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Journal of Applied Physiology... Dec 2011Physical inactivity is associated with an increase in cardiovascular risk that cannot be fully explained by traditional or novel risk factors. Inactivity is also... (Review)
Review
Physical inactivity is associated with an increase in cardiovascular risk that cannot be fully explained by traditional or novel risk factors. Inactivity is also associated with changes in hemodynamic stimuli, which exert direct effects on the vasculature leading to remodeling and a proatherogenic phenotype. In this review, we synthesize and summarize in vivo evidence relating to the impact of local and systemic models of physical inactivity on conduit arteries, resistance vessels, and the microcirculation in humans. Taken together, the literature suggests that a rapid inward structural remodeling of vessels occurs in response to physical inactivity. The magnitude of this response is dependent on the "dose" of inactivity. Moreover, changes in vascular function are found at resistance and microvessel levels in humans. In conduit arteries, a strong interaction between vascular function and structure is present, which results in conflicting data regarding the impact of inactivity on conduit artery function. While much of the cardioprotective effect of exercise is related to the nitric oxide pathway, deconditioning may primarily be associated with activation of vasoconstrictor pathways. The effects of deconditioning on the vasculature are therefore not simply the opposite of those in response to exercise training. Given the importance of sedentary behavior, future studies should provide further insight into the impact of inactivity on the vasculature and other (novel) markers of vascular health. Moreover, studies should examine the role of (hemodynamic) stimuli that underlie the characteristic vascular adaptations during deconditioning. Our review concludes with some suggestions for future research directions.
Topics: Adaptation, Physiological; Blood Vessels; Cardiovascular Diseases; Humans; Microvessels; Motor Activity; Risk Factors; Sedentary Behavior; Time Factors; Vascular Resistance
PubMed: 21737819
DOI: 10.1152/japplphysiol.00394.2011 -
The FEBS Journal Aug 2019Chondroitin sulfate E (CS-E) is a glycosaminoglycan containing type-E disaccharide units (sulfated at C-4 and C-6 of N-acetylgalactosamine). CS-E is covalently linked to... (Review)
Review
Chondroitin sulfate E (CS-E) is a glycosaminoglycan containing type-E disaccharide units (sulfated at C-4 and C-6 of N-acetylgalactosamine). CS-E is covalently linked to a core protein to form chondroitin sulfate proteoglycans (PGs) that are secreted or associated with the plasma membrane of several types of cells. CS-E-containing PGs selectively interact with growth factors and chemokines and control various cellular and/or tissue processes. Angiogenesis is a process that is highly regulated in physiological conditions but deregulated in pathologies, leading to excess or deficient blood vessel formation. Angiogenesis regulation is orchestrated by numerous growth factors, such as vascular endothelial growth factor A, fibroblast growth factors and pleiotrophin, whose functions can be affected by CS-containing PGs. In the present review, we focus on the emerging area of CS-mediated angiogenesis and particularly on the critical assessment of data related to a potential role of CS-E in controlling endothelial cell functions, focusing on angiogenesis regulation and vascular homeostasis in health and disease.
Topics: Animals; Blood Vessels; Chemokines; Chondroitin Sulfates; Humans; Intercellular Signaling Peptides and Proteins; Neovascularization, Physiologic
PubMed: 30932321
DOI: 10.1111/febs.14830 -
Vascular Pharmacology Nov 2014Notch signaling plays many important roles in homeostasis and remodeling in the vessel wall, and serves a critical role in the communication between endothelial cells... (Review)
Review
Notch signaling plays many important roles in homeostasis and remodeling in the vessel wall, and serves a critical role in the communication between endothelial cells and smooth muscle cells. Within blood vessels, Notch signaling integrates with multiple pathways by mechanisms including direct protein–protein interaction, cooperative or synergistic regulation of signal cascades, and co-regulation of transcriptional targets. After establishment of the mature blood vessel, the spectrum and intensity of Notch signaling change during phases of active remodeling or disease progression. These changes can be mediated by regulation via microRNAs and protein stability or signaling, and corresponding changes in complementary signaling pathways. Notch also affects endothelial cells on a system level by regulating key metabolic components. This review will outline the most recent findings of Notch activity in blood vessels, with a focus on how Notch signals integrate with other molecular signaling pathways controlling vascular phenotype.
Topics: Animals; Blood Vessels; Endothelial Cells; Humans; Myocytes, Smooth Muscle; Phenotype; Receptors, Notch; Signal Transduction
PubMed: 25464152
DOI: 10.1016/j.vph.2014.10.003 -
Advances in Experimental Medicine and... 2014Platelets are small, anucleated cells that participate in primary hemostasis by forming a hemostatic plug at the site of a blood vessel's breach, preventing blood loss.... (Review)
Review
Platelets are small, anucleated cells that participate in primary hemostasis by forming a hemostatic plug at the site of a blood vessel's breach, preventing blood loss. However, hemostatic events can lead to excessive thrombosis, resulting in life-threatening strokes, emboli, or infarction. Development of multi-scale models coupling processes at several scales and running predictive model simulations on powerful computer clusters can help interdisciplinary groups of researchers to suggest and test new patient-specific treatment strategies.
Topics: Animals; Blood Coagulation; Blood Platelets; Blood Vessels; Cell Communication; Hemostasis; Humans; Platelet Activation; Platelet Adhesiveness; Systems Biology
PubMed: 25480638
DOI: 10.1007/978-1-4939-2095-2_5 -
Yakugaku Zasshi : Journal of the... 2020The thymus is a vital organ for functional immune systems, and is the site of T cell development, which plays a central role in cellular immune defenses. Unlike other... (Review)
Review
The thymus is a vital organ for functional immune systems, and is the site of T cell development, which plays a central role in cellular immune defenses. Unlike other major organs, the thymus is highly dynamic in size and structure. It shrinks immediately upon bacterial infection, aging, pregnancy, mental stress, nutritional deficiency, and more. The reduction in size and function of the thymus during such biological events is called thymic involution or thymic atrophy; thymic involution is a particularly important issue because dysfunctional T cell immunity increases the risks of tumorigenesis and infectious diseases. However, the molecular mechanisms underlying thymic involution remain obscure. Our recent study indicated that blood vessels are remodeled during thymic involution that occurs upon aging, estradiol-treatment, or nutritional deficiency. We also found that prostanoid synthesis is induced during thymic involution. Treatment with non-steroidal anti-inflammatory drugs (NSAIDs), aspirin or etodolac, at least partially inhibited thymic involution-induced remodeling of the blood vessels, suggesting that prostanoids are involved in blood vessel remodeling. Our results revealed the potential role of blood vessel remodeling during thymic involution, which can lead to biological stress-induced immunosenescence.
Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Blood Vessels; Humans; Mice; Prostaglandins; Stress, Physiological; Stress, Psychological; T-Lymphocytes; Thymus Gland; Vascular Remodeling
PubMed: 32238633
DOI: 10.1248/yakushi.19-00221-1 -
BioMed Research International 2021Aiming at the current problem of insufficient extraction of small retinal blood vessels, we propose a retinal blood vessel segmentation algorithm that combines...
Aiming at the current problem of insufficient extraction of small retinal blood vessels, we propose a retinal blood vessel segmentation algorithm that combines supervised learning and unsupervised learning algorithms. In this study, we use a multiscale matched filter with vessel enhancement capability and a U-Net model with a coding and decoding network structure. Three channels are used to extract vessel features separately, and finally, the segmentation results of the three channels are merged. The algorithm proposed in this paper has been verified and evaluated on the DRIVE, STARE, and CHASE_DB1 datasets. The experimental results show that the proposed algorithm can segment small blood vessels better than most other methods. We conclude that our algorithm has reached 0.8745, 0.8903, and 0.8916 on the three datasets in the sensitivity metric, respectively, which is nearly 0.1 higher than other existing methods.
Topics: Algorithms; Databases, Factual; Humans; Image Processing, Computer-Assisted; Retinal Vessels
PubMed: 34124247
DOI: 10.1155/2021/5561125 -
Physiology (Bethesda, Md.) Jul 2014Blood vessels are composed of two primary cell types, endothelial cells and smooth muscle cells, each providing a unique contribution to vessel function. Signaling... (Review)
Review
Blood vessels are composed of two primary cell types, endothelial cells and smooth muscle cells, each providing a unique contribution to vessel function. Signaling between these two cell types is essential for maintaining tone in mature vessels, and their communication is critical during development, and for repair and remodeling associated with blood vessel growth. This review will highlight the pathways that endothelial cells and smooth muscle cells utilize to communicate during vessel formation and discuss how disruptions in these pathways contribute to disease.
Topics: Animals; Cell Communication; Endothelium, Vascular; Humans; Muscle, Smooth, Vascular; Neovascularization, Physiologic; Signal Transduction; Vascular Diseases
PubMed: 24985327
DOI: 10.1152/physiol.00047.2013 -
Methods in Molecular Biology (Clifton,... 2022Human tissue-engineered blood vessels (TEBVs) that exhibit vasoactivity can be used to test drug toxicity, modulate pro-inflammatory cytokines, and model disease states...
Human tissue-engineered blood vessels (TEBVs) that exhibit vasoactivity can be used to test drug toxicity, modulate pro-inflammatory cytokines, and model disease states in vitro. We developed a novel device to fabricate arteriole-scale human endothelialized TEBVs in situ with smaller volumes and higher throughput than previously reported. Both primary and induced pluripotent stem cell (iPSC)-derived cells can be used. Four collagen TEBVs with 600μm inner diameter and 2.9 mm outer diameter are fabricated by pipetting a solution of collagen and medial cells into a three-layer acrylic mold. After gelation, the TEBVs are released from the mold and dehydrated. After suturing the TEBVs in place and changing the mold parts to form a perfusion chamber, the TEBVs are endothelialized in situ, and then media is perfused through the lumen. By removing 90% of the water after gelation, the TEBVs become mechanically strong enough for perfusion at the physiological shear stress of 0.4 Pa within 24 h of fabrication and maintain function for at least 5 weeks.
Topics: Arterioles; Blood Vessels; Collagen; Humans; Induced Pluripotent Stem Cells; Perfusion; Tissue Engineering
PubMed: 34591300
DOI: 10.1007/978-1-0716-1708-3_7 -
Angiogenesis Apr 2016Cardiovascular function depends on patent, continuous and stable blood vessel formation by endothelial cells (ECs). Blood vessel development initiates by vasculogenesis,...
Cardiovascular function depends on patent, continuous and stable blood vessel formation by endothelial cells (ECs). Blood vessel development initiates by vasculogenesis, as ECs coalesce into linear aggregates and organize to form central lumens that allow blood flow. Molecular mechanisms underlying in vivo vascular 'tubulogenesis' are only beginning to be unraveled. We previously showed that the GTPase-interacting protein called Rasip1 is required for the formation of continuous vascular lumens in the early embryo. Rasip1(-/-) ECs exhibit loss of proper cell polarity and cell shape, disrupted localization of EC-EC junctions and defects in adhesion of ECs to extracellular matrix. In vitro studies showed that Rasip1 depletion in cultured ECs blocked tubulogenesis. Whether Rasip1 is required in blood vessels after their initial formation remained unclear. Here, we show that Rasip1 is essential for vessel formation and maintenance in the embryo, but not in quiescent adult vessels. Rasip1 is also required for angiogenesis in three models of blood vessel growth: in vitro matrix invasion, retinal blood vessel growth and directed in vivo angiogenesis assays. Rasip1 is thus necessary in growing embryonic blood vessels, postnatal angiogenic sprouting and remodeling, but is dispensable for maintenance of established blood vessels, making it a potential anti-angiogenic therapeutic target.
Topics: Aging; Animals; Aorta; Carrier Proteins; Female; Gene Deletion; Human Umbilical Vein Endothelial Cells; Humans; Integrases; Intracellular Signaling Peptides and Proteins; Mice; Neovascularization, Physiologic; Pregnancy; Retinal Vessels
PubMed: 26897025
DOI: 10.1007/s10456-016-9498-5 -
Journal of Anatomy Oct 2002In the adult lung the pulmonary arteries run alongside the airways and the pulmonary veins show a similar branching pattern to the arteries, though separated from them.... (Review)
Review
In the adult lung the pulmonary arteries run alongside the airways and the pulmonary veins show a similar branching pattern to the arteries, though separated from them. During early fetal development the airways act as a template for pulmonary blood vessel development in that the vessels form by vasculogenesis around the branching airways. In later lung development the capillary bed is essential for alveolar formation. This paper reviews evidence for the interaction of the airways and blood vessels in both normal and abnormal lung development.
Topics: Animals; Bronchial Arteries; Bronchopulmonary Dysplasia; Gestational Age; Humans; Infant, Newborn; Infant, Premature; Lung; Mammals; Organogenesis; Pulmonary Artery; Pulmonary Veins
PubMed: 12430957
DOI: 10.1046/j.1469-7580.2002.00097.x