Activités cholinestérasiques dans le foie de Poulet Rôle de l'endoderme dans l'apparition d'activités cholinestérasiques dans la composante mésenchymateuse du tissu hépatique

Development ◽  
1971 ◽  
Vol 26 (3) ◽  
pp. 481-495
Author(s):  
Par Elisabeth Houssaint ◽  
Nicole Le Douarin
Keyword(s):  
Endothelial Cells ◽  
Chick Embryo ◽  
Cholinesterase Activity ◽  
Enzymic Activity ◽  
The Body ◽  
Hepatic Tissue ◽  
Experimental Procedure ◽  
Septum Transversum ◽  
Cholinesterase Activities

Cholinesterases in the chick liver. The role of the endoderm in the appearance of the activity of cholinesterases in the hepatic mesenchyme The histochemical method of Koelle & Friedenwald (1949), as modified by Gerebtzoff (1953), has been used to investigate the distribution of cholinesterases in the chick embryonic and adult liver. Non-specific cholinesterases and, in a lower proportion acetylcholinesterase, have been detected in the endothelial cells of blood sinusoids of both adult and embryonic hepatic tissue. The hepatocytes do not show any cholinesterase activity. Cholinesterases appear precociously in the liver mesenchyme, since they already occur in the septum transversum of the 3-day-old chick embryo. An experimental procedure preventing the invasion of the hepatic mesenchymal Anlage by the endodermic cords has been used. The experimentally isolated hepatic mesenchyme shows an important cholinesterase activity; therefore this activity does not depend on the presence of the hepatocytes. The grafting of the determined hepatic endodern in the somatopleura of the 3-day-old chick embryo results in the development of hepatic tissue in the body wall. In this experimentally produced liver, cholinesterase activities are present in the endothelial cells which have arisen from somatopleura mesenchymal cells, though normally somatopleural mesenchyme does not possess these enzymes. The role of the endoderm in the appearance of this enzymic activity in the somatopleural mesenchyme is discussed.

scholarly journals Lymphatic system and adipose tissue: Crosstalk in health and disease

2021 ◽  
Vol 18 (3) ◽  
pp. 336-344
Author(s):  
V. V. Klimontov ◽  
D. M. Bulumbaeva
Keyword(s):  
Endothelial Cells ◽  
Adipose Tissue ◽  
Molecular Mechanisms ◽  
Lymphatic System ◽  
Lymphatic Vessels ◽  
Inflammatory Cells ◽  
The Body ◽  
Push Button ◽  
Secondary Lymphedema

The lymphatic system (LS) is one of the main integrative systems of the body, providing protective and transport functions. In recent years, interactions between LS and adipose tissue (AT) have been of particular interest. Lymphatic vessels play an important role in metabolic and regulatory functions of AT, acting as a collector of lipolysis products and adipokines. In its turn, hormones and adipocytokines that produced in adipocytes (including leptin, adiponectin, IL-6, TNF-α, etc.) affect the function of lymphatic endothelial cells and control the growth of lymphatic vessels. Cooperation between LS and AT becomes pathogenetically and clinically important in lymphedema and obesity. It is known that both primary and secondary lymphedema are characterized by increased fat accumulation which is associated with the severity of lymphostasis and inflammation. Similarly, in obesity, the drainage function of LS is impaired, which is accompanied by perilymphatic mononuclear infiltration in the AT. The development of these changes is facilitated by endocrine dysfunction of adipocytes and impaired production of adipocytokines. The increase in the production of inflammatory mediators and the disruption of the traffic of inflammatory cells causes a further deterioration in the outflow of interstitial fluid and exacerbates the inflammation of the AT, thereby forming a vicious circle. The role of lymphangiogenesis in AT remodeling in obesity needs further research. Another promising area of research is the study of the role of intestinal LS in the development of obesity and related disorders. It has been shown that the transport of chylomicrons from the intestine depends on the expression of a number of molecular mediators (VEGF-C, DLL-4, neuropilin-1, VEGFR-1, CD36/FAT, etc.)in the endotheliocytes of the intestinal lymphatic vessels, as well as the functioning of «push-button» and “zippering” junctions between endothelial cells. New approach to the treatment of obesity based on blockade of lymphatic chylomicrontransport has been experimentally substantiated. Further identification of the molecular mechanisms and signaling pathways that determine the remodeling of AT in lymphedema and obesity are likely to provide new approaches to the treatment of these diseases.

Junctional Adhesion Molecule-1 Is Involved in bFGF-Induced Angiogenesis In Vivo.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 840-840
Author(s):  
Vesselina G. Cooke ◽  
Meghna U. Naik ◽  
William Skarnes ◽  
Ulhas P. Naik
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Blood Vessels ◽  
Adhesion Molecule ◽  
The Body ◽  
Cell Junctions ◽  
Fluorescein Angiogram ◽  
And Migration

Abstract Neovascularization is a multistep process that occurs in the body in both physiological and pathological conditions. We have recently shown that Junctional Adhesion Molecule-1 (JAM-1), a member of the Ig superfamily of molecules, is involved in endothelial cell adhesion and migration, leading to angiogenesis. In quiescent endothelial cells, JAM-1 is located at the cell-cell junctions where it forms a complex with integrin αvβ3. Upon treatment of the cells with growth factors, such as bFGF, JAM-1 dissociates from its complex with αvβ3 and redistributes to the cell surface. Blockage of the extracellular domain of JAM-1 inhibits bFGF-induced endothelial cell morphology, proliferation and angiogenesis. Additionally, functional knock-down of JAM-1 using the RNAi technique in endothelial cells showed decreased adhesion and migration of these cells, indicating a possible role for JAM-1 in angiogenesis. In this report, we show that JAM-1 has an important role in bFGF-induced angiogenesis in vivo. Here we present for the first time the generation JAM-1 knock-out mice, using the gene trap strategy. We have successfully confirmed the JAM-1 −/− genotype via Southern, Northern, and Western blot analyses. JAM-1 −/− mice are viable and do not seem to have any external abnormalities, except that they appear to be smaller in size. Retinal fluorescein angiogram revealed no evidence for morphological defects in the vasculature of JAM-1 −/− mice. To evaluate the role of JAM-1 in angiogenesis, we performed an aortic ring assay with both wild type and JAM-1−/− mice. Mouse thoracic aortas were harvested, cross-sectioned into rings of 1-mm thickness, and cultured in a three-dimensional Matrigel supplied with 50 ng/ml bFGF. Vascular sproutings were counted every other day for a period of 7 days at which time they were stained with crystal violet and photographed. Aortic rings from WT mice treated with bFGF showed a 2.8-fold increase in microvessel growth, compared to WT controls with no supplementation of bFGF. In contrast, microvessel sproutings in bFGF treated aortic rings from JAM-1 −/− mice were no more than the vessels in the WT control mice. These results suggest that JAM-1 may be important for bFGF induced angiogenesis. To further confirm the role of JAM-1 in angiogenesis, WT and JAM-1 −/− mice were injected in their flank region with Matrigel containing 80 ng/ml bFGF and 60 U/ml heparin. Two weeks after injection, Matrigel plugs were excised, embedded in paraffin, and the presence of blood vessels was visualized by H&E staining. Matrigel plugs from control WT mice that were not treated with bFGF showed no vascularization, while bFGF supplied Matrigel plugs from WT mice showed a robust vessel growth. Interestingly, bFGF-treated Matrigel plugs form JAM-1−/− mice failed to produce any blood vessels. These ex vivo and in vivo studies using JAM-1−/− mice suggest that JAM-1 has a unique and essential role in bFGF-induced angiogenesis.

scholarly journals Lymphovenous hemostasis and the role of platelets in regulating lymphatic flow and lymphatic vessel maturation

Blood ◽  
2016 ◽  
Vol 128 (9) ◽  
pp. 1169-1173 ◽  
Author(s):  
John D. Welsh ◽  
Mark L. Kahn ◽  
Daniel T. Sweet
Keyword(s):  
Endothelial Cells ◽  
Lymphatic Vessel ◽  
Vascular System ◽  
Lymphatic Vessels ◽  
Lymph Flow ◽  
The Body ◽  
Lymphatic Endothelial Cells ◽  
Lymphatic Circulation ◽  
Vessel Maturation

Abstract Aside from the established role for platelets in regulating hemostasis and thrombosis, recent research has revealed a discrete role for platelets in the separation of the blood and lymphatic vascular systems. Platelets are activated by interaction with lymphatic endothelial cells at the lymphovenous junction, the site in the body where the lymphatic system drains into the blood vascular system, resulting in a platelet plug that, with the lymphovenous valve, prevents blood from entering the lymphatic circulation. This process, known as “lymphovenous hemostasis,” is mediated by activation of platelet CLEC-2 receptors by the transmembrane ligand podoplanin expressed by lymphatic endothelial cells. Lymphovenous hemostasis is required for normal lymph flow, and mice deficient in lymphovenous hemostasis exhibit lymphedema and sometimes chylothorax phenotypes indicative of lymphatic insufficiency. Unexpectedly, the loss of lymph flow in these mice causes defects in maturation of collecting lymphatic vessels and lymphatic valve formation, uncovering an important role for fluid flow in driving endothelial cell signaling during development of collecting lymphatics. This article summarizes the current understanding of lymphovenous hemostasis and its effect on lymphatic vessel maturation and synthesizes the outstanding questions in the field, with relationship to human disease.

scholarly journals THE ROLE OF A NATURAL ANTIBODY IN THE REJECTION OF MOUSE TUMOR CELLS BY THE CHICK EMBRYO

1957 ◽  
Vol 106 (1) ◽  
pp. 111-126 ◽  
Author(s):  
Howard Green ◽  
Allan L. Lorincz
Keyword(s):  
Chick Embryo ◽  
Tumor Cells ◽  
The Body ◽  
Mouse Tumor ◽  
Internal Organs ◽  
Tissue Sections ◽  
Viable Cells ◽  
Viable Tumor

Cells of the Krebs ascites tumor of mice grow well in the body of the chick embryo until about the 17th day of incubation, when degeneration of the tumor can be seen in tissue sections and viable tumor cells begin to disappear from the internal organs of the embryo. This death of tumor cells follows the appearance in the chick embryo of serum gamma globulins. Among these are antibodies which can agglutinate the tumor cells in vitro, and destroy their viability. These antibodies occur in the blood without the introduction of any foreign antigen. Their possible origin is discussed. Small numbers of mouse tumor cells growing in the chick embryo are completely eliminated shortly after the time when antibodies ordinarily become detectable. When the number of cells present is larger, viable cells persist longer, and at still higher cell numbers, the embryo or chick is unable to eliminate the tumor, and is itself killed by it. Gamma globulins of older birds injected into young chick embryos bearing growing tumor clear the embryonic organs of viable tumor cells.

scholarly journals The role of the lymphatic system in the homeostasis of the interstitial fluid in the lung and pleural liquid

2019 ◽  
Vol 18 (1) ◽  
pp. 104-112 ◽  
Author(s):  
G. I. Lobov
Keyword(s):  
Endothelial Cells ◽  
Respiratory System ◽  
Interstitial Fluid ◽  
Lymphatic System ◽  
Lymphatic Vessels ◽  
Current Data ◽  
The Body ◽  
Almost All ◽  
Preclinical And Clinical Studies

Accomplishments in the identifcation of lymphatic endothelial cells and the ability to differentiate them from the endothelial cells of blood vessels have contributed to progress in recent decades in studying the role of the lymphatic system in the body. Preclinical and clinical studies of the last decade have shown that changes in the lymphatic vascular network are observed in almost all lung diseases. At the same time, it remains unclear whether the lymphatic vessels and lung nodes are being part of the overall process of lung remodeling or they make a defnite contribution to the pathogenesis of diseases of the respiratory system. This review presents current data on the morphology and physiology of lymphatic vessels and nodes, their role in the regulation of interstitial fluid homeostasis, lipid transportation and immune responses as well as describes the mechanisms of regulation of the transport function of lymphatic vessels. Data on the role of the lymphatic system of the lungs in the exchange of fluid in the interstitial space of the lungs are presented in the review. The results of studies of the last two decades on the formation and reabsorption of pleural fluid and the role of various lymphatic networks in regulating its volume are described. Finally, modern ideas on the mechanisms of pulmonary edema are outlined and important questions of the lymphatic biology of the respiratory system are identifed, still remaining unanswered today.

The Role of VWF In BBB Permeability Associated with Hypoxia/Reoxygenation

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 2102-2102
Author(s):  
Georgette L. Suidan ◽  
Simon F. De Meyer ◽  
Alexander Brill ◽  
Stephen M. Cifuni ◽  
Denisa D. Wagner
Keyword(s):  
Endothelial Cells ◽  
Ischemia Reperfusion ◽  
Critical Role ◽  
The Body ◽  
Wild Type ◽  
Junction Protein ◽  
Bbb Permeability ◽  
Deficient Mice ◽  
Hypoxia Reoxygenation

Abstract Abstract 2102 Aberrant blood brain barrier (BBB) permeability is a hallmark pathology in many diseases of the central nervous system (CNS) including hypoxia, epilepsy, multiple sclerosis and ischemic stroke. Generalized hypoxia is a pathological condition in which the body as a whole is deprived of adequate oxygen supply. Hypoxia occurs in healthy people when they ascend to high altitudes, where it can cause altitude sickness, often manifested by headache, leading to potentially fatal complications such as high altitude cerebral edema (HACE). Hypoxia followed by reoxygenation (H/R) is also commonly used as a model to investigate pathology associated with ischemia/reperfusion as the latter condition is present in several disease states including stroke. In animal models, H/R has been shown to cause tight junction protein abnormalities, increased BBB paracellular permeability and edema. von Willebrand Factor (VWF) is a glycoprotein that is synthesized exclusively by endothelial cells and megakaryocytes. Endothelial cell-derived VWF is secreted constitutively and stored in Weibel-Palade bodies (WPB) from where it is released by regulated secretion into the plasma and subendothelium in response to endothelial activation. It has been demonstrated in vitro that exposure of cultured endothelial cells to hypoxia results in WPB exocytosis and VWF secretion. While it is known that VWF is expressed abundantly by cerebral endothelial cells, very little is known about the role of VWF in endothelial biology, particularly, in regulation of the BBB under stressful conditions. Several studies have shown that VWF protein is up regulated in plasma of patients with several neurological conditions involving BBB disruption such as stroke, severe head injury, cerebral malaria and cerebral venous sinus thrombosis. As it is known that C57BL/6 (wild-type) mice have increased BBB permeability induced by H/R, we investigated the status of BBB integrity in VWF-deficient mice (also on the C57BL/6 background). For these experiments, we used a mouse model of normobaric hypoxia (24 hours of 6% oxygen) followed by reoxygenation (1 hour ~21% oxygen). VWF antigen levels were measured by ELISA and BBB permeability was assessed by quantification of Evan's blue dye leakage into the brain. Our data indicate that plasma VWF levels in wild-type mice are significantly increased after hypoxia when compared to normoxic controls. Upon comparison with wild-type mice, we have determined that VWF-deficient mice have significantly less BBB permeability after H/R suggesting that VWF plays a role in BBB integrity under stressful conditions. We have previously reported that VWF-deficient mice have a defect in regulated P-selectin secretion (Denis et al., PNAS, 2001). To determine if the maintenance of BBB integrity found in VWF-deficient mice was due to lack of P-selectin we utilized an aptamer which inhibits P-selectin (Archemix). Inhibition of P-selectin in wild-type animals resulted in similar BBB permeability when compared to controls. Our findings suggest a critical role for VWF in BBB permeability after hypoxia/reoxygenation that is independent of P-selectin. Disclosures: No relevant conflicts of interest to declare.

Endothelial cells in human cytomegalovirus infection: One host cell out of many or a crucial target for virus spread?

2009 ◽  
Vol 102 (12) ◽  
pp. 1057-1063 ◽  
Author(s):  
Christian Sinzger ◽  
Barbara Adler
Keyword(s):  
Endothelial Cells ◽  
Human Cytomegalovirus ◽  
Cell Types ◽  
The Body ◽  
Cell Type ◽  
Cell Culture Systems ◽  
Human Cytomegalovirus Infection ◽  
Productive Replication

SummaryEndothelial cells (EC) are assumed to play a central role in the spread of human cytomegalovirus (HCMV) throughout the body. Results from in-situ analyses of infected tissues and data from cell culture systems together strongly suggest that vascular EC can support productive replication of HCMV and thus contribute to its haematogeneous dissemination. By inducing an angiogenic response, HCMV may even promote growth of its own habitat. The particular role of EC is further supported by the fact that entry of HCMV into EC is dependent on a complex of the envelope glycoproteins gH and gL with a set of proteins (UL128–131A) which is dispensable for HCMV entry into most other cell types. These molecular requirements may also be reflected by cell type-dependent differences in entry routes, i.e. endocytosis versus fusion at the plasma membrane. An animal model with trackable murine CMV is now available to clarify the pathogenetic role of EC during haematogeneous dissemination of this virus.

Extracellular Mitochondria in Traumatic Brain Injury Induced Coagulopathy

2019 ◽  
Vol 46 (02) ◽  
pp. 167-175
Author(s):  
Zilong Zhao ◽  
Yuan Zhou ◽  
Min Li ◽  
Jianning Zhang ◽  
Jing-Fei Dong
Keyword(s):  
Traumatic Brain Injury ◽  
Endothelial Cells ◽  
Brain Injury ◽  
Tissue Injury ◽  
The Body ◽  
Secondary Tissue ◽  
Dilutional Coagulopathy ◽  
Poor Outcomes ◽  
Traumatic Impact

AbstractTraumatic brain injury (TBI) induced coagulopathy remains a significant clinical challenge, with unmet needs for standardizing diagnosis and optimizing treatments. TBI-induced coagulopathy is closely associated with poor outcomes in affected patients. Recent studies have demonstrated that TBI induces coagulopathy, which is mechanistically distinct from the deficient and dilutional coagulopathy found in patients with injuries to the body/limbs and hemorrhagic shock. Multiple causal and disseminating factors have been identified to cause TBI-induced coagulopathy. Among these are extracellular mitochondria (exMTs) released from injured cerebral cells, endothelial cells, and platelets. These circulating exMTs not only express potent procoagulant activity but also promote inflammation, and could remain metabolically active to become a major source of oxidative stress. They activate platelets and endothelial cells to propagate TBI-induced coagulopathy and secondary tissue injury after primary traumatic impact. In this review, we discuss recent advances in our understanding of the role of exMTs in the development of TBI-induced coagulopathy.

scholarly journals Regulation of Oxidative Stress in Corneal Endothelial Cells by Prdx6

Antioxidants ◽  
2018 ◽  
Vol 7 (12) ◽  
pp. 180 ◽  
Author(s):  
Matthew Lovatt ◽  
Khadijah Adnan ◽  
Gary Peh ◽  
Jodhbir Mehta
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Corneal Endothelium ◽  
Corneal Dystrophy ◽  
The Body ◽  
Corneal Endothelial Cells ◽  
Functional Studies ◽  
Age Dependent ◽  
Cellular Integrity

The inner layer of the cornea, the corneal endothelium, is post-mitotic and unable to regenerate if damaged. The corneal endothelium is one of the most transplanted tissues in the body. Fuchs’ endothelial corneal dystrophy (FECD) is the leading indication for corneal endothelial transplantation. FECD is thought to be an age-dependent disorder, with a major component related to oxidative stress. Prdx6 is an antioxidant with particular affinity for repairing peroxidised cell membranes. To address the role of Prdx6 in corneal endothelial cells, we used a combination of biochemical and functional studies. Our data reveal that Prdx6 is expressed at unusually high levels at the plasma membrane of corneal endothelial cells. RNAi-mediated knockdown of Prdx6 revealed a role for Prdx6 in lipid peroxidation. Furthermore, following induction of oxidative stress with menadione, Prdx6-deficient cells had defective mitochondrial membrane potential and were more sensitive to cell death. These data reveal that Prdx6 is compartmentalised in corneal endothelial cells and has multiple functions to preserve cellular integrity.

scholarly journals Morphological, Histological Changes and Acetyl Cholinesterase Activity in Chick Embryos After Exposure to Abamectin Insecticide

2021 ◽  
Vol 2 (02) ◽  
pp. 64-69
Author(s):  
Banan Taha ◽  
Rabeea Mohammed
Keyword(s):  
Chick Embryo ◽  
Cholinesterase Activity ◽  
Yolk Sac ◽  
The Body ◽  
Streptomyces Avermitilis ◽  
Enzyme Analysis ◽  
Acetyl Cholinesterase ◽  
Cell Degeneration ◽  
Histological Changes ◽  
Adverse Impacts

Abamectin is a bio-insecticide, derived from the soil bacteria Streptomyces avermitilis. This insecticide is used in public health and agriculture to protect crops. Major adverse impacts of Abamectin are neurological symptoms acting on the peripheral nervous system. The aim of the current study is to reveal the toxic effects of Abamectin on chick embryo Ross 308 including morphological and histological changes and acetyl cholinesterase activity. 120 fresh fertilized eggs were divided into 6 groups; two of them were used as control. After 2 days of incubation, the eggs were injected with 100 µL of Abamectin solution (diluted at concentrations 360, 540, 900 and 1800 ppm) into the yolk sac. The Results showed that the mortality increased significantly in chicks treated with Abamectin, but had a lower weight in comparison to the control groups. Treated chicks started hatching at day 22 but were physically weak with drooping limbs, paralysis and then died after 24 hours of hatching. Some chicks did not normally hatch and needed assistance. They characterized by limb defects, failure retraction of yolk sac with bleeding. Histological examination of the liver showed hepatic cell degeneration, congestion in the central vein, infiltration of inflammatory cells and hepatocytes necrosis. Furthermore, the Acetyl cholinesterase enzyme analysis showed a significant decrease in the enzyme activity which leads to inhibition the activity of the body systems. It is concluded that low and high concentration of Abamectin has adverse impacts on chick embryo by changing some of morphological, histological characteristics and acetyl cholinesterase activity.

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