Precocity of the endothelial proliferation during a course of rapid goitrogenesis

1984 ◽  
Vol 105 (4) ◽  
pp. 487-491 ◽  
Author(s):  
M.-C. Many ◽  
J.-F. Denef ◽  
S. Haumont
Keyword(s):  
Endothelial Cells ◽  
Cellular Proliferation ◽  
Pulse Labelling ◽  
Follicular Cells ◽  
Microscopical Level ◽  
Light Microscopical Level ◽  
Endothelial Proliferation ◽  
C3h Mice ◽  
Thyroid Hyperplasia

Abstract. Thyroid hyperplasia was induced in C3H mice by a low iodine diet feeding supplemented with propylthiouracil. The morphological modifications associated to the development of hyperplasia were analyzed at light microscopical level and the cellular proliferation was studied by autoradiography after a pulse labelling with [3H]thymidine. The initial modification during the course of hyperplasia is the development of the vascularization. It includes the dilatation of the capillaries, which occurs before any extended modification of the follicular cells and any change of the thyroid weight, and the proliferation of endothelial cells which starts earlier than that of follicular cells.

Immunolabelling of glomerular deposits in kidney biopsies routinely fixed in glutaraldehyde

1989 ◽  
Vol 47 ◽  
pp. 910-911
Author(s):  
Ś Lhoták ◽  
I. Alexopoulou ◽  
G. T. Simon
Keyword(s):  
Uv Light ◽  
Kidney Diseases ◽  
Light Chains ◽  
Microscopical Level ◽  
Accurate Identification ◽  
Light Microscopical Level ◽  
Dense Deposits ◽  
Cacodylate Buffer ◽  
Glomerular Deposits ◽  
Prognostic Importance

Various kidney diseases are characterized by the presence of dense deposits in the glomeruli. The type(s) of immunoglobulins (Igs) present in the dense deposits are characteristic of the disease. The accurate Identification of the deposits is therefore of utmost diagnostic and prognostic importance. Immunofluorescence (IF) used routinely at the light microscopical level is unable to detect and characterize small deposits found in early stages of glomerulonephritis. Although conventional TEM is able to localize such deposits, it is not capable of determining their nature. It was therefore attempted to immunolabel at EM level IgG, IgA IgM, C3, fibrinogen and kappa and lambda Ig light chains commonly found in glomerular deposits on routinely fixed ( 2% glutaraldehyde (GA) in 0.1M cacodylate buffer) kidney biopsies.The unosmicated tissue was embedded in LR White resin polymerized by UV light at -10°C. A postembedding immunogold technique was employed

scholarly journals Modulatory effect of curcumin on survival of irradiated human intestinal microvascular endothelial cells: role of Akt/mTOR and NF-κB

2010 ◽  
Vol 298 (6) ◽  
pp. G865-G877 ◽  
Author(s):  
Parvaneh Rafiee ◽  
David G. Binion ◽  
Michael Wellner ◽  
Behnaz Behmaram ◽  
Martin Floer ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Radiation Therapy ◽  
Mammalian Target Of Rapamycin ◽  
Microvascular Endothelial Cells ◽  
Antiangiogenic Effect ◽  
Small Interference Rna ◽  
Cell Cycle Reentry ◽  
Endothelial Proliferation ◽  
Low Levels ◽  
Microvascular Endothelial

Radiation therapy is an essential modality in the treatment of colorectal cancers. Radiation exerts an antiangiogenic effect on tumors, inhibiting endothelial proliferation and survival in the tumor microvasculature. However, damage from low levels of irradiation can induce a paradoxical effect, stimulating survival in endothelial cells. We used human intestinal microvascular endothelial cells (HIMEC) to define effects of radiation on these gut-specific endothelial cells. Low-level irradiation (1–5 Gy) activates NF-κB and the phosphatidylinositol 3-kinase (PI3K)/Akt pathway, which is involved in cell cycle reentry and cell survival in HIMEC. A downstream target of PI3K/Akt is mammalian target of rapamycin (mTOR), which contributes to endothelial proliferation and angiogenesis. The aim of this study was to investigate the signaling molecules involved in the radiosensitizing effects of curcumin on HIMEC subjected to low levels of irradiation. We have demonstrated that exposure of HIMEC to low levels of irradiation induced Akt and mTOR phosphorylation, which was attenuated by curcumin, rapamycin, LY294002, and mTOR small interference RNA (siRNA). Activation of NF-κB by low levels of irradiation was inhibited by curcumin, SN-50, and mTOR siRNA. Curcumin also induced apoptosis by induction of caspase-3 cleavage in irradiated HIMEC. In conclusion, curcumin significantly inhibited NF-κB and attenuated the effect of irradiation-induced prosurvival signaling through the PI3K/Akt/mTOR and NF-κB pathways in these gut-specific endothelial cells. Curcumin may be a potential radiosensitizing agent for enhanced antiangiogenic effect in colorectal cancer radiation therapy.

Notch2 Suppression Mimicking Changes in Human Pulmonary Hypertension Modulates Notch1 and Promotes Endothelial Cell Proliferation

2021 ◽  
Author(s):  
Sanghamitra Sahoo ◽  
Yao Li ◽  
Daniel de Jesus ◽  
John Charles Sembrat II ◽  
Mauricio M Rojas ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Target Genes ◽  
Pulmonary Arteries ◽  
Notch Receptor ◽  
Endothelial Cell Proliferation ◽  
Tissue Samples ◽  
Endothelial Proliferation ◽  
Human Pulmonary Artery

Pulmonary arterial hypertension (PAH) is a fatal cardiopulmonary disease characterized by increased vascular cell proliferation with resistance to apoptosis and occlusive remodeling of the small pulmonary arteries in humans. The Notch family of proteins are proximal signaling mediators of an evolutionarily conserved pathway that effect cell proliferation, fate determination, and development. In endothelial cells (ECs), Notch receptor 2 (Notch2) has been shown to promote endothelial apoptosis. However, a pro- or anti-proliferative role for Notch2 in pulmonary endothelial proliferation and ensuing PAH is unknown. Herein, we postulated that suppressed Notch2 signaling drives pulmonary endothelial proliferation in the setting of PAH. We observed that levels of Notch2 are ablated in lung and PA tissue samples from PAH patients compared to non-PAH controls. Interestingly, Notch2 expression was attenuated in human pulmonary artery endothelial cells (hPAECs) exposed to vasoactive factors including hypoxia, TGFβ, ET-1, and IGF-1. Gene silencing of Notch2 increased EC proliferation and reduced apoptosis. At the molecular level, Notch2-deficient hPAECs activated Akt, Erk1/2 and anti-apoptotic protein Bcl-2, and reduced levels of p21cip and Bax. Intriguingly, loss of Notch2 elicits a paradoxical activation of Notch1 and transcriptional upregulation of canonical Notch target genes Hes1, Hey1 and Hey2. Further, reduction in Rb and increased E2F1 binding to the Notch1 promoter appear to explain the upregulation of Notch1. In aggregate, our results demonstrate that loss of Notch2 derepresses Notch1 and elicits aberrant EC hallmarks of PAH. The data underscore a novel role for Notch in the maintenance of endothelial cell homeostasis.

scholarly journals Fabrication of aortic bioprosthesis by decellularization, fibrin glue coating and re-endothelization: a cell scaffold approach

2019 ◽  
Vol 8 (3) ◽  
pp. 197-210 ◽  
Author(s):  
Sonal Walawalkar ◽  
Shahdab Almelkar
Keyword(s):  
Endothelial Cells ◽  
Fibrin Glue ◽  
Cellular Proliferation ◽  
Graft Patency ◽  
Cell Viability Assay ◽  
Ethanol Group ◽  
Viability Assay ◽  
Group I ◽  
Group Ii ◽  
Cellular Dna

Abstract Aortic dysfunctions (aneurysm, aortitis) lead to the most serious conditions related to aortic wall with life-threatening complications. The most common modality of management for such conditions is replacement (diseased part) of aorta by a larger diameter stent (reconstructive vascular surgery) which in itself is a big trial. The most natural way is to use a re-endothelized scaffold. Developing a scaffold with biomimetic properties is an experimental aim for most of the scientists and surgeons. We aim to structure a strategy to overcome the well-known problems associated with aorta. In this study, we plan to remold a larger diameter blood vessel such as aorta from xenogeneic origin using different protocols to decellularize and comparing them with normal aorta. The chemicals and enzymes used for bovine aorta decellularization are 1% SDS (group II), 70% ethanol + 0.25% trypsin (group III), 70% ethanol (group IV), and 0.25% trypsin (group V). Group I served as control (without decellularization). Histology and SEM study were conducted for cellular presence/absence in all scaffolds. Later, the scaffolds were coated with the fibrin glue (FG) and endothelial cells were proliferated over them. 3D images were taken showing the remolding of the endothelial cells on FG-coated surfaces. The re-endothelization was confirmed by lectin and vWF+/+ expression. Graft elasticity and burst pressure were confirmed by biomechanical tensile testing. Further, the absence of host tissue DNA and presence of cellular DNA after re-endothelialization were confirmed by PicoGreen assay. The acceptability for metabolically active cellular proliferation on scaffolds and its non-toxicity were proved by cell viability assay. Current findings accomplish that larger diameter aorta extracellular matrix scaffold (group II) can be fabricated and re-endothelialized to develop non-thrombotic surfaces with improved graft patency with promising results compared to other fabricated scaffold groups.

scholarly journals The Ratio of Factor VIIa:Tissue Factor Content within Microvesicles Determines the Differential Influence on Endothelial Cells

TH Open ◽  
2019 ◽  
Vol 03 (02) ◽  
pp. e132-e145 ◽  
Author(s):  
Yahya Madkhali ◽  
Sophie Featherby ◽  
Mary Collier ◽  
Anthony Maraveyas ◽  
John Greenman ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Coronary Artery ◽  
Tissue Factor ◽  
Cellular Proliferation ◽  
Molar Ratio ◽  
Activity Levels ◽  
Human Coronary Artery ◽  
Determining Factors ◽  
Mcf 7

AbstractTissue factor (TF)-positive microvesicles from various sources can promote cellular proliferation or alternatively induce apoptosis, but the determining factors are unknown. In this study the hypothesis that the ratio of fVIIa:TF within microvesicles determines this outcome was examined. Microvesicles were isolated from HepG2, BxPC-3, 786-O, MDA-MB-231, and MCF-7 cell lines and microvesicle-associated fVIIa and TF antigen and activity levels were measured. Human coronary artery endothelial cells (HCAECs) were incubated with these purified microvesicles, or with combinations of fVIIa-recombinant TF, and cell proliferation/apoptosis was measured. Additionally, by expressing mCherry-PAR2 on HCAEC surface, PAR2 activation was quantified. Finally, the activation of PAR2 on HCAEC or the activities of TF and fVIIa in microvesicles were blocked prior to addition of microvesicles to cells. The purified microvesicles exhibited a range of fVIIa:TF ratios with HepG2 and 786-O cells having the highest (54:1) and lowest (10:1) ratios, respectively. The reversal from proapoptotic to proliferative was estimated to occur at a fVIIa:TF molar ratio of 15:1, but HCAEC could not be rescued at higher TF concentrations. The purified microvesicles induced HCAEC proliferation or apoptosis according to this ruling. Blocking PAR2 activation on HCAEC, or inhibiting fVIIa or TF-procoagulant function on microvesicles prevented the influence on HCAEC. Finally, incubation of HCAEC with recombinant TF resulted in increased surface exposure of fVII. The induction of cell proliferation or apoptosis by TF-positive microvesicles is dependent on the ratio of fVIIa:TF and involves the activation of PAR2. At lower TF concentrations, fVIIa can counteract the proapoptotic stimulus and induce proliferation.

scholarly journals A study of histological changes of human placenta in rural population of eastern India

2018 ◽  
Vol 7 (8) ◽  
pp. 3280
Author(s):  
Mrinal Kanti Karmakar ◽  
Sambit Kar ◽  
S. M. Kumar ◽  
Subir Kumar Chattopadhyay ◽  
L. K. Vaid ◽  
...  
Keyword(s):  
Umbilical Cord ◽  
Cellular Proliferation ◽  
Histological Study ◽  
Normal Growth ◽  
Normal Pregnancy ◽  
Eastern India ◽  
Histological Changes ◽  
Endothelial Proliferation ◽  
Umbilical Cord Insertion ◽  
Normal Placenta

Background: Placenta is essential for maintenance of pregnancy and for promoting normal growth and development of fetus. It forms the morphological record of anatomical condition, intrauterine events and intrapartum events of gestation. Present study has been undertaken to record the data on the morphology and histology of placenta from mothers with hypertension and diabetes.Methods: This study showed several significant morphological and histological differences in the placenta of the mother with GDM and hypertensive placenta. The histological study of the placenta was done under microscope and number of syncytial knots, cytotrophoblastic cellular proliferation, fibrinoid necrosis, endothelial proliferation, calcified and hyalinised villous spots were noted per low power field in the diabetics and hypertensive group in comparison to control group.Results: All other parameters including area, thickness, diameter, and circumference of GDM placenta show a significant increase when compared with normal placenta. The gross anatomic features of placentae e.g infarcted areas, calcified areas and marginal insertion of the umbilical cord in the study group show significant increase in value (p>0.01) in diabetic and hypertensive groups when compared to that of the control or normal group.Conclusions: In present study we found that hypertensive placentae tend to be slightly smaller in size, weight, volume, area, thickness, diameter, circumference and feto-placental ratio than normal placentae but the parameters were found to be significantly greater than that of normal placentae in case of diabetic placentae. No significant differences were found in umbilical cord insertion. In normal pregnancy cases we found several histological findings which were increased in hypertensive and diabetic cases.

Some ultrastructural aspects of Crithidia guilhermei n.sp. isolated from Phaenicia cuprina (Diptera: Calliphoridae)

1986 ◽  
Vol 64 (12) ◽  
pp. 2837-2842 ◽  
Author(s):  
Maurilio J. Soares ◽  
Reginaldo P. Brazil ◽  
Amilcar Tanuri ◽  
Wanderley de Souza
Keyword(s):  
Freeze Fracture ◽  
Kinetoplast Dna ◽  
Microscopical Level ◽  
Thin Sections ◽  
Crithidia Luciliae ◽  
Transmission Electron ◽  
Light Microscopical Level ◽  
Attachment Region ◽  
Phaenicia Sericata ◽  
A New Species

A flagellate trypanosomatid was isolated from the fly Phaenicia cuprina captured in Rio de Janeiro, Brazil. It grows well in liver infusion – trypticase medium, in the form of choanomastigotes, typical of the genus Crithidia. Morphometrical data obtained at the light microscopical level indicated that the new isolated Crithidia is smaller than Crithidia luciliae, a parasite isolated from Phaenicia sericata. Transmission electron microscopy of thin sections revealed that this trypanosomatid has a flagellar pocket divided into two compartments, one basal and the other apical, separated by a region of attachment of the flagellum to the cell body. The attachment region was characterized in freeze-fracture replicas. The flagellate has a compact kinetoplast DNA network. As in endosymbiote-containing trypanosomatids previously described, no subpellicular microtubules were seen in the regions where the mitochondria touched the plasma membrane, although no endosymbiotes were found in this flagellate. Electrophoretic mobility of six enzymes showed that the parasite could not be grouped in any of the isoenzymic pattern groups of other Crithidia spp. These observations indicate that the trypanosomatid isolated from P. cuprina is a new species of Crithidia. The flagellate is described as Crithidia guilhermei n.sp.

Antiproliferative, antiangiogenesis, and reversal of chemoresistance by specific cathepsin L inhibitors

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. e14643-e14643
Author(s):  
A. Rebbaa ◽  
E. Dyskin ◽  
E. Dier ◽  
C. Gallati ◽  
C. Honko ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Endothelial Cells ◽  
Tumor Growth ◽  
Anticancer Agents ◽  
Cellular Proliferation ◽  
Cathepsin L ◽  
Neuroblastoma Cell ◽  
Drug Candidate ◽  
Dependent Manner

e14643 Background: Uncontrolled proliferation, enhanced angiogenesis and the development of resistance to therapy are hallmarks of cancer; therefore, the development of approaches to simultaneously target these three processes would be the most desirable. Previous work from our laboratory has demonstrated that NapSul-Ile-Trp-CHO (NSITC), a specific inhibitors of cathepsin L, and its analogs strongly inhibited cancer cell proliferation and suppressed the development of drug resistance in vitro (Zheng X. et al., 2004 Cancer Res. 64:1773–80). In the present study, we sought to investigate the validity of these observations in vivo, and to dissect the underlying mechanism(s). Methods: Nude mice (Strain CD1) bearing xenografts of doxorubicin resistant neuroblastoma cell line SKN-SH/R were challenged with doxorubicin (1.5 mg/Kg) alone, NSITC (20 mg/kg) alone or the combination of both. The effect of NSITC on tumor angiogenesis was also investigated using the Chick Chorioallantoic Membrane (CAM). Putative mechanisms by which NSITC inhibits cellular proliferation, drug resistance and angiogenesis were studied using cancer and endothelial cells maintained in culture. Results: The in vivo data indicated that doxorubicin alone had no effect on tumor growth, however NSITC alone exerted 40% inhibition and the combination of both drugs reduced tumor growth by about 90%. NSITC also caused a 125% inhibition of blood vessel branching in the CAM model (at 1 μg/CAM). Investigation of the underlying mechanisms of its action revealed that at low concentration, NSITC forces cancer cells into senescence, preventing them from developing resistance to classical anticancer agents, and at high concentrations, it induced autophagic cell death. NSITC also strongly inhibited the proliferation and invasion of endothelial cells in a dose dependent manner with more than 90% inhibition at 20 μM. Conclusions: Overall, these findings suggest that NSITC has multi-anticancer functions and thus, may represent a potential drug candidate for the treatment of aggressive malignancies. No significant financial relationships to disclose.

Induction of endothelial proliferation and angiogenesis through activating the ERK1/2/EGF pathway mediate by CXC chemokine receptor 2 by chemokine (C-X-C motif) ligand 1.

2013 ◽  
Vol 31 (6_suppl) ◽  
pp. 138-138 ◽  
Author(s):  
Makito Miyake ◽  
Steve Goodison ◽  
Evan Gomes ◽  
Wasia Rizwani ◽  
Shanti Ross ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Chemokine Receptor ◽  
Cellular Proliferation ◽  
Human Endothelial Cell ◽  
Endothelial Cell Proliferation ◽  
Cxc Chemokine ◽  
Inhibition Of Angiogenesis

138 Background: Endothelial cell growth and proliferation are critical for tumoral angiogenesis. We report here that blockade of Chemokine (C-X-C motif) ligand 1 (CXCL1) results in reduction of human endothelial cell proliferation and its ability to induce angiogenesis. Methods: Two human endothelial cell lines, HUVEC and HDMEC, were used in the in vitro assays. Proliferation assay and matrigel tube formation assay were performed to test the inhibitory effect of anti-CXCL antibody on the activity of endothelial cells in vitro. Matrigel plug assay in nude mice was performed to test the in vivo angiogenic activity of CXCL1. Results: CXCL1 interacts with its receptor CXC chemokine Receptor 2 and induces endothelial cell proliferation, whereas blockade of CXCL1 is associated with reduction in cellular proliferation through a decrease in levels of cyclin D and cdk4 and inhibition of angiogenesis through EGF and ERK 1/2. Targeting CXCL1 inhibits neoangiogenesis but has no effect on disrupting established vasculature. Furthermore targeting CXCL1 is associated with reduction in migration of human endothelial cells in an in vitro model. Additionally, neutralizing antibody against CXCL1 in a xenograft angiogenesis model resulted in inhibition of angiogenesis. Conclusions: CXCL1-induced regulation of angiogenesis has not been studied extensively in human cancers, thus these findings illustrate a novel contribution of CXCL1 interactions in pathological angiogenesis. Therefore, the ability to selectively modulate CXCL1, specifically in tumoral angiogenesis, may promote the development of novel oncologic therapeutic strategies.

Differential Expression of SKI Oncogene Protein in Hemangiomas

2009 ◽  
Vol 141 (2) ◽  
pp. 213-218 ◽  
Author(s):  
M. Teresa ◽  
Melin Tan ◽  
Mark Tarango ◽  
Lou Fink ◽  
Martin Mihm ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Differential Expression ◽  
Cellular Proliferation ◽  
Vascular Tissue ◽  
Senior Author ◽  
Tissue Array ◽  
Basic Science Study ◽  
Immunohistochemical Studies ◽  
Ski Protein ◽  
Oncogene Protein

OBJECTIVE: The pathogenesis for benign tumorigenesis in hemangiomas is unknown. Oncogene proteins may be influential in this process. SKI proteins have been previously described in various malignancies. We investigated the differential expression of the SKI (sarcoma viral oncogene) protein in hemangiomas. STUDY DESIGN: Prospective basic science study. SUBJECTS AND METHODS: Paraffin-embedded hemangioma tissues were obtained from the senior author from 2005 to 2006. We created the first vascular tissue array composed of 12 hemangioma specimens at various stages of growth and anatomic location. Two cores were taken from each sample. Controls were also included. Immunohistochemical studies were performed using SKI, CD31, and Ki67. RESULTS: All 12 hemangioma tissues overexpressed the SKI protein. The staining pattern was perinuclear within the endothelial cells. The intensity of staining was inversely proportional to the growth stage. The endothelial cells that were SKI-positive were involved in active cell division. CONCLUSION: SKI oncogene protein is differentially and specifically expressed in hemangioma tissues. SKI acts as a transcriptional co-repressor and inhibits the TGF-β pathway, thus leading to uncontrolled cellular proliferation and transformation. All vascular controls were negative for SKI staining. CLINICAL SIGNIFICANCE OF STUDY: The SKI oncogene protein is upregulated by hemangiomas and may play a role in hemangioma tumorigenesis.

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