Abnormal blood vessels formed by human liver cavernous hemangioma endothelial cells in nude mice are suitable for drug evaluation

2009 ◽  
Vol 78 (3) ◽  
pp. 379-385 ◽  
Author(s):  
Wen-jian Zhang ◽  
Lian-qiu Wu ◽  
Hong-lin Liu ◽  
Li-ya Ye ◽  
Yu-ling Xin ◽  
...  
1994 ◽  
Vol 72 (01) ◽  
pp. 044-053 ◽  
Author(s):  
N Chomiki ◽  
M Henry ◽  
M C Alessi ◽  
F Anfosso ◽  
I Juhan-Vague

SummaryIndividuals with elevated levels of plasminogen activator inhibitor type 1 are at risk of developing atherosclerosis. The mechanisms leading to increased plasma PAI-1 concentrations are not well understood. The link observed between increased PAI-1 levels and insulin resistance has lead workers to investigate the effects of insulin or triglyceride rich lipoproteins on PAI-1 production by cultured hepatocytes or endothelial cells. However, little is known about the contribution of these cells to PAI-1 production in vivo. We have studied the expression of PAI-1 in human liver sections as well as in vessel walls from different territories, by immunocytochemistry and in situ hybridization.We have observed that normal liver endothelial cells expressed PAI-1 while parenchymal cells did not. However, this fact does not refute the role of parenchymal liver cells in pathological states.In healthy vessels, PAI-1 mRNA and protein were detected primarily at the endothelium from the lumen as well as from the vasa vasorum. In normal arteries, smooth muscle cells were able to produce PAI-1 depending on the territory tested. In deeply altered vessels, PAI-1 expression was observed in neovessels scattering the lesions, in some intimal cells and in smooth muscle cells. Local increase PAI-1 mRNA described in atherosclerotic lesions could be due to the abundant neovascularization present in the lesion as well as a raised expression in smooth muscle cells. The increased PAI-1 in atherosclerosis could lead to fibrin deposit during plaque rupture contributing further to the development and progression of the lesion.


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

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Maria I. Alvarez-Vergara ◽  
Alicia E. Rosales-Nieves ◽  
Rosana March-Diaz ◽  
Guiomar Rodriguez-Perinan ◽  
Nieves Lara-Ureña ◽  
...  

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.


RSC Advances ◽  
2017 ◽  
Vol 7 (60) ◽  
pp. 37612-37626 ◽  
Author(s):  
Vishal Nemaysh ◽  
Pratibha Mehta Luthra

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


2001 ◽  
Vol 125 (1) ◽  
pp. 67-71 ◽  
Author(s):  
Mark W. Lingen

Abstract The basic signs and symptoms of inflammation and wound healing have been appreciated for thousands of years. However, the specific cells involved and their roles in this complex environment are still being elucidated today. In 1926, the origin of the phagocytic mononuclear ameboid wandering cell (macrophage) had not been determined. One popular theory was that the cells were differentiated from the endothelial cells of the nearby blood vessels, whereas others believed that the cells came from the peripheral blood or resting wandering cells. The purpose of this article is to review the seminal article published by Lang regarding this topic nearly 75 years ago. In addition, this article will review what is now known with regard to the role of the macrophage and endothelial cells in the development of angiogenesis, which is arguably the most critical component of successful inflammatory process or wound healing.


1991 ◽  
Vol 3 (2) ◽  
pp. 22-26
Author(s):  
Xu Xiulan ◽  
Jia Libin ◽  
Zheng Yahai ◽  
Gan Chen ◽  
Gu Jianren ◽  
...  

Development ◽  
2014 ◽  
Vol 141 (21) ◽  
pp. 4121-4126 ◽  
Author(s):  
J. C. Pelton ◽  
C. E. Wright ◽  
M. Leitges ◽  
V. L. Bautch

2010 ◽  
Vol 30 (10) ◽  
pp. 2401-2410 ◽  
Author(s):  
Eunok Im ◽  
Ruta Motiejunaite ◽  
Jorge Aranda ◽  
Eun Young Park ◽  
Lorenzo Federico ◽  
...  

ABSTRACT We previously reported that vascular endothelial growth factor (VEGF)-dependent activation of phospholipase Cγ1 (PLCγ) regulated tube stability by competing with phosphoinositide 3-kinase (PI3K) for their common substrate. Here we describe an additional mechanism by which PLCγ promoted regression of tubes and blood vessels. Namely, it increased the level of autotaxin (ATX), which is a secreted form of lysophospholipase D that produces lysophosphatidic acid (LPA). LPA promoted motility of endothelial cells, leading to disorganization/regression of tubes in vitro. Furthermore, mice that under- or overexpressed members of this intrinsic destabilization pathway showed either delayed or accelerated, respectively, regression of blood vessels. We conclude that endothelial cells can be instructed to engage a PLCγ-dependent intrinsic destabilization pathway that results in the production of soluble regression factors such as ATX and LPA. These findings are likely to potentiate ongoing efforts to prevent, manage, and eradicate numerous angiogenesis-based diseases such as proliferative diabetic retinopathy and solid tumors.


2019 ◽  
Vol 47 ◽  
Author(s):  
Viviane Motta dos Santos Moretto ◽  
Luciana Maria Curtio Soares ◽  
Esthefanie Nunes ◽  
Uiara Hanna Araújo Barreto ◽  
Valéria Régia Franco Sousa ◽  
...  

Background: Cerebral cavernous hemangioma is a rare neoplasm of vascular origin in the brain, characterized by abnormally dilated vascular channels surrounded by endothelium without muscle or elastic fibers. Presumptive diagnosis is performed by magnetic resonance or computed tomography (CT) scanning and can be confirmed by histopathology. The prognosis of intracranial cavernous hemangioma is poor, with progression of clinical signs culminating in spontaneous death or euthanasia. The purpose of this paper is to report a case of cerebral cavernous hemangioma in a dog, presenting the clinical findings, tomographic changes, and pathological findings.Case: This case involved a 2-year-old medium sized mixed breed female dog presenting with apathy, hyporexia, ataxia, bradycardia, dyspnea, and seizure episodes for three days. Hemogram and serum biochemistry of renal and hepatic function and urinalysis did not reveal any visible changes. CT scanning was also performed. The scans revealed a hyperdense nodule of 15.9 x 14 mm, with well defined borders, and a hypodense halo without post-contrast enhancement and mass effect in the right parietal lobe was observed in both transverse and coronal sections. Based on the image presented in the CT scans, the nodule was defined as a hemorrhagic brain lesion. The animal died after a seizure. The right telencephalon was subjected to necropsy, which revealed a reddish-black wel-defined nodule 1.7 cm in diameter extending from the height of the piriform lobe to the olfactory trine at the groove level and extending towards the lateral ventricle, with slight compression and deformation of the thalamus but no other macroscopic alterations in the other organs. The histopathology indicated that this nodular area in the encephalus contained moderate, well-delimited but unencapsulated cellularity, composed of large vascular spaces paved with endothelial cells filled with erythrocytes, some containing eosinophilic fibrillar material (fibrin) and others with organized thrombus containing occasional neutrophil aggregates. The endothelial cells had cytoplasm with indistinct borders, elongated nuclei, scanty crust-like chromatin, and cellular pleomorphism ranging from discrete to moderate, without mitotic figures.Discussion: The histological findings characterized the morphological changes in the brain as cavernous hemangioma, and the growth and compression of this neoplasm were considered the cause of the clinical signs of this dog. The main complaint was seizures, although ataxia and lethargy were also noted. These clinical signs are often related to changes in the anterior brain and brainstem. The literature does not list computed tomography as a complementary diagnostic method in cases of cerebral cavernous hemangioma in dogs, but CT scanning was useful in confirming cerebral hemorrhage. The main differential diagnosis for cerebral cavernous hemangioma would be a hamartoma, but what differentiates them histologically is the presence of normal interstices between the blood vessels, since no intervening neural tissue occurs in the case of cerebral hemangioma. Therefore, even in the absence of immunohistochemistry to more confidently confirm a cavernous hemangioma, the clinical signs, CT scans and especially the pathological findings were consistent with a case of cerebral cavernous hemangioma, a benign neoplasm with a poor prognosis due to the severe neurological changes it causes and its difficult treatment.


2021 ◽  
Author(s):  
Leyla Dogan ◽  
Ruben Scheuring ◽  
Nicole Wagner ◽  
Yuichiro Ueda ◽  
Philipp Woersdoerfer ◽  
...  

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.


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