Bovine Vascular Endothelial Cells Research Articles

391 Inhibitory effect of aprotinin on the destruction of bovine vascular endothelial cells(CPAE) in culture by choriocarcinoma cells(SMT-cc1)

391 Inhibitory effect of aprotinin on the destruction of bovine vascular endothelial cells(CPAE) in culture by choriocarcinoma cells(SMT-cc1)

Soluble CD14 and lipopolysaccharide-binding protein from bovine serum enable bacterial lipopolysaccharide-mediated cytotoxicity and activation of bovine vascular endothelial cells in vitro.

Bacterial endotoxin (lipopolysaccharide, LPS) has potent proinflammatory properties toward many cell types, including vascular endothelial cells. Bovine endothelial cells are often used for investigations involving the vascular endothelium in vitro, and other bovine products such as fetal bovine serum are also widely utilized in research laboratories. Evidence is presented that soluble CD14 (sCD14) is present in bovine serum and that LPS-mediated activation and cytotoxicity to bovine endothelial cells in vitro are dependent on sCD14. LPS-mediated activation of endothelial cells was quantitated by measuring tissue factor expression using an activated factor X-related chromogenic assay. Concentrations of 0.1-5.0% fetal bovine serum in the culture medium promoted LPS-induced tissue factor expression on bovine endothelial cells, and anti-CD14 monoclonal antibody (mAb) (20 micrograms/ml) inhibited tissue factor expression, whereas control antibodies did not. LPS-mediated damage to endothelial cells was assayed using the MTT tetrazolium assay. We found that either serum or recombinant human soluble CD14 (rsCD14, 20-2000 ng/ml) was required for LPS-related endothelial cell damage and that anti-CD14 mAb inhibited cytotoxicity. In addition, bovine LPS-binding protein (LBP, 20 ng/ml) purified from bovine serum had no effect on LPS-mediated cytotoxicity, but bovine LBP greatly enhanced the cytotoxic effect of LPS plus rsCD14. Western blot analysis performed on fractionated bovine serum samples with anti-CD14 mAb revealed immunoreactivity with a 50-55-kd protein, a size consistent with sCD14. Evidence of endothelial cell-associated CD14 was not detected using an immunofluorescence technique on cell preparations, nor by Northern blot analysis. These results indicate the existence of sCD14 in bovine serum and that soluble bovine serum factors including sCD14 and LBP facilitate presentation of LPS to receptive cells.

Effects of Glucose and an Aldose Reductase Inhibitor on Albumin Permeation Through a Layer of Cultured Bovine Vascular Endothelial Cells

The effects of high glucose concentrations on the selective permeability of a layer of cultured bovine vascular endothelial cells (ECs) were investigated. ECs were derived from the intima of the thoracic aorta and permeability to nonglycated albumin, glycated albumin, and fluorescein dextrans (FDs) of molecular mass to albumin was measured. ECs were cultured on a filter coated with type I collagen and preincubated in the presence of various glucose concentrations for 96 h. Human serum albumin was glycated by incubation with glucose in vitro. Nonglycated and glycated albumin were separated by affinity column chromatography. The permeation rates of nonglycated and glycated albumin as well as those of neutral and anionic FD through the EC layer were increased by preincubation of cells with high glucose concentrations (22.2 and 44.4 mmol/l). The permeation rate of glycated albumin was significantly less than that of nonglycated albumin at all glucose concentrations tested, whereas the permeation rate of anionic FD was significantly lower than that of neutral FD only at a physiological glucose concentration (5.6 mmol/l). The aldose reductase inhibitor ponalrestat partially inhibited the high glucose-induced increase in trans-endothelial permeation of albumin (both nonglycated and glycated), but had no effect on the increased permeation of FD. These results indicate that high glucose concentrations enhance trans-endothelial permeability to albumin and FD and may disturb the barrier function of vascular ECs. Furthermore, metabolism of glucose via the polyol pathway may contribute to abnormalities in trans-endothelial permeability.

Signal transduction pathways of bacterial lipopolysaccharide-stimulated bovine vascular endothelial cells

Increased procoagulant activity of vascular endothelial cells may be an important component in the pathogenesis of intravascular coagulation associated with gram-negative bacterial diseases. Two bovine endothelial cell (BEC) lines isolated from pulmonary arteries (ENS-2 and ENT-18) were used in this study to investigate procoagulant signal transduction pathways of endotoxin (lipopolysaccharide, LPS)--stimulated BECs. The endothelial cell line ENS-2 was sensitive to LPS as demonstrated by tissue factor (TF) expression, but in contrast, the ENT-18 endothelial cell line was unusually resistant to the effects of LPS. No remarkable quantitative difference in binding of radiolabeled LPS was detected between the two endothelial cell lines. A protein kinase C (PKC) activator (phorbol 12-myristate 13-acetate, PMA) failed to induce TF expression in either cell line at concentrations ranging from 0.05 to 1.00 microM when used as a sole stimulus for the endothelial cells. However, when PMA was used in combination with LPS, PMA enhanced the stimulatory effect of LPS on the endothelial cells. In parallel experiments, PKC inhibitors (H-7 and GF 109203X) interfered with the stimulatory effect of LPS on the cells by decreasing tissue factor expression. We also found that an activator of adenylate cyclase, forskolin, similarly inhibited LPS-induced tissue factor activity. In contrast, protein tyrosine kinase inhibitors (genistein, lavendustin A) had no inhibitory effect on LPS-induced endothelial cell tissue factor expression. Our results collectively suggest that activation of PKC is an important step in stimulation of endothelial cells by LPS, and that LPS and phorbol esters may synergize to produce an enhanced stimulatory effect. Our results also suggest participation of cAMP in controlling LPS-mediated stimulation of endothelial cells, but fail to demonstrate a role for protein tyrosine kinase activity.

Plasmin Modulators, Aprotinin and Anti-Catalytic Plasmin Antibody, Efficiently Inhibit Destruction of Bovine Vascular Endothelial Cells by Choriocarcinoma Cells

The interaction of human gestational choriocarcinoma cell line, SMT-cc1, with bovine vascular endothelial cells, CPAE, was examined in an in vitro coculture model. SMT-cc1 cells have urokinase-type plasminogen activator (uPA) on their cell surface, and more than half of the cell-associated uPA is enzymatically inactive single-chain uPA (pro-uPA). uPA is bound to a specific surface receptor that is not completely saturated. Also, the plasmin activity is detected on their cell surface. We measured the ability of added SMT-cc1 cells to cause morphological changes in CPAE cells, leading to destruction of CPAE cells. SMT-cc1 cells that adhered to CPAE cell monolayers were capable of causing CPAE cell destruction, followed by detachment, within 6 hr after coculture. Nonspecific serine proteinase inhibitor, aprotinin, and anti-catalytic antibody against plasmin(ogen) effectively inhibited the destruction/detachment in a dose-dependent manner. SMT-cc1 cell-mediated CPAE cell destruction was suppressed for 6 hr in the presence of aprotinin, at a concentration of 20 μg/ml, or anti-plasmin antibody, at a concentration of ⩾10 μg/ml, suggesting that the destruction is closely related to the proteolytic enzyme, plasmin. We suggest that the destruction of endothelial cells by some tumor cells is associated with tumor cell-associated proteolytic activity, and the uPA-plasmin cascade plays an important role as a critical step during blood-borne metastasis.

Molecular adaptation of vascular endothelial cells to oxidative stress.

Cellular organisms respond at the cellular and molecular level when confronted with sudden changes in environment, and molecular adaptation represents the ability of the cells to acclimate themselves to their new environment. In this study we examined the response of bovine vascular endothelial cells (VEC) to the oxidative stress by exposing the cultured cells to two different concentrations of H2O2, 0.04 or 0.08 mM, for 18-24 h. H2O2-exposed VEC displayed good viability (85-90% for 0.04 mM H2O2; 75-80% for 0.08 mM H2O2) and exhibited normal morphology. H2O2 treatment of the VEC was associated with the expression of a number of new proteins, as demonstrated by two-dimensional gel electrophoresis of total cell lysate. Cells exposed to 0.04 mM H2O2 expressed 25 new proteins, whereas 19 newly expressed proteins were detected when the cells were exposed to 0.08 mM H2O2. Western blot analysis of H2O2-treated VEC using specific antibodies to heat-shock proteins (HSP) identified one of these proteins as a member of the HSP 70 family. In addition, H2O2 induced an increase in antioxidative enzyme activities in the VEC, including superoxide dismutase, catalase, and glutathione peroxidase. Moreover, these changes were a truly adaptive phenomenon because challenging the VEC with brief exposure to toxic levels of H2O2 (1 mM for 30 min) showed increased viability (by Trypan blue exclusion test) and decreased injury (by lactate dehydrogenase supernatant-to-cellular ratio determination) in adapted cells (preexposed to 0.04 or 0.08 mM H2O2) compared with control cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of basic fibroblast growth factor in the migration of bovine vascular endothelial cells

Role of basic fibroblast growth factor in the migration of bovine vascular endothelial cells

O-19 - Stimulatory effects of platelets on endothelin-1 production in cultured bovine vascular endothelial cells.

O-19 - Stimulatory effects of platelets on endothelin-1 production in cultured bovine vascular endothelial cells.

Effects of nicardipine on tube formation of bovine vascular endothelial cells in vitro.

The purpose of this study was to assess the effect of nicardipine, a Ca2+ channel blocker, on angiogenesis in vitro. Bovine carotid artery endothelial cells were cultured between type I collagen gel layers with 10(-9) to 10(-5) M nicardipine. The morphological changes were monitored by phase-contrast microscopy and photographed. The total length of tubular structures was measured with an image analyzer system. Endothelial proliferation and migration assays were also performed with the same doses of nicardipine. Cultured endothelial cells form tubular structures between collagen gel layers. Tube formation of endothelial cells was suppressed by culture with 10(-9) to 10(-5) M nicardipine in a dose-dependent manner. Migration of endothelial cells was also suppressed by the same doses of nicardipine. However, proliferation of endothelial cells was not enhanced. Nicardipine acts as an inhibitor of angiogenesis in vitro by inhibiting the migration of endothelial cells. This result suggests that nicardipine may have therapeutic potential in angiogenic disorders such as tumor growth, atherogenesis, and diabetic retinopathy.

Granulocyte-colony stimulating factor stimulates immunoreactive endothelin-1 release from cultured bovine endothelial cells

We examined the effect of human recombinant granulocyte-colony stimulating factor (G-CSF) on the release of immunoreactive endothelin-1 (ET-1) from cultured bovine vascular endothelial cells. G-CSF dose dependenlly (10 −8-10 −6M) increased the release of immunoreactive ET-1 as a function of time under a serum-free condition. Coaddition of G-CSF and thrombin induced an additive effect on immunoreactive ET-i release. Neither Ca 2+ channel antagonist nor cyclooxygenase inhibitor affected immunoreactive ET-1 release stimulated by G-CSF These results suggest that G-CSF, in addition to its effect on granulocyte progenitor has a direct effect on vascular endothelium to induce the release of immunoreactive ET-1.

IL-6 increases endothelial permeability in vitro.

The effect of interleukin 6 (IL-6) on endothelial permeability was examined by measuring fluorescein isothiocyanate-labeled albumin flux across an endothelial cell monolayer. Bovine vascular endothelial cells (BVEC) were cultured up to confluency on collagen-coated polycarbonate micropore filters and then the filters were mounted on modified Boyden chambers. Treatment of the BVEC with IL-6 at 100 ng/ml for 21 h caused a remarkable increase in the permeability of fluorescein isothiocyanate-labeled albumin across the endothelial monolayer. This effect of IL-6 was concentration dependent, in the range from 10-200 ng/ml of IL-6. The effect of IL-6 was also time dependent, the maximal level being reached at 21 h from the beginning of the treatment. This stimulatory effect of IL-6 on albumin clearance was completely abolished by the addition of anti-IL-6 antibody. Light microscopic observation of a cross-section of a monolayer showed that the IL-6-induced increase in the permeability was correlated with changes in cell shape and rearrangement of intracellular actin fibers. IL-6 did not show any cytotoxicity toward or growth inhibition of endothelial cells, even at more than 200 ng/ml. The enhancing effect of IL-6 on the increase in the permeability was reversible; when IL-6 was removed by a medium change and the cells were incubated for a further 24 h without IL-6, the permeability was restored to the control level. These results suggest that IL-6 can induce an increase in endothelial permeability in vitro by rearranging actin filaments and by changing the shape of endothelial cells.

Effect of 15-deoxyspergualin, a microbial angiogenesis inhibitor, on the biological activities of bovine vascular endothelial cells

We found recently that 15-deoxyspergualin, an analog of spergualin, which is an antibiotic and includes a spermidine moiety in its structure, exhibits anti-angiogenic activity. We have now carried out in vitro experiments with bovine vascular endothelial cells to determine which events occurring during angiogenesis are affected by this microbial angiogenesis inhibitor. 15-Deoxyspergualin did not inhibit the production of urokinase-type plasminogen activator (u-PA) or type IV collagenase by vascular endothelial cells. The direct inhibition of u-PA activity by 15-deoxyspergualin was not observed either. The angiostatic antibiotic neither affected the migration of vascular endothelial cells nor inhibited the endothelial cell proliferation in a two-dimensional culture system. We also examined the effect of 15-deoxyspergualin on the proliferation of endothelial cells in a three-dimensional culture system involving collagen gel, in which cell growth resembles more closely the endothelial cell proliferation during in vivo angiogenesis than that in a two-dimensional culture system without collagen gel. The antibiotic inhibited cell proliferation in a dose-dependent manner, indicating that the three-dimensional culture system is useful for finding a new angiogenesis inhibitor with a different mode of action from those of angiogenesis inhibitors found by using a two-dimensional assay system; however, no cause-effect relationship has yet been established. Taken together, these results suggest the possible involvement of the inhibition of vascular endothelial cell growth by 15-deoxyspergualin in its angiogenesis-inhibitory effect. 15-Deoxyspergualin appears to be a promising candidate as an angiogenesis inhibitor for controlling aberrant angiogenic responses occurring in different states, including tumor development.(ABSTRACT TRUNCATED AT 250 WORDS)

Inhibitory effects of interleukin 6 on prostaglandin I 2 production in cultured bovine vascular endothelial cells

The effect of interleukin 6 (IL-6) upon arachidonic acid (AA) metabolism was studied in cultured bovine vascular endothelial cells (BVECs). Although, in those BVECs pretreated with IL-6 for 48 h, there was no effect upon cell proliferation, it was discovered that IL-6 suppressed the conversion of AA to prostaglandin I 2 (PGI 2) in cellular homogenates. First signs of the suppression occurred 3 h after incubation, and thereafter the suppression increased with time until it leveled off at 12 h. This effect of IL-6 was concentration-dependent, ranging from 20 ng/ml to a maximum of 100 ng/ml with IL-6 at 47% of control. IL-6 had no effect upon AA conversion when exogenously added to the BVEC homogenates. To investigate the mechanism of the suppression induced by IL-6, we studied its effect upon PGI 2 synthesizing enzymes. We found that IL-6 had no effect upon the release of AA from phospholipids, but inhibited cyclooxygenase, the key enzyme for PGI 2 production from AA. To amplify PGI 2 production, AA was added exogenously to both control and IL-6-treated BVECs, and in this case also, the conversion activity in IL-6-treated BVEC's was suppressed. Through immunoblot analysis with an antibody to cyclooxygenase, it was determined that the level of cyclooxygenase protein was lowered in IL-6-treated cells. This is the first report to confirm down expression of cyclooxygenase in addition to the first observation as to the effect of IL-6 on endothelial cells.

Calcium overload and ischemic myocardial injury.

HomeCirculationVol. 83, No. 2Calcium overload and ischemic myocardial injury. Free AccessAbstractPDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessAbstractPDF/EPUBCalcium overload and ischemic myocardial injury. J D Marsh and T S Smith J D MarshJ D Marsh Search for more papers by this author and T S SmithT S Smith Search for more papers by this author Originally published1 Feb 1991https://doi.org/10.1161/01.CIR.83.2.709Circulation. 1991;83:709–711 Previous Back to top Next FiguresReferencesRelatedDetailsCited By Nemade H, Chaudhari U, Acharya A, Hescheler J, Hengstler J, Papadopoulos S and Sachinidis A (2018) Cell death mechanisms of the anti-cancer drug etoposide on human cardiomyocytes isolated from pluripotent stem cells, Archives of Toxicology, 10.1007/s00204-018-2170-7, 92:4, (1507-1524), Online publication date: 1-Apr-2018. Givvimani S, Pushpakumar S, Metreveli N, Veeranki S, Kundu S and Tyagi S (2015) Role of mitochondrial fission and fusion in cardiomyocyte contractility, International Journal of Cardiology, 10.1016/j.ijcard.2015.03.352, 187, (325-333), Online publication date: 1-May-2015. Wang X, Wang L, Fu C, Zhang P, Wu Y and Ma J (2014) Ranolazine Attenuates the Enhanced Reverse Na+-Ca2+ Exchange Current via Inhibiting Hypoxia-Increased Late Sodium Current in Ventricular Myocytes, Journal of Pharmacological Sciences, 10.1254/jphs.13202FP, 124:3, (365-373), . Tang Q, Ma J, Zhang P, Wan W, Kong L and Wu L (2012) Persistent sodium current and Na+/H+ exchange contributes to the augmentation of the reverse Na+/Ca2+ exchange during hypoxia or acute ischemia in ventricular myocytes, Pflügers Archiv - European Journal of Physiology, 10.1007/s00424-011-1070-y, 463:4, (513-522), Online publication date: 1-Apr-2012. Zheng J, Ma J, Zhang P, Hu L, Fan X and Tang Q (2009) Milrinone inhibits hypoxia or hydrogen dioxide-induced persistent sodium current in ventricular myocytes, European Journal of Pharmacology, 10.1016/j.ejphar.2009.06.021, 616:1-3, (206-212), Online publication date: 1-Aug-2009. Davidson S and Yellon D (2005) The role of nitric oxide in mitochondria . Focus on “Modulation of mitochondrial Ca 2+ by nitric oxide in cultured bovine vascular endothelial cells” , American Journal of Physiology-Cell Physiology, 10.1152/ajpcell.00277.2005, 289:4, (C775-C777), Online publication date: 1-Oct-2005. Caesar R (1999) Herz Pathologie, 10.1007/978-3-642-58620-0_7, (103-276), . Chávez E, Téllez F, Pichardo J, Milán R, Cuéllar A, Carbajal K and Cruz D (1996) On the protection by ketorolac of reperfusion-induced heart damage, Comparative Biochemistry and Physiology Part C: Pharmacology, Toxicology and Endocrinology, 10.1016/S0742-8413(96)00058-8, 115:1, (95-100), Online publication date: 1-Sep-1996. Rose U, Couwenberg P, Jansen J, Bindels R and Van Os C (1994) Effects of substrate-free anoxia and veratridine on intracellular calcium concentration in isolated rat ventricular cardiomyocytes, Pflügers Archiv, 10.1007/BF00374851, 428:2, (142-149), Online publication date: 1-Sep-1994. Nakamura T, Goda K, Okamoto T, Kishi T, Nakamura T and Goshima K (1993) Contractile and morphological impairment of cultured fetal mouse myocytes induced by oxygen radicals and oxidants. Correlation with intracellular Ca2+ concentration., Circulation Research, 73:4, (758-770), Online publication date: 1-Oct-1993. Thornell L, Holmbom B, Eriksson A, Reiz S, Marklund S and N�slund U (1992) Enzyme and immunohistochemical assessment of myocardial damage after ischaemia and reperfusion in a closed-chest pig model, Histochemistry, 10.1007/BF00271069, 98:6, (341-353), . Miyata H, Lakatta E, Stern M and Silverman H (1992) Relation of mitochondrial and cytosolic free calcium to cardiac myocyte recovery after exposure to anoxia., Circulation Research, 71:3, (605-613), Online publication date: 1-Sep-1992. Hayashida K, Miyara S, Shinozaki K, Takegawa R, Yin T, Rolston D, Choudhary R, Guevara S, Molmenti E and Becker L (2021) Inhaled Gases as Therapies for Post–Cardiac Arrest Syndrome: A Narrative Review of Recent Developments, Frontiers in Medicine, 10.3389/fmed.2020.586229, 7 February 1, 1991Vol 83, Issue 2 Advertisement Article InformationMetrics Copyright © 1991 by American Heart Associationhttps://doi.org/10.1161/01.CIR.83.2.709 Originally publishedFebruary 1, 1991 PDF download Advertisement

Both cultured bovine and human vascular endothelial cells possess histamine receptors but express them differently

Both cultured bovine and human vascular endothelial cells possess histamine receptors but express them differently

The respective 27 kDa and 28 kDa protein kinase C substrates in vascular endothelial and MCF-7 cells are most probably heat shock proteins

The phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA) stimulated the phosphorylation of two distinct 27 kDa and 28 kDa proteins, respectively, in bovine vascular endothelial cells and in MCF-7 human breast cancer cells. These protein phosphorylation events were correlated to striking opposite cell growth responses to TPA, i.e., stimulation of vascular endothelial cell proliferation and inhibition of MCF-7 cell growth. Exposure of both vascular endothelial and MCF-7 cells to heat shock induced synthesis of the respective 27 kDa and 28 kDa proteins among a set of common and distinct other proteins as well as an increase in the degree of phosphorylation of the two 27 kDa and 28 kDa proteins. These results suggest that the two protein kinase C substrates very likely belong to the family of low molecular mass stress proteins.

Action of calcitonin gene‐related peptide upon bovine vascular endothelial and smooth muscle cells grown in isolation and co‐culture

1. Bovine aortic endothelial cells (BAE) and smooth muscle cells (BASM) were grown separately and in co-culture. 2. Calcitonin gene-related peptide (CGRP) caused dose-dependent activation of adenylate cyclase in each cell type when grown in isolation. The concentration of CGRP causing half-maximal activation in BAE and BASM was 200 nM and 310 nM, respectively. 3. In cells grown in co-culture exposure to bradykinin produced dose-dependent elevations in cyclic GMP content which were maximal 1 min after application of the agonist. 4. CGRP (1 nM-1 microM) did not stimulate a rise in cyclic GMP in co-cultures. 5. Displaceable CGRP binding was identified throughout the wall of the bovine aorta. 6. We conclude that CGRP receptors coupled to adenylate cyclase are present on BAE and BASM, but there is no coupling of these receptors to the release of any agent (such as endothelium-derived relaxing factor) that activates guanylate cyclase.

高比重リポ蛋白(HDL)の血管内皮細胞の増殖促進作用に関する研究

In cultured bovine pulmonary endothelial cells (EC), human high density lipoproteins (HDL) induced DNA synthesis, which was measured by the incorporation of 3H-thymidine, in the complete absence of the serum. Neither the apolipoprotein components of HDL, apoHDL/cholesterol/DMPC (dimyristoyl phosphatidylcholine) vesicles, not the 25OH-cholesterol stimulated DNA synthesis. Co-incubation with phorbol-12-myristate-l3-acetate (PMA) did not affect the HDL-stimulated DNA synthesis. Diltiazem, one of the calcium channel blockers, inhibited DNA synthesis both in the quiescent and HDL-stimulated EC. The 45Ca2+ uptake was not changed by incubation with HDL. These results suggest that HDL-stimulated DNA synthesis was not directly linked to the activation of protein kinase C or the extracellular Ca3 uptake.The d<1.019g/cm3 fraction and LDL-stimulated DNA synthesis, in the presence of excessive amounts of these or IntralipidsR, did not cause any additional stimulation of DNA synthesis by HDL. Furthermore, oleic acid enhanced DNA synthesis in the quiscent EC, but not in the HDL (1mg prot/ml)-stimulated EC, thereby suggesting that lipoproteins may provide the fatty acids necessary for the proliferation of bovine vascular endothelial cells.

Effect of cell substratum on lateral mobility of lipids in the plasma membrane of vascular endothelial cells

Bovine vascular endothelial cells can be maintained in a highly differentiated state in vitro, either by the addition of fibroblast growth factor (FGF) to the culture medium or by plating the cells on extracellular matrix (ECM)-coated dishes. Under these conditions the cells proliferate actively and at confluence form a tightly packed monolayer composed of nonoverlapping polarized cells. A fluorescence recovery after photobleaching method was used to determine the lateral mobility coefficient D of the lipophilic fluorescent probe, 5 N-(hexadecanoyl)-aminofluorescein (HEDAF), in the basal and apical plasma membranes of endothelial cells under various culture conditions (cells on glass coverslips in the presence or absence of FGF, or cells plated on ECM in the exponential growth phase or at confluence). A heterogeneous distribution of lateral diffusion coefficients D was found in a given cell population. Nevertheless, for the basal membrane, a “mean” D value close to 2.0 × 10 −9 cm 2/s was found for all the culture conditions. The “mean” D value of HEDAF in the apical pole was slightly higher when sparse cells were exposed to FGF ( D = 2.2 × 10 −9cm 2/s) and was further enhanced when cells were growing or confluent on ECM-coated coverslips ( D = 2.7 × 10 −9cm 2/s). On the other hand, when the cells were maintained in the absence of FGF on glass coverslips, similar “mean” D values were found in both cell poles ( D = 2.0 × 10 −9cm 2/s). These results show that lateral mobility of lipids in endothelial plasmalemma varies in response to external factors such as FGF and the ECM.

Endothelial cell contraction increases Candida adherence to exposed extracellular matrix.

Bovine vascular endothelial cells treated with EDTA, urea, or thrombin underwent a marked, reversible contraction resulting in exposure of the subendothelial extracellular matrix (ECM). Candida yeasts adhered more to contracted monolayers than to confluent monolayers (P less than 0.01) by preferentially adhering to the ECM. Two strains of Candida albicans and one strain of Candida tropicalis bound avidly to exposed ECM, but Pseudomonas aeruginosa did not. However, treatment of endothelium with forskolin, which induces cell shape changes without exposure of the ECM, did not cause an increase in adherence.