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PubMed1993

Transcytosis of protein through the mammalian cerebral epithelium and endothelium. II. Adsorptive transcytosis of WGA-HRP and the blood-brain and brain-blood barriers.

Morphological evidence of the potential for adsorptive transcytosis of protein through the mammalian blood-brain fluid barriers, first reported from this laboratory in the mouse, has been confirmed and expanded upon in rats injected intravenously or into the lateral cerebral ventricle/subarachnoid space with with exogenous lectin wheatgerm agglutinin (WGA) conjugated to horseradish peroxidase (HRP). Blood-borne WGA-HRP rapidly enters cerebral endothelia by the process of adsorptive endocytosis and labels the vascular tree throughout the CNS. At 3 h post-injection and longer, WGA-HRP occupies the perivascular clefts and labels perivascular cells and basal lamina; this suspected transendothelial transfer of the lectin conjugate from blood to brain involves specific constituents of the endothelial endomembrane system of organelles (e.g., plasmalemma, vesicles, endosomes, Golgi complex). Within 6 h, reaction product is evident in extracellular clefts beyond the perivascular basal lamina and labels endocytic vesicles, endosomes, and dense bodies within cells and processes of the neuropil. Exposure of the abluminal surface of blood-brain barrier endothelia for 1-18 h to WGA-HRP delivered into the cerebral ventricles or subarachnoid space indicates blood-brain barrier endothelia do not engage in demonstrable adsorptive endocytosis at the abluminal surface. In this preparation, no endothelial organelles comparable to those sequestering blood-borne WGA-HRP are labelled with the lectin conjugate; hence, significant adsorptive transcytosis of WGA-HRP through cerebral endothelia from brain to blood is unlikely. The demonstrable difference in membrane internalization of the luminal versus abluminal plasmalemma of blood-brain barrier endothelia suggests the blood-brain barrier is polarized regarding adsorptive endocytosis of WGA-HRP. If adsorptive transcytosis of macromolecules through the blood-brain barrier does occur, the process appears unidirectional, from blood to brain but not from brain to blood. Absence of demonstrable endocytosis at the abluminal front is an enigma in the scheme of transcytosis through the blood-brain barrier from blood to brain insofar as exocytosis and endocytosis are complementary events in the cellular secretory process. This unconventional membrane behavior associated with the abluminal plasmalemma argues against a significant transcytosis of blood-borne protein through blood-brain barrier endothelia. The potential for transcytosis of macromolecules through the blood-cerebrospinal fluid barrier of choroid plexus epithelia is not as problemmatic as that through blood-brain barrier endothelia; additional evidence is provided to suggest choroid plexus epithelia participate in adsorptive endocytosis circumferentially and adsorptive transcytosis of WGA-HRP bidirectionally between the blood and cerebrospinal fluid.

Adsorption↗

PubMed1994

Is the intrasomal phase of fast axonal transport driven by oscillations of intracellular calcium?

An hypothesis is presented suggesting that the delivery of vesicle-packaged protein from the neuronal soma to the axonal transport system is physiologically coupled to spontaneous fluctuations of intracellular calcium (Cai). Evidence is reviewed that oscillations of Cai, commonly detected as agonist- or voltage-triggered waves and spikes propagating through the cytosol, also occur as spontaneous events. Endogenously-generated oscillations are examined since intrasomal transport persists in the absence of extracellular signals or nerve impulse activity. Vesicle budding from the endoplasmic reticulum (ER) may be a key step at which anterograde transport is regulated by events related to the release and reuptake of ER stores of Ca2+.

Animals↗

PubMed1992

Lanthanum tracer and freeze-fracture studies suggest that compartmentalisation of early bone matrix may be related to initial mineralisation.

In adult bone the calcified matrix and enclosed osteocytes are separated from the extracellular space by a continuous layer of bone lining cells. It thus appears that bone matrix is compartmentalised and, as such, may constitute a 'milieu intérieur' which is different from the general extracellular space. Since adult bone matrix is compartmentalised and matrix vesicles also form a microcompartment, it is conceivable that compartmentalisation, in early osteogenesis, may be a requirement for the initial events of the mineralisation process. We have therefore conducted an ultrastructural, tracer, and freeze-fracture study to determine the stage in which bone matrix becomes compartmentalised and also to find out whether there are tight junctions between osteoblasts. The results show that in early nonmineralised stages and in incipient mineralisation, lanthanum penetrates all intercellular spaces and the newly forming bone matrix which is rich in matrix vesicles and collagen. With the progression of mineralisation, when all matrix vesicles appear mineralised and calcification is 'spreading' to the surrounding matrix, lanthanum is restricted to intercellular spaces and conspicuous macular tight junctions are present between osteoblasts. We suggest that matrix vesicles act as microcompartments for calcification when the early bone matrix is in continuity with the surrounding extracellular space. In later stages, when lanthanum fails to penetrate the matrix, matrix vesicles may no longer be necessary because the bone matrix itself is compartmentalised, thus allowing for localised changes in composition that might favour mineral deposition.

Animals↗

PubMed1994

A distinct class of intracellular storage vesicles, identified by expression of the glucose transporter GLUT4.

Some cell types have cytoplasmic storage vesicles whose fusion with the cell surface is triggered by an extracellular signal. To explore the relationship between different classes of storage vesicles, we expressed, in the neuro-endocrine cell line PC12, the facilitative glucose transporter GLUT4, which is stored in small cytoplasmic vesicles in fat and muscle cells and mobilized to the cell surface when insulin is present. PC12 cells have two known types of storage vesicles, secretory granules and synaptic vesicles, but GLUT4 is targeted to neither. It is recovered, however, in a class of small vesicles that sediment approximately twice as fast as synaptic vesicles. Immunoelectron microscopy confirmed the presence of such small vesicles in transfected PC12 cells. By velocity sedimentation analysis, GLUT4 vesicles efficiently exclude the synaptic vesicle markers synaptophysin, SV2, and synaptobrevin; the transferrin receptor, a marker of conventional endocytosis; and the polymeric immunoglobulin receptor, a marker of transcytosis. The exclusion of synaptophysin and the transferrin receptor from most of the GLUT4-containing structures was confirmed by confocal immunofluorescence microscopy. Like synaptic vesicles, therefore, GLUT4 vesicles of PC12 cells appear to be a unique type of organelle. A GLUT4-containing organelle of identical sedimentation properties was found in transfected fibroblast cell lines and in rat adipocytes. On stimulation of the adipocytes with insulin, GLUT4 was translocated from the peak of small vesicles to faster sedimenting membranes. We propose that the class of vesicles described here is present in a wide range of cell types and is involved in transient modification of the cell surface.

3T3 Cells↗

PubMed1986

Prelesional events in atherogenesis. Accumulation of extracellular cholesterol-rich liposomes in the arterial intima and cardiac valves of the hyperlipidemic rabbit.

Biochemical, physiologic, and ultrastructural modifications which appear in the aortic intima and atrioventricular valves before monocyte diapedesis and foam cell formation were investigated in rabbits fed a cholesterol-rich diet. In the first 2 weeks of the diet, while plasma beta-VLDL cholesterol was increased up to 15-fold, the intima showed an enhanced uptake and deposition of dietary 3H-cholesterol, 125I-beta-VLDL, and the fluorescent beta-VLDL-1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine conjugate. beta-VLDL-gold complex perfused in situ was transcytosed across endothelium by plasmalemmal vesicles. Concomitantly, within the intima, a progressive accumulation of extracellular densely packed uni- or multilamellar vesicles took place. These commonly occurred in cell-free subendothelial spaces and were not associated with any sign of cytolysis. In freeze-fracture preparations, these vesicles appeared as smooth surfaces, suggesting the absence of translamellar proteins. Upon incubation with filipin, these extracellular liposomes (EL) displayed characteristic approximately 20 nm filipin-sterol complexes, revealing the presence of preparations unesterified cholesterol in the phospholipid lamellas. EL deposition was paralleled by proliferation of basal lamina-like material, microfibrils, and proteoglycans, and continued to increase during foam cell formation. For the entire period of our experiments, the endothelium was morphologically intact, and no platelet involvement was detected. The results show that an early prelesional ultrastructural change in lesion-prone aortic and valvular areas is the accumulation of extracellular phospholipid liposomes rich in unesterified cholesterol.

Animals↗

PubMed1988

Rod photoreceptors dissociated from the adult rabbit retina.

Rod photoreceptors have been isolated from the adult rabbit retina using enzymatic and mechanical dissociation procedures; their fine structure, synaptic activity, and long-term viability were examined using conventional electron-microscopic, quick-freezing, and cell culture techniques. Freshly dissociated photoreceptors were well-preserved compared to their counterparts in the intact retina. About half of the cells, however, exhibited broad continuity between inner and outer segments. Quick-frozen, freeze-substituted rods differed from chemically fixed cells in 3 respects: (1) there was an increased amount of granular matrix in the cytoplasm, mitochondria, and rough endoplasmic reticulum; (2) branching and anastomosing profiles of smooth endoplasmic reticulum had disappeared from the inner segment; and (3) the number of synaptic vesicles within the spherule was highly variable, in some cases leaving synaptic ribbons completely denuded of their halo of vesicles. Light-adapted, solitary rod cells continued to be synaptically active: their endings were capable of endocytosis when placed in the dark in the presence of extracellular ferritin and tracer was incorporated into vesicles and vacuoles; this uptake was much reduced when the cells were incubated with the tracer in the light. Thus, synaptic vesicle regeneration was stimulated in the dark, suggesting that vesicles underwent exocytosis in the dark. Isolated rod cells adhered poorly to most standard substrates; without proper adhesion, cells deteriorated in 2-4 hr. However, photoreceptors did adhere to glutaraldehyde-fixed Vitrogen gels and could be maintained for over 48 hr on this substrate if kept in a complete medium at 22 degrees C. In contrast, Müller cells adhered quickly to a laminin substrate with their endfoot processes. The differential adhesion properties of Müller and photoreceptor cells may be useful in obtaining pure populations of glial cells or neurons from the adult mammalian retina.

Animals↗

PubMed2005

Cleavage of L1 in exosomes and apoptotic membrane vesicles released from ovarian carcinoma cells.

PURPOSE: The L1 adhesion molecule (CD171) is overexpressed in human ovarian and endometrial carcinomas and is associated with bad prognosis. Although expressed as a transmembrane molecule, L1 is released from carcinoma cells in a soluble form. Soluble L1 is present in serum and ascites of ovarian carcinoma patients. We investigated the mode of L1 cleavage and the function of soluble L1. EXPERIMENTAL DESIGN: We used ovarian carcinoma cell lines and ascites from ovarian carcinoma patients to analyze soluble L1 and L1 cleavage by Western blot analysis and ELISA. RESULTS: We find that in ovarian carcinoma cells the constitutive cleavage of L1 proceeds in secretory vesicles. We show that apoptotic stimuli like C2-ceramide, staurosporine, UV irradiation, and hypoxic conditions enhance L1-vesicle release resulting in elevated levels of soluble L1. Constitutive cleavage of L1 is mediated by a disintegrin and metalloproteinase 10, but under apoptotic conditions multiple metalloproteinases are involved. L1 cleavage occurs in two types of vesicles with distinct density features: constitutively released vesicles with similarity to exosomes and apoptotic vesicles. Both types of L1-containing vesicles are present in the ascites fluids of ovarian carcinoma patients. Soluble L1 from ascites is a potent inducer of cell migration and can trigger extracellular signal-regulated kinase phosphorylation. CONCLUSIONS: We suggest that tumor-derived vesicles may be an important source for soluble L1 that could regulate tumor cell function in an autocrine/paracrine fashion.

ADAM Proteins↗

PubMed2002

Regulation of peptidergic vesicle mobility by secretagogues.

Neuropeptides are released into the extracellular space from large secretory granules. In order to reach their release sites, these granules are translocated on microtubules and thought to interact with filamentous actin as they approach the cell membrane. We have used a green fluorescent protein-tagged neuropeptide prohormone (prepro-orphanin FQ) to visualize vesicle trafficking dynamics in NS20Y cells and cultures of primary hippocampal neurons. We found that the majority of secretory granules were mobile and accumulated at both the tips of neurites as well as other apparently specialized cellular sites. We also used live-cell imaging to test the notion that peptidergic vesicle mobility was regulated by secretagogues. We show that treatment with forskolin appeared to increase vesicle rates of speed, while depolarization with high K+ had no effect, even though both treatments stimulated neuropeptide secretion. In cultured hippocampal neurons the green fluorescent protein-tagged secretory vesicles were routed to both dendrites and axons, indicating that peptidergic vesicle transport was not polarized. Basal peptidergic vesicle mobility rates in hippocampal neurons were the same as those in NS20Y cells. Taken together, these studies suggest that secretory vesicle mobility is regulated by specific classes of secretagogues and that neuropeptide containing secretory vesicles may be released from dendritic structures.

Animals↗

PubMed1987

Transmitter localization and vesicle turnover at a serotoninergic synapse between identified leech neurons in culture.

An electron microscopic study has been made of chemical synapses that develop between identified nerve cells isolated from the CNS of the leech and maintained in culture. Structures resembling synapses were observed in pairs of Retzius cells and P sensory cells at which chemical transmission had been demonstrated by recording with microelectrodes. Vesicle recycling was shown by following the uptake of extracellular markers after stimulation. The membrane separation between the presynaptic Retzius cell (which is known to liberate serotonin) and the postsynaptic P cell was wider in synaptic than in extrasynaptic regions. The Retzius cell contained clusters of clear vesicles apposed to thickenings of the presynaptic membrane. These clear vesicle clusters were capped by a layer of dense core vesicles that did not contact the presynaptic membrane thickenings. Subsynaptic cisternae were found in the postsynaptic cell opposite the presynaptic membrane thickenings. Occasional slight postsynaptic membrane thickenings were seen. Extracellular material was observed within the synaptic cleft. Similar synaptic structures developed between pairs of Retzius cells in culture; even a single Retzius cell was able to form autapses upon itself. Structures resembling transmitter release sites were found in Retzius cells at a distance from any postsynaptic membranes. These are presumed to be locations for the diffuse release of transmitter. Presynaptic structures resembling release sites were never observed in P cells apposed to Retzius cells. Antibody to serotonin (5-HT) labelled with colloidal gold showed serotonin to be localized in the dense core vesicles in Retzius cells. Stimulation of pairs of Retzius and P cells by raised concentrations of K+ resulted in uptake of extracellular markers. Only Retzius cells became labelled. Ferritin was found in cisternae, in dense core vesicles, and in clear vesicles. HRP was found in cisternae and in clear vesicles. Colloidal gold was taken up by coated vesicles and was occasionally found in both clear and dense core vesicles. The uptake of extracellular markers following stimulation was blocked by high Mg++. These results show that structures develop between pairs of cells at which chemical transmission develops and that transmitter release leads to turnover of dense core and clear vesicles.

Animals↗

PubMed1990

The ultrastructure of imaginal disc cells in primary cultures and during cell aggregation in continuous cell lines.

We have examined the ultrastructure of cellular vesicles in primary cultures of wing imaginal disc cells of Drosophila melanogaster. These cells maintain the apico-basal polarity characteristic of epithelial cells. The apical surfaces secrete extracellular material into the lumen of the vesicle from plasma membrane plaques at the tip of microvilli. During the course of one passage, cells from the established cell lines grow to confluence and then aggregate into discrete condensations joined by aligned bridges of cells. Cells in these aggregates are tightly packed, and there appears to be a loss of the epithelial polarity characteristic of the vesicle cells. Elongated cell extensions containing numerous microtubules are found in aggregates, and we suggest that these may be epithelial feet involved in the aggregation process. Virus particles are commonly found both within the nucleus and the cytoplasm of cells in the aggregates.

Animals↗

PubMed2000

A rab3 homolog in sea urchin functions in cell division.

Rabs are monomeric GTP binding proteins belonging to the ras superfamily that function throughout the secretory pathway. Members of the rab3 family function in the final steps of the secretory pathway, vesicle fusion with the plasma membrane. In contrast to mammalian systems with several rab3 isoforms (rab3A-D), a single family member homologue of rab3 is present in the rapidly dividing cleavage stage sea urchin embryo that localizes to numerous vesicles enriched at the cell cortex. We hypothesized that whereas the contents of these rab3-positive vesicles may contribute to the embryonic extracellular matrix, the membrane and its constituent proteins may be important for other aspects of cell division. We tested the function of rab3 in cell division by the microinjection of either antibodies or competing effector domain peptides to interfere with its function. We found that perturbing rab3 function results in cessation of cell division, whereas cells injected with either heat-inactivated antibodies or control scrambled peptides develop as normal. Moreover, neither endocytosis nor general membrane topology are affected by rab3 perturbation. Thus, we conclude that rab3-associated vesicles and/or their contents are critical for cell division.

Animals↗

PubMed1986

Endocytosis in sickle erythrocytes: a mechanism for elevated intracellular Ca2+ levels.

Staining of sickle cells with the fluorescent probes chlortetracycline (a Ca2+ probe) and diindocarbocyanine (a general membrane probe) revealed the presence of Ca2+-containing vesicles which are not found in normal erythrocytes. These vesicles increase in number upon deoxygenation, and are apparently formed by endocytosis, as judged by the use of the extracellular fluorescent probe lucifer yellow. The presence of vesicles is not restricted to any particular morphological or density class of cells in the general population.

Anemia, Sickle Cell↗

PubMedDate not supplied

Cell volume regulation in liver.

The maintenance of liver cell volume in isotonic extracellular fluid requires the continuous supply of energy: sodium is extruded in exchange for potassium by the sodium/potassium ATPase, conductive potassium efflux creates a cell-negative membrane potential, which expelles chloride through conductive pathways. Thus, the various organic substances accumulated within the cell are osmotically counterbalanced in large part by the large difference of chloride concentration across the cell membrane. Impairment of energy supply leads to dissipation of ion gradients, depolarization and cell swelling. However, even in the presence of ouabain the liver cell can extrude ions by furosemide-sensitive transport in intracellular vesicles and subsequent exocytosis. In isotonic extracellular fluid cell swelling may follow an increase in extracellular potassium concentration, which impairs potassium efflux and depolarizes the cell membrane leading to chloride accumulation. Replacement of extracellular chloride with impermeable anions leads to cell shrinkage. During excessive sodium-coupled entry of amino acids and subsequent stimulation of sodium/potassium-ATPase by increase in intracellular sodium activity, an increase in cell volume is blunted by activation of potassium channels, which maintain cell membrane potential and allow for loss of cellular potassium. Cell swelling induced by exposure of liver cells to hypotonic extracellular fluid is followed by regulatory volume decrease (RVD), cell shrinkage induced by reexposure to isotonic perfusate is followed by regulatory volume increase (RVI). Available evidence suggests that RVD is accomplished by activation of potassium channels, hyperpolarization and subsequent extrusion of chloride along with potassium, and that RVI depends on the activation of sodium hydrogen ion exchange with subsequent activation of sodium/potassium-ATPase leading to the respective accumulation of potassium and bicarbonate. In addition, exposure of liver to anisotonic perfusates alters glycogen degradation, glycolysis and probably urea formation, which are enhanced by exposure to hypertonic perfusates and depressed by hypotonic perfusates.

Animals↗

PubMed1988

Norepinephrine uptake dependent upon apparent Mg++-ATPase activity and proton transport in storage vesicles in axoplasm.

A Ca++-dependent secretion of norepinephrine ([3H]NE) was evoked in adrenergic nerve endings in rat heart ventricle slices incubated in a modified Krebs-HCO3 medium containing choline Cl as the replacement for NaCl (Ch+-Ca++). Exogenous ATP inhibited secretion and lithium ion, a known inhibitor of NE uptake dependent upon Mg++-ATPase activity in vesicles (but not ouabain) prevented the response to ATP (Bogdanski, 1983,1986). It was suggested that vesicles attached to the axolemma recaptured [3H]NE from the extracellular fluid. This report indicates that other known inhibitors of uptake in isolated vesicles also inhibited the response to ATP in the attached vesicles. Included were two inhibitors of Mg++-ATPase activity, N-ethylmaleimide (NEM) and dicyclohexylcarbodiimide (DCCD), and the proton transporters 2,4-dinitrophenol (2,4-DNP 1.0 mM) and chlorpromazine (CPZ). Potassium ionophores (valinomycin with 2,4-DNP 0.1 mM, and nigericin) and a pH neutralizing reagent for vesicles (NH3 from ammonium sulfate in solution) were also effective. The uptake inhibitors, except 2,4-DNP, could also increase the rate of depletion of stored NE and its deamination in nonsecreting nerve endings incubated in Krebs-HCO3 (KRB) medium. Valinomycin by itself stimulated uptake in the presence of ATP. It is suggested that mechanisms of uptake and retention of NE in isolated vesicles (symposium (1982) Fed. Proc. 41:2742-2780) apply to the axoplasmic vesicles as well. Thus, the activity of Mg++-ATPase drives proton transport to establish the electrochemical gradients of H+, which drive the transport of NE. A lowering of the gradients can mobilize amines and evoke secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗

PubMed1992

Na(+)-Ca2+ antiporter activity of rat hepatocytes. Effect of adrenalectomy on Ca2+ uptake and release from plasma membrane vesicles.

The presence and mode of Na(+)-Ca2+ antiporter activity were studied in hepatocytes isolated from sham-operated or adrenalectomized rats and in inside-out plasma membrane vesicles isolated from rat liver. Decreasing extracellular Na+ (Na+o) immediately increased cytosolic free calcium (Ca2+i). The rise in Ca2+i was proportional to the reduction in Na+o and was caused by an increased calcium influx, presumably on the Na(+)-Ca2+ antiporter operating in the reverse mode. Perfusing the cells with Ca(2+)-free media stimulated Ca2+ efflux and decreased Ca2+i, an effect dependent on Na+o. This suggests an activation of the forward mode of Na(+)-Ca2+ exchange. There was little difference in these parameters between sham and adx groups. In contrast, steady-state calcium uptake by inside-out plasma membrane vesicles was inhibited 40% after adrenalectomy. The decreased calcium uptake was not caused by a deficiency in the ATP-dependent Ca2+ pump, whose Km and Vmax were unaffected by adrenalectomy, but by an Na(+)-dependent leak from the vesicles. Ca2+ efflux was proportional to the extravesicular Na+ concentration, suggesting that the calcium leak may take place on a Na(+)-Ca2+ antiporter. This Na(+)-dependent calcium efflux was significantly increased in vesicles prepared from adx rat livers. These results suggest that hepatocytes have functional Na(+)-Ca2+ antiporters that can operate in both forward and reverse modes. Under normal conditions, the Na(+)-Ca2+ antiporter apparently operates in the reverse mode as a Ca2+ influx pathway. The increase in Na(+)-dependent Ca2+ efflux evoked by adrenalectomy in plasma membrane vesicles could explain the recent results we obtained in hepatocytes isolated from adx rats, showing increased calcium influx, increased Ca2+i, increased intracellular calcium sequestration, and increased plasmalemmal calcium cycling.

Adrenalectomy↗

PubMed1983

Binding of mannosylated ferritin to chicken bone marrow macrophages.

Ferritin conjugated to diazo p-aminophenylmannoside and mannan was used for ultrastructural visualization of binding and endocytosis via the mannose receptor. Conjugates were bound by live macrophages but not by glutaraldehyde-fixed cells. Binding was inhibited by 0.1 mM mannan and 0.2 M alpha-methylmannoside, and strongly reduced, but not abolished, after trypsin degradation of surface receptors. Binding sites were rapidly assembled on coated pits, which often showed a polar distribution on the cell surface and entered the cell following the direction of microtubuli. Some coated vesicles occasionally kept in touch with the extracellular space. 10-min exposure to the conjugate resulted in changes in the surface morphology, such as a loss of infoldings and increased membrane tension. Ferritin accumulated in large smooth vesicles with coated membrane regions. It was mostly detached from the membrane and agglutinated into big clumps, together with fibrillar material and small vesicles which may derive from the vesicle membrane.

Animals↗

PubMed1991

The role of the growth plate in longitudinal bone growth.

The epiphyseal growth plate is the main site of longitudinal growth of the long bones. At this site, cartilage is formed by the proliferation and hypertrophy of cells and synthesis of the typical extracellular matrix. The formed cartilage is then calcified, degraded, and replaced by osseous tissue. Proliferation and differentiation of cartilage cells (i.e., chondrocytes) as studied mostly in culture, is regulated by various endocrine, paracrine, and autocrine agents such as growth hormone, insulin-like growth factor-I (IGF-I), transforming growth factor (TGE-beta), and vitamin D metabolites (1,25-dihydroxycholecalciferol and 24,25-dihydroxycholecalciferol). Avian chondrocyte proliferation is enhanced by agents which use adenosine 3':5'-cyclic monophosphate as a second messenger, such as parathyroid hormone or prostaglandin-E2, and is depressed by guanosine 3':5'-cyclic monophosphate agonists, such as atrial natriuretic peptide. Several of the regulating agents also affect synthesis of the main extracellular components (i.e., collagen and proteoglycans) and their transfer to the extracellular space. Cartilage calcification involves matrix vesicles secreted by the chondrocytes at a specific stage. Calcification probably involves some initial nucleation agent and participation of phosphatases. During sexual maturation, the growth plate closes by an unknown mechanism and longitudinal bone growth ceases. Disorders in the metabolism of the controlling agents or the cellular responses in growth plate may lead to several deformities classified as dysplasias. In poultry, this class of disorders is represented by chondrodystrophy and dyschondroplasia.

Animals↗

PubMed1990

Electrostatic properties of fiber cell membranes from the frog lens.

The electrostatic properties of lens fiber cell membranes have been investigated by recording the electrophoretic mobility of membrane vesicles formed from isolated fiber cells. The vesicles appear to be sealed and have external surfaces that are representative of the extracellular surface of fiber cells. The average mobility of a vesicle in normal Ringer's solution was 0.9 microns/s per v/cm, which gives a zeta potential of -9 mV, a value similar to that reported for other cells (McLaughlin, S. 1989. Annu. Rev. Biophys. Biophys. Chem. 18:113-136.). There was no significant difference in the mobility of vesicles formed from peripheral, middle cortical, or nuclear fiber cells. Vesicle surface changes were titrated using Ca and Mg and each had a pK of approximately 2, which is similar to that for the most common phospholipids. We also titrated these charges with varying pH and found the most significant changes in mobility at pH values between 5 and 6. The majority of lipids found in biological membranes are not titratable in this pH range, so the pH effect is probably through a membrane protein charged group. These experimental data in conjunction with the previously measured extracellular voltage gradient (Mathias, R. T., and J. L. Rae. 1985. Am. J. Physiol. 249:C181-C190) imply that electroosmosis can generate a fluid velocity of approximately 0.6 mm/h, directed from the aqueous or vitreous toward the center of the lens, along intercellular clefts.

Animals↗