free, 3D bioprinted vessels from a combination of rat vascular smooth muscle cells and fibroblasts that remain patent and retain the tensile and mechanical strength of native vessels.

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Isayama, Noriko, Goki Matsumura, Hideki Sato, Shojiro Matsuda, and Kenji Yamazaki. "Histological maturation of vascular smooth muscle cells in in situ tissue-engineered vasculature." Biomaterials 35, no. 11 (April 2014): 3589–95. http://dx.doi.org/10.1016/j.biomaterials.2014.01.006.

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Li, Jian-Jun, Yao-Qi Huang, Ross Basch, and Simon Karpatkin. "Thrombin Induces the Release of Angiopoietin-1 from Platelets." Thrombosis and Haemostasis 85, no. 02 (2001): 204–6. http://dx.doi.org/10.1055/s-0037-1615677.

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SummaryBlood platelets contain angiopoietin-1, a growth factor essential for blood vessel development via stabilization of proliferating endothelial cells. It has recently been reported that angiopoietin-1 can act as a vascular stability factor (Nature Medicine 6:460, 2000). In investigating the normal tissue distribution of angiopoietin-1 from surgically-removed frozen specimens by RT-PCR, we found it consistently present in platelets and megakaryocytes, usually absent in relatively non-vascular tissue: breast, colon, lung, skin, kidney, thyroid, testicle, cervix and occasionally present in tissue enriched with vasculature: prostate, endometrium, ovary, under conditions in which mRNA stability was verified by the positive detection of internal control, actin mRNA. The consistent distribution in platelets and relatively absent distribution in non-vascular normal tissue suggested that the well-known role of platelets in maintaining vascular stability, may in part be due to platelet release of angiopoietin-1 following platelet activation. In this communication we report the incidence of Ang-1 in various normal tissues and demonstrate that thrombin-treated human platelets release angiopoietin-1 in vitro.

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Banerjee, Indroneal, John W. Fuseler, Colby A. Souders, Stephanie L. K. Bowers, and Troy A. Baudino. "The Role of Interleukin-6 in the Formation of the Coronary Vasculature." Microscopy and Microanalysis 15, no. 5 (August 27, 2009): 415–21. http://dx.doi.org/10.1017/s1431927609990353.

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AbstractThe formation and the patterning of the coronary vasculature are critical to the development and pathology of the heart. Alterations in cytokine signaling and biomechanical load can alter the vascular distribution of the vessels within the heart. Changes in the physical patterning of the vasculature can have significant impacts on the relationships of the pressure-flow network and distribution of critical growth and survival factors to the tissue. Interleukin-6 (IL-6) is a pleiotropic cytokine that regulates several biological processes, including vasculogenesis. Using both immunohistological and cardioangiographic analyses, we tested the hypothesis that IL-6-loss will result in decreased vessel density, along with changes in vascular distribution. Moreover, given the impact of vascular patterning on pressure-flow and distribution mechanics, we utilized non-Euclidean geometrical fractal analysis to quantify the changes in patterning resulting from IL-6-loss. Our analyses revealed that IL-6-loss results in a decreased capillary density and increase in intercapillary distances, but does not alter vessel size or diameter. We also observed that the IL-6−/− coronary vasculature had a marked increase in fractal dimension (D value), indicating that IL-6-loss alters vascular patterning. Characterization of IL-6-loss on coronary vasculature may lend insight into the role of IL-6 in the formation and patterning of the vascular bed.

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Mignemi, Nicholas, Heather Cole, Masato Yausa, David Gailani, Jay L. Degen, and Jonathan G. Schoenecker. "Deficiency in Plasminogen Cause Decreased Vascularity in Sold Tissue Organs and Bone." Blood 118, no. 21 (November 18, 2011): 857. http://dx.doi.org/10.1182/blood.v118.21.857.857.

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Abstract Abstract 857 A sufficient vascular supply is critical for proper physiologic function of solid-tissue organs and bone. Tissue vascularity is mediated concomitantly through vascular patency and angiogenesis. Recently, numerous studies have associated plasminogen, the key fibrinolytic protease of the coagulation system, with maintaining vascular patency by preventing fibrin accumulation with in the vasculature. Additionally, plasminogen may also have a direct role in angiogenesis as it has been shown in vitro that inhibitors of plasmin(ogen) suppress formation of capillary structures from normal endothelial cells and cells cultured from plasmin(ogen) deficient mice have reduced capillary sprouting in response to the angiogenic stimulator VEGF-A. Therefore, we hypothesized that plasminogen is essential for developing and maintaining vascularity in solid-tissue organs and revascularization of bone fracture calluses. To determine if there was a discernable difference in vivo between the vascular supply of plasminogen deficient (plg−/−) and wild type mice we performed microfil profusion studies visualized using a Sanco 40 μCT. We determined that plg−/− mice have a diminished renal and hepatic vascularity compared to wild type mice at 3 and 20 weeks of age (Figure 1). Further, we show that plg−/− mice fail to develop a blood supply at the fracture site by week 2 post-fracture whereas the control mice exhibit a highly neovascularized capillary system (Figure 2). Plg −/− mice also fail to develop a mineralized callus around a two week old fracture site demonstrating a role for plasmin(ogen) in osteoblast minimization. These findings demonstrate that disruption of the fibrinolytic system's main proteolytic enzyme plasmin results in decreased vascularity of solid-tissue organs and revascularization of bone fracture calluses. While the role of plasmin(ogen) in vascularity is clear, further studies are warranted to elucidate its mechanisms of action. Studies investigating plasmin(ogen)'s role in vascularity may have importance in variety of biologic conditions and pathologies. For example, aging, diabetes and smoking, all of which are known to incur an acquired deficiency or dysfunction of fibrinolysis lead to complications of vascularity (cardiovascular disease) and are also associated with pathologic bone disease (osteoporosis and poor fracture healing). These data indicate that plasmin(ogen) and its biologic targets may provide future novel therapeutic targets for treatment of pathologies involving impaired vascularization.Figure 1:Vascularization of Kidney and Liver in Wild Type and Plasminogen Deficient Mice: Microfil of both kidney and liver of plasminogen −/− show decreased vascularity as compared to WT mice. Colors denote diameter of the vasculature. Red represent large diameter vessels while green represent smaller diameter.Figure 1:. Vascularization of Kidney and Liver in Wild Type and Plasminogen Deficient Mice: Microfil of both kidney and liver of plasminogen −/− show decreased vascularity as compared to WT mice. Colors denote diameter of the vasculature. Red represent large diameter vessels while green represent smaller diameter.Figure 2:Callus Formation and Vascularization of Transverse Femur Fractures in Wild Type and Plasminogen Deficient Mice: Transverse femur fractures of plasminogen −/− mice show a decrease in mineralizing callus formation as compared to wild type mice. Further, Microfil of transverse femur fracture shows plasminogen −/− mice have significantly less vascular invasion of their callus. Colors denote diameter of the vasculature. Red represent large diameter vessels while green represent smaller diameter.Figure 2:. Callus Formation and Vascularization of Transverse Femur Fractures in Wild Type and Plasminogen Deficient Mice: Transverse femur fractures of plasminogen −/− mice show a decrease in mineralizing callus formation as compared to wild type mice. Further, Microfil of transverse femur fracture shows plasminogen −/− mice have significantly less vascular invasion of their callus. Colors denote diameter of the vasculature. Red represent large diameter vessels while green represent smaller diameter. Disclosures: No relevant conflicts of interest to declare.

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Hoffmann, Nathan E., and John C. Bischof. "Cryosurgery of Normal and Tumor Tissue in the Dorsal Skin Flap Chamber: Part II—Injury Response." Journal of Biomechanical Engineering 123, no. 4 (February 27, 2001): 310–16. http://dx.doi.org/10.1115/1.1385839.

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It has been hypothesized that vascular injury may be an important mechanism of cryosurgical destruction in addition to direct cellular destruction. In this study, we report correlation of tissue and vascular injury after cryosurgery to the temperature history during cryosurgery in an in vivo microvascular preparation. The dorsal skin flap chamber, implanted in the Copenhagen rat, was chosen as the cryosurgical model. Cryosurgery was performed in the chamber on either normal skin or tumor tissue propagated from an AT-1 Dunning rat prostate tumor, as described in a companion paper (Hoffmann and Bischof, 2001). The vasculature was then viewed at 3 and 7 days after cryoinjury under brightfield and FITC-labeled dextran contrast enhancement to assess the vascular injury. The results showed that there was complete destruction of the vasculature in the center of the lesion and a gradual return to normal patency moving radially outward. Histologic examination showed a band of inflammation near the edge of a large necrotic region at both 3 and 7 days after cryosurgery. The area of vascular injury observed with FITC-labeled dextran quantitatively corresponded to the area of necrosis observed in histologic section, and the size of the lesion for tumor and normal tissue was similar at 3 days post cryosurgery. At 7 days after cryosurgery, the lesion was smaller for both tissues, with the normal tissue lesion being much smaller than the tumor tissue lesion. A comparison of experimental injury data to the thermal model validated in a companion paper (Hoffmann and Bischof, 2001) suggested that the minimum temperature required for causing necrosis was −15.6±4.3°C in tumor tissue and −19.0±4.4°C in normal tissue. The other thermal parameters manifested at the edge of the lesion included a cooling rate of ∼28°C/min, 0 hold time, and a ∼9°C/min thawing rate. The conditions at the edge of the lesion are much less severe than the thermal conditions required for direct cellular destruction of AT-1 cells and tissues in vitro. These results are consistent with the hypothesis that vascular-mediated injury is responsible for the majority of injury at the edge of the frozen region in microvascular perfused tissue.

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Reho, John J., and Kamal Rahmouni. "Oxidative and inflammatory signals in obesity-associated vascular abnormalities." Clinical Science 131, no. 14 (June 30, 2017): 1689–700. http://dx.doi.org/10.1042/cs20170219.

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Obesity is associated with increased cardiovascular morbidity and mortality in part due to vascular abnormalities such as endothelial dysfunction and arterial stiffening. The hypertension and other health complications that arise from these vascular defects increase the risk of heart diseases and stroke. Prooxidant and proinflammatory signaling pathways as well as adipocyte-derived factors have emerged as critical mediators of obesity-associated vascular abnormalities. Designing treatments aimed specifically at improving the vascular dysfunction caused by obesity may provide an effective therapeutic approach to prevent the cardiovascular sequelae associated with excessive adiposity. In this review, we discuss the recent evidence supporting the role of oxidative stress and cytokines and inflammatory signals within the vasculature as well as the impact of the surrounding perivascular adipose tissue (PVAT) on the regulation of vascular function and arterial stiffening in obesity. In particular, we focus on the highly plastic nature of the vasculature in response to altered oxidant and inflammatory signaling and highlight how weight management can be an effective therapeutic approach to reduce the oxidative stress and inflammatory signaling and improve vascular function.

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46

Holash, J. A., K. Sugamori, and P. A. Stewart. "The Difference in Vascular Volume between Cerebrum and Cerebellum is in the Pia Mater." Journal of Cerebral Blood Flow & Metabolism 10, no. 3 (May 1990): 432–34. http://dx.doi.org/10.1038/jcbfm.1990.75.

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Previous studies using intravascular tracers have shown that the apparent vascular volume in the cerebellum is 10–60% higher than that in the cerebrum. We questioned whether the extravascular volume in the cerebellum could be accounted for by the vasculature of the pia mater that covers its highly infolded surface. Estimates of vascular volume were made using a previously reported point-counting method. Two counts were done: one in which only intraparenchymal vessels were included, and a second one in which both intraparenchymal vessels and pial vessels were included. We found no differences in intraparenchymal vascular volume between cerebellum and cerebrum. When the pial vessels are included, however, the cerebral vascular volume increases by <6%, whereas the cerebellar vascular volume increases by >30%. We suggest that the higher cerebellar vascular volume measured using intravascular tracers is due to inclusion of the pial vasculature. Since pial vessels do not express blood–brain barrier characteristics as prominently as intraparenchymal vessels, we further suggest that estimates of barrier permeability in cerebellum should not be made using simple models developed for cerebral tissue.

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Jia, Zhiming, Hailin Guo, Hua Xie, Junmei Zhou, Yaping Wang, Xingqi Bao, Yichen Huang, and Fang Chen. "Construction of Pedicled Smooth Muscle Tissues by Combining the Capsule Tissue and Cell Sheet Engineering." Cell Transplantation 28, no. 3 (January 9, 2019): 328–42. http://dx.doi.org/10.1177/0963689718821682.

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The survival of engineered tissue requires the formation of its own capillary network, which can anastomose with the host vasculature after transplantation. Currently, while many strategies, such as modifying the scaffold material, adding endothelial cells, or angiogenic factors, have been researched, engineered tissue implanted in vivo cannot timely access to sufficient blood supply, leading to ischemic apoptosis or shrinkage. Constructing vascularized engineered tissue with its own axial vessels and subsequent pedicled transfer is promising to solve the problem of vascularization in tissue engineering. In this study, we used the tissue expander capsule as a novel platform for vascularizing autologous smooth muscle cell (SMC) sheets and fabricating vascularized engineered tissue with its own vascular pedicle. First, we verified which time point was the most effective for constructing an axial capsule vascular bed. Second, we compared the outcome of SMC sheet transplantation onto the expander capsule and classical dorsal subcutaneous tissue, which was widely used in other studies for vascularization. Finally, we transplanted multilayered SMC sheets onto the capsule bed twice to verify the feasibility of fabricating thick pedicled engineered smooth muscle tissues. The results indicated that the axial capsule tissue could be successfully induced, and the capsule tissue 1 week after full expansion was the most vascularized. Quantitative comparisons of thickness, vessel density, and apoptosis of cell sheet grafts onto two vascular beds proved that the axial capsule vascular bed was more favorable to the growth and vascularization of transplants than classical subcutaneous tissue. Furthermore, thick vascularized smooth muscle tissues with the vascular pedicle could be constructed by multi-transplanting cell sheets onto the capsule bed. The combination of axial capsule vascular bed and cell sheet engineering may provide an efficient strategy to overcome the problem of slow or insufficient vascularization in tissue engineering.

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Nitzsche, Bianca, Wen Wei Rong, Andrean Goede, Björn Hoffmann, Fabio Scarpa, Wolfgang M. Kuebler, Timothy W. Secomb, and Axel R. Pries. "Coalescent angiogenesis—evidence for a novel concept of vascular network maturation." Angiogenesis 25, no. 1 (December 14, 2021): 35–45. http://dx.doi.org/10.1007/s10456-021-09824-3.

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AbstractAngiogenesis describes the formation of new blood vessels from pre-existing vascular structures. While the most studied mode of angiogenesis is vascular sprouting, specific conditions or organs favor intussusception, i.e., the division or splitting of an existing vessel, as preferential mode of new vessel formation. In the present study, sustained (33-h) intravital microscopy of the vasculature in the chick chorioallantoic membrane (CAM) led to the hypothesis of a novel non-sprouting mode for vessel generation, which we termed “coalescent angiogenesis.” In this process, preferential flow pathways evolve from isotropic capillary meshes enclosing tissue islands. These preferential flow pathways progressively enlarge by coalescence of capillaries and elimination of internal tissue pillars, in a process that is the reverse of intussusception. Concomitantly, less perfused segments regress. In this way, an initially mesh-like capillary network is remodeled into a tree structure, while conserving vascular wall components and maintaining blood flow. Coalescent angiogenesis, thus, describes the remodeling of an initial, hemodynamically inefficient mesh structure, into a hierarchical tree structure that provides efficient convective transport, allowing for the rapid expansion of the vasculature with maintained blood supply and function during development.

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Arrigoni, Chiara, Davide Camozzi, and Andrea Remuzzi. "Vascular Tissue Engineering." Cell Transplantation 15, no. 1_suppl (January 2006): 119–25. http://dx.doi.org/10.3727/000000006783982430.

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Nerem, Robert M., and Dror Seliktar. "Vascular Tissue Engineering." Annual Review of Biomedical Engineering 3, no. 1 (August 2001): 225–43. http://dx.doi.org/10.1146/annurev.bioeng.3.1.225.

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