Lasertechniques treatment of vascular malformations

Phlebologie ◽  
2010 ◽  
Vol 39 (03) ◽  
pp. 167-175
Author(s):  
M. Poetke ◽  
P. Urban ◽  
H.-P. Berlien
Keyword(s):  
Endothelial Cells ◽  
Spontaneous Regression ◽  
Vascular System ◽  
Vascular Malformations ◽  
Clinical Importance ◽  
Vascular Structure ◽  
Laser Application ◽  
Vascular Morphogenesis ◽  
Structural Abnormalities

SummaryVascular malformations are structural abnormalities, errors of vascular morphogenesis, which can be localized in all parts of the vascular system. All vascular malformations by definition, are present at birth and grow proportionately with the child; their volume can change. In contrast to the haemangiomas, which only proliferate from the endothelial cells the division in stages is of clinical importance. Vascular malformations are divided from the part of vascular system, which is affected.In principle the techniques of laser application in congenital vascular tumours like haemangiomas and in vascular malformations are similar, but the aim is different. In tumours the aim is to induce regression, in vascular malformations the aim is to destroy the pathologic vascular structure because there is no spontaneous regression. This means that the parameters for treatment of vascular malformations must be more aggressive than for vascular tumours.

scholarly journals Endothelial cells on the move: dynamics in vascular morphogenesis and disease

2020 ◽  
Vol 2 (1) ◽  
pp. H29-H43
Author(s):  
Catarina G Fonseca ◽  
Pedro Barbacena ◽  
Claudio A Franco
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Blood Vessels ◽  
Vascular System ◽  
Endothelial Cell Migration ◽  
Network Stability ◽  
Cell Dynamics ◽  
Vascular Morphogenesis ◽  
Endothelial Cell Differentiation ◽  
Shape Changes

The vascular system is a hierarchically organized network of blood vessels that play crucial roles in embryogenesis, homeostasis and disease. Blood vessels are built by endothelial cells – the cells lining the interior of blood vessels – through a process named vascular morphogenesis. Endothelial cells react to different biomechanical signals in their environment by adjusting their behavior to: (1) invade, proliferate and fuse to form new vessels (angiogenesis); (2) remodel, regress and establish a hierarchy in the network (patterning); and (3) maintain network stability (quiescence). Each step involves the coordination of endothelial cell differentiation, proliferation, polarity, migration, rearrangements and shape changes to ensure network integrity and an efficient barrier between blood and tissues. In this review, we highlighted the relevance and the mechanisms involving endothelial cell migration during different steps of vascular morphogenesis. We further present evidence on how impaired endothelial cell dynamics can contribute to pathology.

Vascular endothelial cell–specific phosphotyrosine phosphatase (VE-PTP) activity is required for blood vessel development

Blood ◽  
2006 ◽  
Vol 107 (12) ◽  
pp. 4754-4762 ◽  
Author(s):  
Sebastian Bäumer ◽  
Linda Keller ◽  
Astrid Holtmann ◽  
Ruth Funke ◽  
Benjamin August ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Blood Vessels ◽  
Vascular System ◽  
Vascular Malformations ◽  
Vascular Endothelial Cell ◽  
Tyrosine Kinase Receptor ◽  
Phosphotyrosine Phosphatase ◽  
Fibronectin Type Iii ◽  
Cell Layers ◽  
Vessel Development

AbstractVE-PTP, a receptor-type phosphotyrosine phosphatase, associates with the tyrosine kinase receptor Tie-2 and VE-cadherin and enhances the adhesive function of the latter. Here, VE-PTP was found to be restricted to endothelial cells, with a preference for arterial endothelium. Mutant mice expressing a truncated, secreted form of VE-PTP lacking the cytoplasmic and transmembrane domains and the most membrane-proximal extracellular fibronectin type III repeat, showed severe vascular malformations causing lethality at 10 days of gestation. Although blood vessels were initially formed, the intraembryonic vascular system soon deteriorated. Blood vessels in the yolk sac developed into dramatically enlarged cavities. In explant cultures of mutant allantoides, endothelial cells were found next to vessel structures growing as cell layers. No signs for enhanced endothelial apoptosis or proliferation were observed. Thus, the activity of VE-PTP is not required for the initial formation of blood vessels, yet it is essential for their maintenance and remodeling.

scholarly journals A Review on the Histological Types of Hemangioma

2021 ◽  
pp. 36-39
Author(s):  
M. Nagameenalochini
Keyword(s):  
Endothelial Cells ◽  
Vascular Malformations ◽  
Benign Neoplasms ◽  
Histological Types ◽  
Vascular Morphogenesis ◽  
Localized Defects

Even after the approved classification of congenital vascular tumours/malformations which was first published by Mulliken and Glowacki, in the year 1982, there is still a significant amount of confusion to categorize hemangiomas and vascular malformations. Hemangiomas are considered to be true, benign neoplasms arising from endothelial cells and must be clearly differentiated from localized defects of vascular morphogenesis, i.e., vascular malformations.

The Vascular Structure of the Kidney of Mallards and Doves

1999 ◽  
Vol 5 (S2) ◽  
pp. 1192-1193
Author(s):  
H. Ditrich
Keyword(s):  
Vascular System ◽  
Venous Drainage ◽  
Portal System ◽  
Physiological Data ◽  
Vascular Structure ◽  
Serial Sections ◽  
Functional Importance ◽  
Additional Material ◽  
Functional Studies ◽  
Primitive Feature

The architecture of the kidney of birds (and also reptiles) is, unlike in mammalians, mainly determined by the organization of the blood vascular system. Besides arterial supply and venous drainage, the renal portal system forms a main structural component. While the latter was often regarded as a “primitive” feature in the literature, morphological and physiological data reveal its great functional importance.Microvascular corrosion casts studied in the scanning electron microscope permit the visualization of minute vessels, retaining their 3D-arrangement. Additionally, when compared with graphical reconstructions of serial sections, this method avoids several inherent artifacts like fixation and dehydration shrinkage as well as the compression of the object by the sectioning blade. Most of the studies on avian kidneys with this technique used the domestic chicken as a model. In order to provide additional material for comparative and functional studies, data on the intrarenal vascular structure of other species are required.

scholarly journals Studying dynamic stress effects on the behaviour of THP-1 cells by microfluidic channels

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Semra Zuhal Birol ◽  
Rana Fucucuoglu ◽  
Sertac Cadirci ◽  
Ayca Sayi-Yazgan ◽  
Levent Trabzon
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Vascular System ◽  
Circulatory System ◽  
Disease Process ◽  
Microfluidic Channels ◽  
Shear Stresses ◽  
Stress Effects ◽  
Adhesion Behavior ◽  
Cycling System

AbstractAtherosclerosis is a long-term disease process of the vascular system that is characterized by the formation of atherosclerotic plaques, which are inflammatory regions on medium and large-sized arteries. There are many factors contributing to plaque formation, such as changes in shear stress levels, rupture of endothelial cells, accumulation of lipids, and recruitment of leukocytes. Shear stress is one of the main factors that regulates the homeostasis of the circulatory system; therefore, sudden and chronic changes in shear stress may cause severe pathological conditions. In this study, microfluidic channels with cavitations were designed to mimic the shape of the atherosclerotic blood vessel, where the shear stress and pressure difference depend on design of the microchannels. Changes in the inflammatory-related molecules ICAM-1 and IL-8 were investigated in THP-1 cells in response to applied shear stresses in an continuous cycling system through microfluidic channels with periodic cavitations. ICAM-1 mRNA expression and IL-8 release were analyzed by qRT-PCR and ELISA, respectively. Additionally, the adhesion behavior of sheared THP-1 cells to endothelial cells was examined by fluorescence microscopy. The results showed that 15 Pa shear stress significantly increases expression of ICAM-1 gene and IL-8 release in THP-1 cells, whereas it decreases the adhesion between THP-1 cells and endothelial cells.

scholarly journals Vascular endothelial cell specification in health and disease

Angiogenesis ◽  
2021 ◽  
Author(s):  
Corina Marziano ◽  
Gael Genet ◽  
Karen K. Hirschi
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Current Knowledge ◽  
Vascular Malformations ◽  
Immune Surveillance ◽  
Vascular Endothelial Cell ◽  
Lymphatic Vessels ◽  
Lymphatic Endothelial Cell ◽  
The Body ◽  
Vascular Networks

AbstractThere are two vascular networks in mammals that coordinately function as the main supply and drainage systems of the body. The blood vasculature carries oxygen, nutrients, circulating cells, and soluble factors to and from every tissue. The lymphatic vasculature maintains interstitial fluid homeostasis, transports hematopoietic cells for immune surveillance, and absorbs fat from the gastrointestinal tract. These vascular systems consist of highly organized networks of specialized vessels including arteries, veins, capillaries, and lymphatic vessels that exhibit different structures and cellular composition enabling distinct functions. All vessels are composed of an inner layer of endothelial cells that are in direct contact with the circulating fluid; therefore, they are the first responders to circulating factors. However, endothelial cells are not homogenous; rather, they are a heterogenous population of specialized cells perfectly designed for the physiological demands of the vessel they constitute. This review provides an overview of the current knowledge of the specification of arterial, venous, capillary, and lymphatic endothelial cell identities during vascular development. We also discuss how the dysregulation of these processes can lead to vascular malformations, and therapeutic approaches that have been developed for their treatment.

scholarly journals The first “Slit” is the deepest: the secret to a hollow heart

2008 ◽  
Vol 182 (2) ◽  
pp. 221-223 ◽  
Author(s):  
Iiro Taneli Helenius ◽  
Greg J. Beitel
Keyword(s):  
Cell Shape ◽  
Vascular System ◽  
Hollow Heart ◽  
Autocrine Signaling ◽  
Lumen Formation ◽  
Membrane Surfaces ◽  
Vascular Morphogenesis ◽  
Cell Biol ◽  
Shape Changes

Tubular organs are essential for life, but lumen formation in nonepithelial tissues such as the vascular system or heart is poorly understood. Two studies in this issue (Medioni, C., M. Astier, M. Zmojdzian, K. Jagla, and M. Sémériva. 2008. J. Cell Biol. 182:249–261; Santiago-Martínez, E., N.H. Soplop, R. Patel, and S.G. Kramer. 2008. J. Cell Biol. 182:241–248) reveal unexpected roles for the Slit–Robo signaling system during Drosophila melanogaster heart morphogenesis. In cardioblasts, Slit and Robo modulate the cell shape changes and domains of E-cadherin–based adhesion that drive lumen formation. Furthermore, in contrast to the well-known paracrine role of Slit and Robo in guiding cell migrations, here Slit and Robo may act by autocrine signaling. In addition, the two groups demonstrate that heart lumen formation is even more distinct from typical epithelial tubulogenesis mechanisms because the heart lumen is bounded by membrane surfaces that have basal rather than apical attributes. As the D. melanogaster cardioblasts are thought to have significant evolutionary similarity to vertebrate endothelial and cardiac lineages, these findings are likely to provide insights into mechanisms of vertebrate heart and vascular morphogenesis.

Antibodies to kidney endothelial cells contribute to a “leaky” glomerular barrier in patients with chronic kidney diseases

2012 ◽  
Vol 302 (7) ◽  
pp. F884-F894 ◽  
Author(s):  
Nidia Maritza Hernandez ◽  
Anna Casselbrant ◽  
Meghnad Joshi ◽  
Bengt R. Johansson ◽  
Suchitra Sumitran-Holgersson
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Endothelial Dysfunction ◽  
Kidney Diseases ◽  
Clinical Importance ◽  
Human Kidney ◽  
Cell Permeability ◽  
Chronic Kidney Diseases ◽  
Esrd Patients

Anti-endothelial cell antibodies (AECA) have been reported to cause endothelial dysfunction, but their clinical importance for tissue-specific endothelial cells is not clear. We hypothesized that AECA reactive with human kidney endothelial cells (HKEC) may cause renal endothelial dysfunction in patients with chronic kidney diseases. We report that a higher fraction (56%) of end-stage renal disease (ESRD) patients than healthy controls (5%) have AECA reactive against kidney endothelial cells ( P <0.001). The presence of antibodies was associated with female gender ( P < 0.001), systolic hypertension ( P < 0.01), and elevated TNF-α ( P < 0.05). These antibodies markedly decrease expression of both adherens and tight junction proteins VE-cadherin, claudin-1, and zonula occludens-1 and provoked a rapid increase in cytosolic free Ca2+and rearrangement of actin filaments in HKEC compared with controls. This was followed by an enhancement in protein flux and phosphorylation of VE-cadherin, events associated with augmented endothelial cell permeability. Additionally, kidney biopsies from ESRD patients with AECA but not controls demonstrated a marked decrease in adherens and tight junctions in glomerular endothelium, confirming our in vitro data. In summary, our data demonstrate a causal link between AECA and their capacity to induce alterations in glomerular vascular permeability.

Increased hemangioblast commitment, not vascular disorganization, is the primary defect in flt-1 knock-out mice

Development ◽  
1999 ◽  
Vol 126 (13) ◽  
pp. 3015-3025 ◽  
Author(s):  
G.H. Fong ◽  
L. Zhang ◽  
D.M. Bryce ◽  
J. Peng
Keyword(s):  
Endothelial Cells ◽  
Population Density ◽  
Cell Fate ◽  
Vascular System ◽  
Primitive Streak ◽  
Cellular Level ◽  
Wild Type ◽  
Primary Defect ◽  
Knock Out ◽  
Vascular Channels

We previously demonstrated the essential role of the flt-1 gene in regulating the development of the cardiovascular system. While the inactivation of the flt-1 gene leads to a very severe disorganization of the vascular system, the primary defect at the cellular level was unknown. Here we report a surprising finding that it is an increase in the number of endothelial progenitors that leads to the vascular disorganization in flt-1(−/−) mice. At the early primitive streak stage (prior to the formation of blood islands), hemangioblasts are formed much more abundantly in flt-1(−/−) embryos. This increase is primarily due to an alteration in cell fate determination among mesenchymal cells, rather than to increased proliferation, migration or reduced apoptosis of flt-1(−/−) hemangioblasts. We further show that the increased population density of hemangioblasts is responsible for the observed vascular disorganization, based on the following observations: (1) both flt-1(−/−) and flt-1(+/+) endothelial cells formed normal vascular channels in chimaeric embryos; (2) wild-type endothelial cells formed abnormal vascular channels when their population density was significantly increased; and (3) in the absence of wild-type endothelial cells, flt-1(−/−) endothelial cells alone could form normal vascular channels when sufficiently diluted in a developing embryo. These results define the primary defect in flt-1(−/−) embryos at the cellular level and demonstrate the importance of population density of progenitor cells in pattern formation.

Abstract 558: Microchanneled Polysaccharide Hydrogel Laden With Endothelial Cells and Mesenchymal Stem Cells With VEGF Facilitate Formation of Vascular Structures and Are Effective for Repairing Tissue Ischemia

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Sangho Lee ◽  
Min Kyung Lee ◽  
Hyunjoon Kong ◽  
Young-sup Yoon
Keyword(s):  
Stem Cells ◽  
Endothelial Cells ◽  
Mesenchymal Stem Cells ◽  
Cell Survival ◽  
Vascular Structure ◽  
Hindlimb Ischemia ◽  
Alginate Hydrogel ◽  
Vessel Formation

Various hydrogels are used to create vascular structure in vitro or to improve cell engraftment to overcome low cell survival in vivo, a main hurdle for bare cell therapy Recently we developed a modified alginate hydrogel within which microchannels are aligned to guide the direction and spatial organization of loaded cells. We investigated whether these cell constructs in which HUVECs and human mesenchymal stem cells (hMSCs) are co-loaded in this novel microchanneled hydrogel facilitate formation of vessels in vitro and in vivo, and enhance recovery of hindlimb ischemia. We crafted a modified alginate hydrogel which has microchannels, incorporates a cell adhesion peptide RGD, and was encapsulated with VEGF. We then compared vascular structure formation between the HUVEC only (2 x 105 cells) group and the HUVEC plus hMSC group. In the HUVEC+hMSC group, we mixed HUVECs and hMSCs at the ratio of 3:1. For cell tracking, we labeled HUVECs with DiO, a green fluorescence dye. After loading cells into the microchannels of the hydrogel, these constructs were cultured for seven days and were examined by confocal microscopy. In the HUVEC only group, HUVECs stands as round shaped cells without forming tubular structures within the hydrogel. However, in the HUVEC+hMSC group, HUVECs were stretched out and connected with each other, and formed vessel-like structure following pre-designed microchannels. These results suggested that hMSCs play a critical role for vessel formation by HUVECs. We next determined their in vivo effects using a mouse hindlimb ischemia model. We found that engineered HUVEC+hMSC group showed significantly higher perfusion over 4 weeks compared to the engineered HUVEC only group or bare cell (HUVEC) group. Confocal microscopic analysis of harvested tissues showed more robust vessel formation within and outside of the cell constructs and longer term cell survival in HUVEC+hMSC group compared to the other groups. In conclusion, this novel microchanneled alginate hydrogel facilitates aligned vessel formation of endothelial cells when combined with MSCs. This vessel-embedded hydrogel constructs consisting of HUVECs and MSCs contribute to perfusable vessel formation, prolong cell survival in vivo, and are effective for recovering limb ischemia.

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