Maturation of the glomerular visceral epithelium and capillary endothelium in the puppy kidney

1979 ◽  
Vol 193 (1) ◽  
pp. 1-21 ◽  
Author(s):  
Don A. Hay ◽  
Andrew P. Evan
Keyword(s):  
Capillary Endothelium ◽  
Visceral Epithelium

Cellular Contacts Within the Interhemal Membrane of the Rat Placenta at Term

1974 ◽  
Vol 32 ◽  
pp. 146-147
Author(s):  
William P. Jollie
Keyword(s):  
Osmium Tetroxide ◽  
Uranyl Acetate ◽  
Capillary Endothelium ◽  
En Bloc ◽  
Aldehyde Fixation ◽  
Chorioallantoic Placenta

By routine EM preparative techniques, the tissues which, collectively, separate maternal and fetal bloods in the fully formed chorioallantoic placenta of the rat have been shown to consist of three chorionic layers, or trophoblast, and a layer of allantoic capillary endothelium [Fig. 1]. Relationships between these layers are best demonstrated by special techniques, viz., cacodylate-buffered aldehyde fixation, collidine-buffered osmium tetroxide postfixation, and en bloc staining with uranyl acetate. By using this method on placentas at term, the cells of the outermost chorionic layer (Trophoblast 1) appear to be attached to each other by means of maculae adherentes which sometimes occur in clusters [Fig. 2].

Ultrastructure of pulmonary microvasculature in acute endotoxemia

1978 ◽  
Vol 36 (2) ◽  
pp. 470-471
Author(s):  
R. G. Gerrity ◽  
M. Richardson
Keyword(s):  
Polymorphonuclear Leukocytes ◽  
Alveolar Epithelium ◽  
Endothelial Damage ◽  
Capillary Endothelium ◽  
Type Ii Cells ◽  
Type Ii ◽  
Interstitial Edema ◽  
Pulmonary Capillaries ◽  
Lung Ultrastructure ◽  
Fibrin Thrombi

Dogs were injected intravenously with E_. coli endotoxin (2 mg/kg), and lung samples were taken at 15 min., 1 hr. and 24 hrs. At 15 min., occlusion of pulmonary capillaries by degranulating platelets and polymorphonuclear leukocytes (PML) was evident (Fig. 1). Capillary endothelium was intact but endothelial damage in small arteries and arterioles, accompanied by intraalveolar hemorrhage, was frequent (Fig. 2). Sloughing of the surfactant layer from alveolar epithelium was evident (Fig. 1). At 1 hr., platelet-PML plugs were no longer seen in capillaries, the endothelium of which was often vacuolated (Fig. 3). Interstitial edema and destruction of alveolar epithelium were seen, and type II cells had discharged their granules into the alveoli (Fig. 4). At 24 hr. phagocytic PML's were frequent in peripheral alveoli, while centrally, alveoli and vessels were packed with fibrin thrombi and PML's (Fig. 5). In similar dogs rendered thrombocytopenic with anti-platelet serum, lung ultrastructure was similar to that of controls, although PML's were more frequently seen in capillaries in the former (Fig. 6).

Morphometric SEM study of the effects of ACTH on endothelial fenestrae in the rat adrenal cortex

1984 ◽  
Vol 42 ◽  
pp. 234-235
Author(s):  
J. Curtis ◽  
K. S. Schwartz ◽  
R. P. Apkarian
Keyword(s):  
Anterior Pituitary ◽  
Lipid Droplets ◽  
Adrenocorticotropic Hormone ◽  
Unit Area ◽  
High Density Lipoproteins ◽  
Capillary Endothelium ◽  
Zona Fasciculata ◽  
Sem Study ◽  
Saline Vehicle ◽  
Scanning Electron

A scanning electron microscope (SEM) study was made of the effect of adrenocorticotropic hormone (ACTH) on the size and numbers of fenestrae/unit area in the capillary endothelium of the zona fasciculata (ZF) of the rat adrenal. The stimulatory effect of ACTH on cholesterol uptake via high density lipoproteins in the rat and evidence for the secretion of glucocorticoids by exocytosis of lipid droplets described by Rhodin suggest that endothelial change may accompany these transport phenomena.Twelve rats received two Dexamethasone (DEX) ip injections (25 μg DEX/100 g body wt.), the first at 8 PM and the second at 8 AM the next day, to inhibit the release of endogenous ACTH by the anterior pituitary. The animals were then divided into two groups. Six animals received only saline vehicle and six rats received ACTH (100 ng/100 g body wt.).

scholarly journals Single cell transcriptomic analysis of murine lung development on hyperoxia-induced damage

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Maria Hurskainen ◽  
Ivana Mižíková ◽  
David P. Cook ◽  
Noora Andersson ◽  
Chanèle Cyr-Depauw ◽  
...  
Keyword(s):  
Single Cell ◽  
Lung Development ◽  
Alveolar Epithelium ◽  
Cell Types ◽  
Capillary Endothelium ◽  
Stromal Fibroblasts ◽  
Main Driver ◽  
Macrophage Populations ◽  
Induced Changes ◽  
Cellular Compartments

AbstractDuring late lung development, alveolar and microvascular development is finalized to enable sufficient gas exchange. Impaired late lung development manifests as bronchopulmonary dysplasia (BPD) in preterm infants. Single-cell RNA sequencing (scRNA-seq) allows for assessment of complex cellular dynamics during biological processes, such as development. Here, we use MULTI-seq to generate scRNA-seq profiles of over 66,000 cells from 36 mice during normal or impaired lung development secondary to hyperoxia with validation of some of the findings in lungs from BPD patients. We observe dynamic populations of cells, including several rare cell types and putative progenitors. Hyperoxia exposure, which mimics the BPD phenotype, alters the composition of all cellular compartments, particularly alveolar epithelium, stromal fibroblasts, capillary endothelium and macrophage populations. Pathway analysis and predicted dynamic cellular crosstalk suggest inflammatory signaling as the main driver of hyperoxia-induced changes. Our data provides a single-cell view of cellular changes associated with late lung development in health and disease.

Repair of radiation damage to capillary endothelium

1975 ◽  
Vol 48 (573) ◽  
pp. 727-731 ◽  
Author(s):  
H. S. Reinhold ◽  
G. H. Buisman
Keyword(s):  
Radiation Damage ◽  
Capillary Endothelium

scholarly journals STUDIES ON ENDOTHELIAL REACTIONS

1920 ◽  
Vol 32 (5) ◽  
pp. 533-546 ◽  
Author(s):  
Nathan Chandler Foot
Keyword(s):  
Endothelial Cell ◽  
Vascular Endothelium ◽  
Colloidal Suspension ◽  
Giant Cells ◽  
Epithelioid Cell ◽  
Normal Lung ◽  
Capillary Endothelium ◽  
Alveolar Wall ◽  
Living Animal ◽  
Capillary Walls

1. The injection of a colloidal suspension, or sol, of carbon into the veins of a living animal, as recommended by McJunkin, furnishes an apparently reliable means of tracing the so called epithelioid cell of the pulmonary tubercle from its origin in the vascular endothelium to the lesion. 2. Experimental tubercles are formed in the lung, as in the liver, primarily by cells originating in the capillary endothelium. These cells are probably present in small numbers in the normal lung, lying free both in the alveolar wall and the air vesicles. In response to infection they proliferate in the capillary walls in the vicinity of the invading organisms, migrate in steadily increasing numbers, and, arriving at the site of the infection, further multiply and to some extent fuse to form the syncytia known as giant cells. 3. The epithelial cell takes no active part in the process; its proliferation tends to repair denuded surfaces and is regenerative rather than combative or phagocytic in nature. This cell is free from carbon and stains only diffusely with carmine, in contradistinction to the endothelial cell which readily takes up both pigments in granular form. 4. The cells of endothelial origin not only phagocytose tubercle bacilli, but carry them into the tissues, for example into lymph nodes, by way of the lymphatics, or into other lung lobules by way of the air passages, in which they are readily demonstrable.

Bidirectional transcytosis of IgG by the rat neonatal Fc receptor expressed in a rat kidney cell line: a system to study protein transport across epithelia

2000 ◽  
Vol 113 (7) ◽  
pp. 1277-1285 ◽  
Author(s):  
K.M. McCarthy ◽  
Y. Yoong ◽  
N.E. Simister
Keyword(s):  
Cell Culture ◽  
Collecting Duct ◽  
Rat Kidney ◽  
Fc Receptor ◽  
Capillary Endothelium ◽  
Apical Surface ◽  
Dna Encoding ◽  
Cell Culture Model ◽  
Neonatal Fc Receptor ◽  
Culture Model

The neonatal Fc receptor, FcRn, transports immunoglobulin G (IgG) across cellular barriers between mother and offspring. FcRn also protects circulating IgG from catabolism, probably during transport across the capillary endothelium. Only one cell culture model of transcytosis has been used extensively, the transport of IgA from the basolateral to the apical surface of Madin-Darby canine kidney cells by the polymeric immunoglobulin receptor (pIgR). We report that rat inner medullary collecting duct (IMCD) cells transfected with DNA encoding the (alpha) subunit of rat FcRn specifically and saturably transport Fc when grown as polarized monolayers. Using this system, we have found that transcytosis by FcRn, like transcytosis by the pIgR, depends upon an intact microtubule system. FcRn differs most strikingly from the pIgR in its ability to transport its ligand in both the apical to basolateral and basolateral to apical directions. The phosphatidylinositol 3-kinase inhibitors wortmannin and LY294002 inhibited basolateral to apical transport by FcRn more than apical to basolateral transport, suggesting that there are differences in the mechanisms of transport in the two directions. Lastly, we found that transcytosis by FcRn depends upon vesicular acidification. We anticipate that the IMCD cell culture model will allow further elucidation of the mechanism of IgG transport by FcRn.

The cell biology and pathogenic role of pulmonary intravascular macrophages

1990 ◽  
Vol 258 (2) ◽  
pp. L1-L12 ◽  
Author(s):  
A. E. Warner ◽  
J. D. Brain
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Cell Biology ◽  
Morphological Characteristics ◽  
Laboratory Animals ◽  
Capillary Endothelium ◽  
Phagocytic Cells ◽  
Pulmonary Uptake ◽  
Pulmonary Intravascular Macrophages

Pulmonary intravascular macrophages (PIMs) are an extensive population of mature phagocytic cells adherent to the pulmonary capillary endothelium in selected species. They are not prevalent in lungs of commonly studied laboratory animals, such as rodents, and thus have only been recently appreciated. However, their potential role in host defense and acute lung injury has attracted interest, since a number of studies have demonstrated pulmonary localization of circulating particles, microbes, and endotoxin by PIMs. Those animal species, such as ruminants, that provide useful models of pathogen (or endotoxin)-induced acute lung injury demonstrate rapid pulmonary uptake of bacteria by PIMs. Inflammatory mediators released by activated PIMs may initiate the process and provoke accumulation of neutrophils and platelets. This review summarizes the morphological characteristics of PIMs and their species distribution. The role of these members of the mononuclear phagocyte system, both beneficial and potentially pathogenic, is reviewed. The question of whether PIMs have a role in acute lung injury in humans is also discussed.

Neoplastic and pharmacological influence on the permeability of an in vitro blood-brain barrier

1995 ◽  
Vol 82 (6) ◽  
pp. 1053-1058 ◽  
Author(s):  
Paul A. Grabb ◽  
Mark R. Gilbert
Keyword(s):  
Endothelial Cell ◽  
Rat Brain ◽  
Phospholipase A ◽  
Cell Permeability ◽  
Capillary Endothelium ◽  
Brain Capillary ◽  
Content Type ◽  
Endothelial Cell Permeability ◽  
Fine Print

✓ The authors investigated the effects of glioma cells and pharmacological agents on the permeability of an in vitro blood-brain barrier (BBB) to determine the following: 1) whether malignant glia increase endothelial cell permeability; 2) how glucocorticoids affect endothelial cell permeability in the presence and absence of malignant glia; and 3) whether inhibiting phospholipase A2, the enzyme that releases arachidonic acid from membrane phospholipids, would reduce any malignant glioma—induced increase in endothelial cell permeability. Primary cultures of rat brain capillary endothelium were grown on porous membranes; below the membrane, C6, 9L rat glioma, T98G human glioblastoma, or no cells (control) were cocultured. Dexamethasone (0.1 µM), bromophenacyl bromide (1.0 µM), a phospholipase A2 inhibitor, or nothing was added to culture media 72 hours prior to assaying the rat brain capillary endothelium permeability. Permeability was measured as the flux of radiolabeled sucrose across the rat brain capillary endothelium monolayer and then calculated as an effective permeability coefficient (Pe). When neither dexamethasone nor bromophenacyl bromide was present, C6 cells reduced the Pe significantly (p < 0.05), whereas 9L and T98G cells increased Pe significantly (p < 0.05) relative to rat brain capillary endothelium only (control). Dexamethasone reduced Pe significantly for all cell preparations (p < 0.05). The 9L and T98G cell preparations coincubated with dexamethasone had the lowest Pe of all cell preparations. The Pe was not affected in any cell preparation by coincubation with bromophenacyl bromide (p > 0.45). These in vitro BBB experiments showed that: 1) malignant glia, such as 9L and T98G cells, increase Pe whereas C6 cells probably provide an astrocytic influence by reducing Pe; 2) dexamethasone provided significant BBB “tightening” effects both in the presence and absence of glioma cells; 3) the in vivo BBB is actively made more permeable by malignant glia and not simply because of a lack of astrocytic induction; 4) tumor or endothelial phospholipase A2 activity is probably not responsible for glioma-induced increased in BBB permeability; and 5) this model is useful for testing potential agents for BBB protection and for studying the pathophysiology of tumor-induced BBB disruption.

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