scholarly journals Extensive Cutaneous Scalp Angiosarcoma

2018 ◽  
Vol 2018 ◽  
pp. 1-3 ◽  
Author(s):  
Zabeer Bhatti ◽  
Rameez Bhatti ◽  
Sharon Brangman ◽  
Kerry Whiting ◽  
Amit Dhamoon
Keyword(s):  
Older Adults ◽  
Endothelial Cells ◽  
Blood Vessels ◽  
Clinical Presentation ◽  
De Novo

Angiosarcoma is a cancer that is derived from endothelial cells that line blood vessels and lymphatic channels. Cutaneous angiosarcoma can appear anywhere on the skin and the clinical presentation is highly variable. Most cases appear on the scalp and face de novo. Our case describes a 91-year-old female with cutaneous scalp angiosarcoma. Our case serves to remind physicians that an abnormal skin finding in older adults should raise their index of suspicion for angiosarcoma and an early biopsy should be performed.

scholarly journals Human iPSC-derived mesodermal progenitor cells preserve their vasculogenesis potential after extrusion and form hierarchically organized blood vessels

2021 ◽  
Author(s):  
Leyla Dogan ◽  
Ruben Scheuring ◽  
Nicole Wagner ◽  
Yuichiro Ueda ◽  
Philipp Woersdoerfer ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Blood Vessels ◽  
Progenitor Cells ◽  
Vessel Wall ◽  
De Novo ◽  
Hierarchical Organization ◽  
Wall Structure ◽  
Electron Microscopic ◽  
Vessel Formation

Post-fabrication formation of a proper vasculature remains an unresolved challenge in bioprinting. Established strategies focus on the supply of the fabricated structure with nutrients and oxygen and either rely on the mere formation of a channel system using fugitive inks, or additionally use mature endothelial cells and/or peri-endothelial cells such as smooth muscle cells for the formation of blood vessels in vitro. Functional vessels, however, exhibit a hierarchical organization and multilayered wall structure that is important for their function. Human induced pluripotent stem cell-derived mesodermal progenitor cells (hiMPCs) have been shown to possess the capacity to form blood vessels in vitro, but have so far not been assessed for their applicability in bioprinting processes. Here, we demonstrate that hiMPCs, after formulation into an alginate/collagen type 1 bioink and subsequent extrusion, retain their ability to give rise to the formation of complex vessels that display a hierarchical network in a process that mimicks the embryonic steps of vessel formation by vasculogenesis. Histological evaluations at different time points of extrusion revealed initial formation of spheres, followed by lumen formation and further structural maturation as evidenced by building a multilayered vessel wall and a vascular network. These findings are supported by immunostainings for endothelial and peri-endothelial cell markers as well as electron microscopic analyses at the ultrastructural level. Moreover, capillary-like vessel structures deposited a basement membrane-like matrix structure at the basal side between the vessel wall and the alginate-collagen matrix. These results evidence the applicability and great potential of hiMPCs for the bioprinting of vascular structures mimicking the basic morphogenetic steps of de novo vessel formation during embryogenesis.

Endothelial Cells Induce Multiple Myeloma Cell Proliferation Protect Against Conventional and Novel Therapies.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 2354-2354
Author(s):  
Shaji Kumar ◽  
Noopur Raje ◽  
Teru Hideshima ◽  
Klaus Podar ◽  
Kenji Ishitsuka ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Cell Proliferation ◽  
Endothelial Cells ◽  
Tumor Cell ◽  
Blood Vessels ◽  
Intracellular Signaling ◽  
De Novo ◽  
Cell Contact ◽  
Protective Effects ◽  
Tumor Cell Proliferation

Abstract Angiogenesis or formation of new blood vessels from existing blood vessels, in contrast to vasculogenesis or de novo formation of new vessels, plays an important role in the progression and spread of most cancers. Multiple myeloma (MM) is characterized by increased microvessel density (MVD), a quantitative estimate of angiogenesis, which correlates with stage of disease. MVD increases with progression from MGUS to smoldering MM to newly diagnosed MM and relapsed MM. It is a powerful prognostic factor, predicting for overall survival. To further elucidate the biological basis for the prognostic value of increased angiogenesis in MM, we studied the interactions of MM cells with endothelial cells using HUVECS as a model system. Co-culture of MM cells (MM1.S, OPM2, U266) with HUVECS induced tumor cell proliferation. Enhanced tumor cell proliferation correlated with the number of HUVECs and was greater than that triggered by co-culture with patient bone marrow stromal cells. When HUVECs were fixed prior to co-culture there was a significant decrease in the tumor cell proliferation. Addition of HUVEC conditioned media to the MM cell lines also induced proliferation. Importantly, HUVECS protected against anti-MM agents including conventional agents (Dexamethasone, Doxorubicin, Melphalan) and novel drugs (Revlimid™). The protective effect afforded by co-culture was lost on HUVEC fixation. Intracellular signaling events following MM cell-endothelial cell contact were studied to understand the mechanisms of the proliferative and protective effects. Western blotting demonstrated activation of the JAK/STAT, PI3K/Akt and the MAPK pathways, mediating proliferation and survival. Ongoing studies focused on understanding cytokine as well as adhesion-mediated interactions between the endothelial cells and the MM cells will identify targets for new therapeutic approaches in MM.

scholarly journals Endothelial struts, a mechanism to generate large lumenized blood vessels de novo

2019 ◽  
Author(s):  
Bart Weijts ◽  
Iftach Shaked ◽  
Wenqing Li ◽  
Mark Ginsberg ◽  
David Kleinfeld ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Blood Vessels ◽  
Alternative Model ◽  
Vessel Wall ◽  
De Novo ◽  
Large Diameter ◽  
Lumen Diameter ◽  
The Future

Lumenization of de novo formed blood vessels occurs either through cell hollowing (intracellular lumen)1–3 or cord hollowing (extracellular lumen)4–6 and restricts thereby the initial lumen diameter to one or two endothelial cells (ECs) respectively. However, vasculogenesis can result in large diameter blood vessels, raising the question how these vessels are formed. Here, we describe an alternative model of vasculogenesis that results in the formation of large diameter vessels. In this model, ECs coalesce into a branched network of EC struts within the future lumen of the vessel. These struts maintain the patency of the vessel and serve as a scaffold for the ECs forming the vessel wall, which initially consists out of a few patches of ECs. Together, we show that endothelial struts facilitate the formation of large blood vessels without being bound by the prerequisite of a cord-like structure, nor are they restricted in size.

Platelets Stimulate Thromboplastin Synthesis in Human Endothelial Cells

1983 ◽  
Vol 49 (02) ◽  
pp. 069-072 ◽  
Author(s):  
U L H Johnsen ◽  
T Lyberg ◽  
K S Galdal ◽  
H Prydz
Keyword(s):  
Endothelial Cells ◽  
De Novo ◽  
Umbilical Vein ◽  
Time Dependent ◽  
De Novo Synthesis ◽  
Human Endothelial Cells ◽  
Tumor Promotor ◽  
Coagulation Assay ◽  
Platelet Aggregates ◽  
Umbilical Vein Endothelial Cells

SummaryHuman umbilical vein endothelial cells in culture synthesize thromboplastin upon stimulation with phytohaemagglutinin (PHA) or the tumor promotor 12-O-tetradecanoyl-phorbol-13-acetate (TPA). The thromboplastin activity is further strongly enhanced in a time dependent reaction by the presence of gel-filtered platelets or platelet aggregates. This effect was demonstrable at platelet concentrations lower than those normally found in plasma, it may thus be of pathophysiological relevance. The thromboplastin activity increased with increasing number of platelets added. Cycloheximide inhibited the increase, suggesting that de novo synthesis of the protein component of thromboplastin, apoprotein III, is necessary.When care was taken to remove monocytes no thromboplastin activity and no apoprotein HI antigen could be demonstrated in suspensions of gel-filtered platelets, platelets aggregated with thrombin or homogenized platelets when studied with a coagulation assay and an antibody neutralization technique.

Action of Corynebacterium ovis exotoxin on endothelial cells of blood vessels

Nature ◽  
1978 ◽  
Vol 271 (5642) ◽  
pp. 246-248 ◽  
Author(s):  
H. R. CARNE ◽  
ELEANOR O. ONON
Keyword(s):  
Endothelial Cells ◽  
Blood Vessels

scholarly journals Non-productive angiogenesis disassembles Aß plaque-associated blood vessels

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Maria I. Alvarez-Vergara ◽  
Alicia E. Rosales-Nieves ◽  
Rosana March-Diaz ◽  
Guiomar Rodriguez-Perinan ◽  
Nieves Lara-Ureña ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Blood Vessels ◽  
Molecular Signature ◽  
Loss Of Function ◽  
Local Loss ◽  
Microglial Phagocytosis ◽  
Vascular Phenotype ◽  
Cerebral Microvasculature ◽  
Vascular Component

AbstractThe human Alzheimer’s disease (AD) brain accumulates angiogenic markers but paradoxically, the cerebral microvasculature is reduced around Aß plaques. Here we demonstrate that angiogenesis is started near Aß plaques in both AD mouse models and human AD samples. However, endothelial cells express the molecular signature of non-productive angiogenesis (NPA) and accumulate, around Aß plaques, a tip cell marker and IB4 reactive vascular anomalies with reduced NOTCH activity. Notably, NPA induction by endothelial loss of presenilin, whose mutations cause familial AD and which activity has been shown to decrease with age, produced a similar vascular phenotype in the absence of Aß pathology. We also show that Aß plaque-associated NPA locally disassembles blood vessels, leaving behind vascular scars, and that microglial phagocytosis contributes to the local loss of endothelial cells. These results define the role of NPA and microglia in local blood vessel disassembly and highlight the vascular component of presenilin loss of function in AD.

scholarly journals A novel de novo DDX3X missense variant in a female with brachycephaly and intellectual disability: a case report

2021 ◽  
Vol 47 (1) ◽  
Author(s):  
Giada Moresco ◽  
Jole Costanza ◽  
Carlo Santaniello ◽  
Ornella Rondinone ◽  
Federico Grilli ◽  
...  
Keyword(s):  
Intellectual Disability ◽  
Clinical Presentation ◽  
De Novo ◽  
Clinical Signs ◽  
Missense Variant ◽  
Psychomotor Development ◽  
Helicase Domain ◽  
Protein Activity ◽  
Mrna Metabolism ◽  
Pathogenic Variants

Abstract Background De novo pathogenic variants in the DDX3X gene are reported to account for 1–3% of unexplained intellectual disability (ID) in females, leading to the rare disease known as DDX3X syndrome (MRXSSB, OMIM #300958). Besides ID, these patients manifest a variable clinical presentation, which includes neurological and behavioral defects, and abnormal brain MRIs. Case presentation We report a 10-year-old girl affected by delayed psychomotor development, delayed myelination, and polymicrogyria (PMG). We identified a novel de novo missense mutation in the DDX3X gene (c.625C > G) by whole exome sequencing (WES). The DDX3X gene encodes a DEAD-box ATP-dependent RNA-helicase broadly implicated in gene expression through regulation of mRNA metabolism. The identified mutation is located just upstream the helicase domain and is suggested to impair the protein activity, thus resulting in the altered translation of DDX3X-dependent mRNAs. The proband, presenting with the typical PMG phenotype related to the syndrome, does not show other clinical signs frequently reported in presence of missense DDX3X mutations that are associated with a most severe clinical presentation. In addition, she has brachycephaly, never described in female DDX3X patients, and macroglossia, that has never been associated with the syndrome. Conclusions This case expands the knowledge of DDX3X pathogenic variants and the associated DDX3X syndrome phenotypic spectrum.

scholarly journals Cyclooxygenase-2 Glycosylation Is Affected by Peroxynitrite in Endothelial Cells: Impact on Enzyme Activity and Degradation

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 496
Author(s):  
Sonia Eligini ◽  
Susanna Colli ◽  
Aida Habib ◽  
Giancarlo Aldini ◽  
Alessandra Altomare ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
De Novo ◽  
Cyclooxygenase 2 ◽  
Nitric Oxide Donors ◽  
Metabolic Labeling ◽  
Dependent Manner ◽  
De Novo Synthesis ◽  
Human Endothelial Cells ◽  
Prolonged Incubation ◽  
Cox 2

The exposure of human endothelial cells to 3-morpholinosydnonimine (SIN-1) induced the expression of cyclooxygenase-2 (COX-2) in a dose- and time-dependent manner. Interestingly, after a prolonged incubation (>8 h) several proteoforms were visualized by Western blot, corresponding to different states of glycosylation of the protein. This effect was specific for SIN-1 that generates peroxynitrite and it was not detected with other nitric oxide-donors. Metabolic labeling experiments using 35S or cycloheximide suggested that the formation of hypoglycosylated COX-2 was dependent on de novo synthesis of the protein rather than the deglycosylation of the native protein. Moreover, SIN-1 reduced the activity of the hexokinase, the enzyme responsible for the first step of glycolysis. The hypoglycosylated COX-2 induced by SIN-1 showed a reduced capacity to generate prostaglandins and the activity was only partially recovered after immunoprecipitation. Finally, hypoglycosylated COX-2 showed a more rapid rate of degradation compared to COX-2 induced by IL-1α and an alteration in the localization with an accumulation mainly detected in the nuclear membrane. Our results have important implication to understand the effect of peroxynitrite on COX-2 expression and activity, and they may help to identify new pharmacological tools direct to increase COX-2 degradation or to inhibit its activity.

Stimulation of Tetrahydrobiopterin Synthesis by 17β-Estradiol in Brain Microvascular Endothelial Cells

Pteridines ◽  
2000 ◽  
Vol 11 (4) ◽  
pp. 129-132
Author(s):  
Kazuhiro Shiota ◽  
Masakazu Ishii ◽  
Toshinori Yamamoto ◽  
Shunichi Shimizu ◽  
Yuji Kiuchi
Keyword(s):  
Endothelial Cells ◽  
De Novo ◽  
Vascular Endothelial Cells ◽  
Mrna Level ◽  
Microvascular Endothelial Cells ◽  
No Production ◽  
Brain Microvascular Endothelial Cells ◽  
Protective Effects ◽  
17Β Estradiol ◽  
Microvascular Endothelial

Abstract The purpose of this study was to examine whether 17β-estradiol stimulates the synthesis of tetrahydrobiopterin : BH4), which is one of the cofactors of nitric oxide (NO) synthase, in mouse brain microvascular endothelial cells. Addition of 17()-estradiol to endothelial cells time- and concentration-dependently increased intracellular BH4 level. 17β-Estradiol also stimulated the mRNA level of GTP-cyclohydrolase I (GTPCH), which is a rate-limiting enzyme of the de novo BH4 synthetic pathway. In addition, the 17β-estradiol-induced expression of GTPCH mRNA was strongly attenuated by treatment with an inhibitor of 17β-estradiol receptor 4-hydroxy-tamoxlfen. These results suggest that 17β-estradiol stimulates BH4 synthesis through the induction of GTPCH by tamoxifensensitive receptor in vascular endothelial cells. The 17β-estradiol-induced increase in BH4 level might be implicated in not only NO production, but also protective effects of 17β-estradiol against ischemic brain damage and atherosclerosis, since BH4 is an intracellular antioxidant.

scholarly journals Computational analysis revealing that K634 and T681 mutations modulate the 3D-structure of PDGFR-β and lead to sunitinib resistance

RSC Advances ◽  
2017 ◽  
Vol 7 (60) ◽  
pp. 37612-37626 ◽  
Author(s):  
Vishal Nemaysh ◽  
Pratibha Mehta Luthra
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Blood Vessels ◽  
Computational Analysis ◽  
3D Structure ◽  
Growth Factor Receptor ◽  
Platelet Derived Growth Factor ◽  
Receptor Beta

Platelet-derived growth factor receptor-beta (PDGFR-β) is expressed by endothelial cells (ECs) of tumor-associated blood vessels and regulates primarily early hematopoiesis.

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