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Extracellular matrix deposition by fibroblasts is necessary to promote capillary-like tube formation in vitro.

The contribution of the cellular and fibrillar microenvironment to angiogenesis still remains unclear. Our purpose was to evaluate the effect of the extracellular matrix deposited by fibroblasts on the capacity of human endothelial cells to form capillaries in vitro. We have drastically decreased the amount of extracellular matrix surrounding fibroblasts in our model of endothelialized-reconstructed connective tissue (ERCT) by culturing it without ascorbate. Under these conditions, the number of capillary-like tubes (CLT) formed by endothelial cells was reduced by up to 10-fold after 31 days of culture compared to controls. This decrease was due neither to a variation of MMP-2 and MMP-9 secretion, nor to a reduction in the number of fibroblasts and/or endothelial cells, or a diminution of fibroblast growth factor 2 (FGF2) synthesis. The secretion of vascular endothelial growth factor (VEGF) by fibroblasts accounted for 25-70% of the capillary-like tube formation when tissues were cultured in the presence or absence of ascorbate, as demonstrated by VEGF-blocking studies. The culture of endothelial cells on a similar extracellular matrix but in the absence of living fibroblasts did not promote the formation of CLT, even when tissues were fed with fibroblast-conditioned medium. Thus, the deposition of a rich extracellular matrix by living fibroblasts appeared necessary, but not sufficient to promote capillary-like formation. Fibroblasts seem to induce endothelial cells to spontaneously form CLT by secreting and organizing an abundant extracellular matrix, which creates a microenvironment around cells that could in turn trap growth factors produced by fibroblasts and promote three-dimensional cell organization.

Ascorbic Acid↗

Evaluation of tartrate-resistant acid phosphatase and cathepsin K in ruptured cranial cruciate ligaments in dogs.

OBJECTIVE: To determine localization of tartrate-resistant acid phosphatase (TRAP) and cathepsin K in ruptured and healthy cranial cruciate ligaments (CCL) in dogs. ANIMALS: 30 dogs with ruptured CCL, 8 aged dogs without ruptured CCL, and 9 young dogs without ruptured CCL. PROCEDURE: The CCL was examined histologically and cells containing TRAP and cathepsin K were identified histochemically and immunohistochemically, respectively. RESULTS: Cathepsin K and TRAP were detected within the same cells, principally within the epiligamentous region and to a lesser extent in the core region of ruptured CCL. Numbers of cells containing TRAP and cathepsin K were significantly greater in ruptured CCL, compared with CCL from young or aged dogs, and numbers of such cells were greater in CCL from aged dogs, compared with those of young dogs. In aged dogs, small numbers of cells containing TRAP and cathepsin K were seen in intact CCL associated with ligament fascicles in which there was chondroid transformation of ligament fibroblasts and disruption of the extracellular matrix. CONCLUSIONS AND CLINICAL RELEVANCE: Ruptured CCL contain greater numbers of cells with the proteinases TRAP and cathepsin K than CCL from healthy, young, or aged dogs. Results suggest that cell-signaling pathways that regulate expression of these proteinases may form part of the mechanism that leads to upregulation of collagenolytic ligament remodeling and progressive structural failure of the CCL over time.

Acid Phosphatase↗

Joint development in the Drosophila leg: cell movements and cell populations.

Flexible joints separate the rigid sections of the insect leg, allowing them to move. In Drosophila, the initial patterning of these joints is apparent in the larval imaginal discs from which the adult legs will develop. Here, we describe the later patterning and morphogenesis of the joints, which occurs after pupariation (AP). In the tibial/tarsal joint, the apodeme insertion site provides a fixed marker for the boundary between proximal and distal joint territories (the P/D boundary). Cells on either side of this boundary behave differently during morphogenesis. Morphogenesis begins with the apical constriction of distal joint cells, about 24 h AP. Distal cells then become columnar, causing distal tissue nearest the P/D boundary to fold into the leg. In the last stage of joint morphogenesis, the proximal joint cells closest to the P/D boundary align and elongate to form a "palisade" (a row of columnar cells) over the distal joint cells. The proximal and distal joint territories are characterised by the differential organisation of cytoskeletal and extracellular matrix proteins, and by the differential expression of enhancer trap lines and other gene markers. These markers also define a number of more localised territories within the pupal joint.

Animals↗

Visualization of a luteovirus in the vector aphid's body by two gold immunolabelling techniques: a comparative study.

Two gold immunolabelling techniques using electron microscopy were compared to examine the in situ localization of a luteovirus, potato leafroll virus (PLRV), inside its main aphid vector, Myzus persicae SULZ. With Gildow's technique, virus particles were labelled prior to fixation, embedding by injecting PLRV-specific IgGs into the living aphids. This facilitated the detection of extracellular particles located between the basal lamina and plasmalemma by trapping them in aggregates. The heavy coating of particles by antibodies and gold indicated good labelling sensitivity. Isometric virus-like particles were also observed inside the cytoplasm, but they were non decorated because the cell membrane prevented labelling reagents from entering the cell. With the second technique, ultrathin sections were immunolabelled after fixation-embedding. Since PLRV lost its antigenicity when aphid tissues were normally treated for electron microscopy, the successful application of this technique required fixation in 4% formaldehyde before embedding in Lowicryl at low temperature; it was also necessary to use PLRV-specific monoclonal antibodies to eliminate non-specific reactions. In these conditions, all intra- and extra-cytoplasmic virions present on the surface of sections were surrounded by gold particles, but the antibody coating was not discernible, and, because the resin limited the access of markers to antigens, the inner virus particles were not labelled. In conclusion, both techniques must be applied on the same material to give complementary information.

Acrylic Resins↗

Distal nephron function in Bartter's syndrome: abnormal conductance to chloride in the cortical collecting tubule?

Five patients with the clinical patterns of Bartter's syndrome underwent a series of clearance studies in order to characterize the underlying tubule defect. Free water generation during maximal water diuresis (CH2O), expressed as percentage of the distal delivery (CH2O + CCl), was lower in the patients (72.5 +/- 3.2%) than in controls (84.4 +/- 5.5, p < 0.0001). During maximal water diuresis and furosemide administration (40 mg i.v. as bolus), NaCl reabsorption along the diluting nephron segments could be separated into 2 components, that occurring in the loop of Henle (DRNaHL) and that occurring in tubule segments beyond the macula densa (DRNaDT): DRNaHL was normal, while DRNaDT was reduced (3.1 +/- 0.8 vs. 6.2 +/- 2.5 ml/min in controls, p < 0.015). Thus, according to this furosemide protocol, our patients had normal solute reabsorption in the loop of Henle but reduced NaCl reabsorption in tubule segments beyond the macula densa. During 0.9% saline infusion (2 liters in 2 h, after stimulation of distal Na reabsorption with fludrocortisone) fractional excretion (FE) of K showed a linear rise with the increase of FECl-FEK, however, was much higher in the patients than in controls for every FECl level. In contrast, the infusion of Na2SO4, after fludrocortisone administration, induced similar FEK increases in patients and in controls. Thus, in these patients Na reabsorption in the distal nephron (possibly the cortical collecting tubule) was associated with the generation of a higher than normal electric potential gradient in the presence of Cl but not of another poorly reabsorbable anion, such as SO4(2-). These observations indicate that, in our patients, Henle's loop function is normal, while the collecting tubule function is abnormal. We suggest that NaCl wasting and enhanced tubular secretion of H+ and K in our patients might result from an abnormally low conductance to Cl in distal nephron site(s) where Na reabsorption is electrogenic, possibly the cortical collecting tubule. A larger than normal transtubular electric gradient would be generated by Na reabsorption, causing: (1) a direct stimulation of tubular secretion of K and H+ (leading to hypokalemia and alkalosis) and (2) inhibition of the reabsorption of Na ('trapped' into the tubular lumen by electric forces), with consequent extracellular volume contraction, hyperreninemia and hyperaldosteronism.

Adolescent↗

Denucleation promotes neovascularization of ePTFE in vivo.

Expanded polytetrafluoroethylene (ePTFE) implants are being increasingly used as vascular prostheses and other devices. However the tissue response associated with this and other polymer implants continues to limit any long-term function. One of the major approaches currently being investigated to improve biocompatibility involves surface modification of the base polymer. In this report, we attempted to alter the healing characteristics of ePTFE by denucleation, a process which removes air trapped within the interstices of the material. Additionally, adsorption of extracellular proteins on the denucleated polymer was also tested. After 5 weeks implanted in subcutaneous and epididymal fat sites of rats, the material was explanted and the healing around the implant evaluated histologically. We found that in skin implants, denucleation alone resulted in a substantial reduction in the fibrous capsule which has been previously reported for untreated ePTFE, and an increase in blood vessel development around and within the polymer. Absorption of extracellular matrix proteins prior to implantation resulted in a reduced vascularity of the implants compared with denucleation-only implants. Implants in fat tissue, regardless of treatment, showed very little tissue reaction, either in the number of inflammatory cells, development of a fibrous capsule or neovascularization. These results suggest that the presence of air nuclei within porous material may contribute to the inappropriate healing response associated with these polymers. In addition, they confirm earlier reports that healing around implanted polymers is tissue-specific.

Adipose Tissue↗

A 25 kDa polypeptide is the ligand for p185neu and is secreted by activated macrophages.

Medium conditioned by mouse peritoneal macrophages, activated by muramyl dipeptide (MDP), was used as a possible source of p185neu-specific ligand. MDP-activated macrophage-conditioned medium (MDP-CM) was shown to induce p185neu down-regulation in NEU-expressing NIH3T3 cells in a dose-dependent and temperature-sensitive manner. To exclude the possibility of an indirect action of proteins/metabolites present in MDP-CM on p185neu turnover, a ligand-trapping approach was used. Secreted NEU protein possessing only the extracellular domain but lacking transmembrane and protein kinase domains was expressed in HeLa cells and then purified from conditioned medium, using affinity chromatography on WGA-Sepharose. Co-incubation of the truncated, soluble NEU protein preparation with MDP-CM abolished MDP-CM-induced p185neu down-regulation and reduced self-phosphorylation. It is concluded that a putative p185neu-specific ligand is produced by macrophages activated by MDP. Using MDP-CM, the presence of a 25 kDa polypeptide distinct from EGF, PDGF, FGF, IGF, TGF-alpha and TGF-beta and TNF-alpha, could be demonstrated by decorating a Western blot with soluble NEU and anti-NEU antibodies. Thus, a 25 kDa (non-reduced) p185neu ligand has been described.

3T3 Cells↗

["Autodesmosomes", desmosomes formed between apposing surface membranes of the same cell, in the human chorion laeve and amnion (author's transl)].

An unusual desmosome formation in the human amnion and chorion laeve is described. The macula adherens, found at the cell surface, forms contact zones between different parts of one and the same cell: autodesmosomes. These zones appear to seal off and trap compartments of various sizes formed by invagination of the extracellular space. Furthermore they are indistinguishable morphologically from intracellular desmosomes. Epithelial cells of the chorion laeve display autodesmosomes along the whole cell surface, however the basal surfaces of these cells are particularly rich in these structures. Amnion epithelial cells exhibit autodesmosomes on their basal surface only. These surfaces are deeply indented and the foldings, in many cases, reach into the nuclear region. In this area semidesmosomes are found. It is suggested that autodemosomes are formed by semidesmosomes which have approached and become adjacent to each other. Moreover, the presence, and relationship of the autodesmosomes to the extracellular compartments, perhaps indicate a novel metabolic regulatory function of the chorionic and amnionic cells.

Amnion↗

Cellular and sub-cellular localisation of PrP in the lymphoreticular system of mice and sheep.

Using immunocytochemistry or immunogold electron microscopy, abnormal PrP accumulation was found in lymphoreticular tissues of Suffolk sheep naturally exposed to scrapie and in the spleens of ME7 infected C57 BL mice at 70 days after infection and at the terminal stage of disease at 170 days. Clinically diseased scrapie affected sheep show widespread PrP accumulation within tingible body macrophages (TBMs) and follicular dendritic cells (FDCs) of secondary lymphoid follicles. Serial tonsillar biopsies taken from 171 ARQ/ARQ sheep at 4 months of age did not contain abnormal PrP accumulations but 80% of biopsies were positive by 14 months. In contrast, whole body necropsies of sheep not previously biopsied failed to detect PrP in the tonsil of sheep at 4, 8, 12 or 16 months of age. These findings suggest that the biopsy procedure of susceptible sheep but not resistant sheep may induce tonsillar infection. In spleen of mice both at 70 and 170 dpi, accumulations of PrP were found within lysosomes of TBMs and also at the plasma-lemma of FDCs. In the light zone of follicles of terminally diseased mice, all FDC dendrites were arranged in the form of highly reactive or hyperplastic labrynthine glomerular complexes. PrP was consistently seen between FDC dendrites in association with abundant electron dense antigen-antibody complexes. At 70 days after challenge, labrynthine complexes were rare and invariably labelled for PrP. However, sparse PrP labelling was also seen on simple FDC dendrites at this stage. These observations suggests that scrapie infected FDCs continually release PrP from the cell surface where it accumulates in excess in association with trapped immune complexes and dendritic extension. It is likely that TBMs acquire lysosomal PrP following phagocytosis of effete FDC processes or from the extracellular space. We suggest that the normal function of PrP may involve cell process extension or immune complex trapping.

Animals↗

Extracellular diffusion is fast and isotropic in the stratum radiatum of hippocampal CA1 region in rat brain slices.

Molecular transport in brain extracellular space (ECS) is hindered by the structure of the tissue. Diffusion analysis of small extracellular markers quantifies tissue hindrance, expressed as tortuosity lambda = (D/D*)(1/2), where D is the free diffusion coefficient and D* is the effective diffusion coefficient in tissue. In healthy brain, lambda is approximately 1.6, but the nature of this parameter is poorly understood. We report that the stratum radiatum of the hippocampal CA1 region in vitro, previously shown to be anisotropic (i.e., different along the x-, y-, and z-axes) in in vivo study, is isotropic like somatosensory neocortex but has a reduced lambda. Diffusion of fluorophore-labeled dextran (f-dex, M(r) 3,000) and tetramethylammonium (TMA(+), M(r) 74) was measured in rat brain slices (400 mum) using integrative optical imaging (IOI) and real-time iontophoresis (RTI), respectively. In the stratum radiatum, diffusion of f-dex was similar along the x-, y-, and z-axes (lambda(x), lambda(y); lambda(z) were 1.55, 1.53, and 1.55), but the tortuosity was significantly lower than in the neocortex, where lambda = 1.81. This finding was confirmed by the RTI method, which measured lambda with TMA(+), a much smaller molecule, and determined volume fraction alpha, the proportion of tissue occupied by the ECS. In stratum radiatum, lambda(x), lambda(y), and lambda(z) were 1.47, 1.44, and 1.46, while in neocortex, lambda was 1.65. The ECS volume fraction was similar (0.24) in both regions. It is proposed that in the hippocampus, low lambda reflects a reduced occurrence of concave extracellular microdomains, referred to as dead spaces, which increase tortuosity by transient trapping of markers. Functionally, a low lambda may permit structural plasticity and facilitate extrasynaptic communication. It may also enhance the spread of neuroactive substances and thus contribute to the sensitivity of the hippocampal CA1 region to ischemia and epilepsy.

Animals↗

The location of a closed channel gate in the GABAA receptor channel.

Considerable controversy surrounds the location of the closed channel gate in members of the Cys-loop receptor family of neurotransmitter-gated ion channels that includes the GABAA, glycine, acetylcholine, and 5-HT3 receptors. Cysteine-accessibility studies concluded that the gate is near the cytoplasmic end of the channel in acetylcholine and GABAA receptors but in the middle of the 5-HT3A receptor channel. Zn2+ accessibility studies in a chimeric 5-HT3-ACh receptor suggested the gate is near the channel's cytoplasmic end. In the 4-A resolution structure of the acetylcholine receptor closed state determined by cryoelectron microscopy, the narrowest region, inferred to be the gate, is in the channel's midsection from 9' to 14' but the M1-M2 loop residues at the channel's cytoplasmic end were not resolved in that structure. We used blocker trapping experiments with picrotoxin, a GABAA receptor open channel blocker, to determine whether a gate exists at a position more extracellular than the picrotoxin binding site, which is in the vicinity of alpha1Val257 (2') near the channel's cytoplasmic end. We show that picrotoxin can be trapped in the channel after removal of GABA. By using the state-dependent accessibility of engineered cysteines as reporters for the channel's structural state we infer that after GABA washout, with picrotoxin trapped in the channel, the channel appears to be in the closed state. We infer that a gate exists between the picrotoxin binding site and the channel's extracellular end, consistent with a closed channel gate in the middle of the channel. Given the homology with acetylcholine and 5-HT3 receptors there is probably a similar gate in those channels as well. This does not preclude the existence of an additional gate at a more cytoplasmic location.

Allosteric Regulation↗

Cell migration: may the force be with you.

Effective linkages between the extracellular matrix and the cytoskeleton are crucial for cell migration. New insights into the formation of these links are provided by laser trap experiments and other recent advances.

Animals↗

Ascorbate recycling in human erythrocytes: role of GSH in reducing dehydroascorbate.

Human erythrocytes regenerate ascorbate from its oxidized product, dehydroascorbate. The extent to which such ascorbate recycling occurs by a GSH-dependent mechanism was investigated. In the presence of glucose, erythrocytes took up over 90% of extracellular [14C]dehydroascorbate and rapidly converted it to [14C]ascorbate, which was trapped within the cells. Dehydroascorbate uptake and reduction was not associated with generation of a monoascorbyl free radical intermediate. Uptake and reduction of dehydroascorbate by glucose-depleted erythrocytes coordinately decreased GSH and raised GSSG concentrations in erythrocytes. This effect was reversed by D-glucose, but not by L-lactate. Conversely, depletion of cellular GSH decreased the ability of cells to recycle dehydroascorbate to ascorbate, as reflected in the extent to which cells were able to reduce extracellular ferricyanide. Monoascorbyl free radical was formed during the reduction of extracellular ferricyanide, indicating that one electron transfer steps were involved in this process. In GSH-depleted cells, addition of L-lactate as an energy source for glycolysis-dependent NADH regeneration did cause a partial recovery of the ability of cells to reduce ferricyanide. However, in resealed erythrocyte ghosts containing either 4 mM GSH or 400 mu M NADH, only the GSH-containing ghosts supported regeneration of ascorbate from added dehydroascorbate. These results suggest that in human erythrocytes ascorbate regeneration from dehydroascorbate is largely GSH dependent, and that it occurs through either enzymatic or nonenzymatic reactions not involving the monoascorbyl free radical.

Ascorbic Acid↗

Superoxide production by phagocytosing macrophages in relation to the intracellular distribution of oxygen.

We simultaneously measured the concentration of oxygen ([O2]) within the phagosomal and extracellular compartments of macrophages. By combining electron paramagnetic resonance (EPR) oximetry techniques with that of spin-trapping, we found that a significant difference in oxygen concentration ([O2]) exists between these two compartments and we were able to monitor (1) how [O2] in the extracellular compartment and the rate of mitochondrial consumption affected this difference in [O2], and (2) to what extent this gradient of [O2] influenced production of reactive oxygen species by phagosomes. Under conditions where the [O2] in the inflowing gas was high (210 microM; air), the [O2] in the extracellular and phagosomal compartments was 180 and 141 microM, respectively. This was sufficient to maintain maximum superoxide production in these cells. When extracellular [O2] was reduced to 84 or 36 microM, the [O2] in phagosomes within the cells (31.7 and 7.7 microM, respectively) was too low to maintain superoxide production by the NADPH-oxidase system within the phagosomes. The [O2] in the extracellular compartments of these samples, however, was always sufficient to maintain superoxide production by phagosomes at the cell surface. Our findings suggest that the distribution of oxygen surrounding and within macrophages can influence their ability to perform microbicidal and tumoricidal functions, even at an [O2] in the media that appears to be adequate.

Animals↗

Evaluation of dibromonitrosobenzene sulfonate as a spin trap in biological systems.

In the present study dibromonitrosobenzene sulfonate (DBNBS) was examined for its suitability for spin trapping for ESR detection of superoxide radicals in biological systems. This nitroso spin trap recently has been reported to yield very persistent spin adducts with O2. as well as with various carbon-centered radicals. In the present work the possible toxicity of DBNBS, the partitioning of its spin adducts into cells, and the stability of the adducts and the parent compound inside cells were studied. No significant toxicity was found. In cellular systems, however, DBNBS did not produce detectable adducts with O2.; it also did not detectably trap superoxide generated in the xanthine/xanthine oxidase system. Both DBNBS and a DBNBS adduct performed extracellularly and then added to cell suspensions were rapidly metabolized by cells. Intracellular spin adducts were not detected under any condition. Evidently, in spite of its promising features, DBNBS will not be useful for spin trapping radicals in cellular systems or for detecting superoxide radicals in any biological system.

Benzenesulfonates↗

Leukotriene C4 production by murine mast cells: evidence of a role for extracellular leukotriene A4.

The glutathione-containing leukotriene C4 (LTC4) is a major mediator of smooth muscle contraction and is released by mast cells when antigen interacts with cell-bound IgE. Antigen-stimulated mast cells undergo phospholipase activation. We report a pathway of LTC4 production by mast cells that does not require phospholipase activation but depends on the interaction of activated neutrophils with unstimulated mast cells, using as an intermediate extracellular leukotriene A4 (LTA4). The epoxide LTA4 is released by neutrophils and, together with leukotriene B4 and 5-hydroxyeicosatetraenoic acid, constitutes the major lipoxygenase metabolites found in supernatants of stimulated neutrophils. Five minutes after activation of neutrophils by calcium ionophore A23187 we measured 136 pmol of extracellular LTA4 per 10(7) neutrophils (range 40-300, n = 7) by trapping the epoxide with alcohols. Therefore, we conclude that LTA4 is not just an intracellular leukotriene precursor but is released as a lipoxygenase metabolite. LTA4 is known to be stabilized by albumin and is efficiently converted by mast cells into LTC4 even at low LTA4 concentrations. The LTA4 complexed to albumin is converted into LTC4 rapidly and completely within 10-15 min. More than 50% of the LTA4 presented to mast cells is metabolized to LTC4 at concentrations of LTA4 between 0.2 and 2 nmol of LTA4 per 10(7) mast cells. This observation establishes a potential physiologic role for extracellular LTA4. Therefore, interactions between various cell types that release or utilize LTA4 may provide an important metabolic pathway for the production of leukotrienes.

Animals↗

Intraphagosomal chlorination dynamics and yields determined using unique fluorescent bacterial mimics.

Fluorescein was covalently attached through a cystamine linker group to carboxy-derivatized polyacrylamide microspheres to generate phagocytosable particles containing fluorescent reporter groups. A unique feature of these beads is that the dye was recoverable in near-quantitative yield from intracellular environments by thiol reduction of the cystamine disulfide bond. Fluorescence microscopy indicated that individual neutrophils could bind as many as approximately 20 serum-opsonized beads, although no appreciable cellular association was observed for unopsonized beads. By using methyl viologen to quench external fluorescence, it was demonstrated that 70-90% of the neutrophil-associated fluorescein on opsonized beads was inaccessible to the medium. The particle-bound fluorescein underwent near-stoichiometric conversion to chlorinated derivatives when reacted with HOCl or the cell-free myeloperoxidase (MPO)-H2O2-Cl- system; products were identified by HPLC separation and electrospray ionization mass spectrometry of the recovered dye. Fluorescence changes accompanying phagocytosis were consistent with chlorination of the dye; fluorescence spectrometric and chemical trapping measurements indicated that intraphagosomal chlorination was far more extensive than extracellular chlorination. Yields of recovered chlorofluoresceins determined by HPLC indicated that sufficient HOCl had been produced intracellularly to kill entrapped bacteria. Fluorescein chlorination coincided approximately with phagocytosis and stimulated uptake of O2 by the cells. Demonstration that HOCl is produced within phagosomes in sufficient concentrations to kill bacteria on a time scale associated with death constitutes strong evidence in support of a primary role for HOCl in the microbicidal action of neutrophils.

Blood Bactericidal Activity↗

Lipid accumulation in prosthetic vascular grafts. Experimental study.

The present study demonstrates that the endoprosthetic tissue, developed at the contact of Dacron and Gore-Tex vascular prostheses replacing the infrarenal aortae of healthy dogs, presents a particular lipidic pattern as compared with the adjacent intimal arterial layer. The modified lipidic pattern is characterized by a significant increase in the total amounts of cholesterol, phospholipids, and triglycerides, despite a normal lipidic plasma profile. Histochemical studies showed that lipid droplets are accumulated in the cytoplasm of deeply situated cells and in the extracellular matrix. These findings support the idea that lipids may be trapped within the pseudo-intima of synthetic vascular grafts, even in the absence of a major plasma lipid disorder, and contribute to the prosthesis failure.

Animals↗