bluuebunny/crossref_metadata_2025_split huggingface dataset:
Inhibition by 1,25 dihydroxyvitamin D3 of c‐myc down‐regulation and DNA fragmentation in cytosine arabinoside–induced erythroid differentiation of K562 cells
Authors: Moore Dorothy C. , Carter Darryl L. , Studzinski George P. 
Published: February 2005

AbstractThe effect of 1,25‐dihydroxyvitamin D3 (1,25(OH)2D3) on DNA fragmentation, altered expression of the heat shock protein (hsp) 70 gene, and protooncogenes c‐myc and c‐myb was studied during chemical induction of erythroid differentiation in K562 cells. Preincubation of K562 cells with 1,25(OH)2D3 did not alter the concentration of hemoglobin in cells which did differentiate, but led to a reduction in the accumulation of low molecular weight DNA generated by Ara‐C administration. The extent of this reduction was similar to the degree of inhibition of hemoglobin formation in the culture as the whole. Preincubation with 1,25(OH)2D3 had no effect on the increase of hsp 70 gene expression induced by a 48‐hr treatment with Ara‐C, but prevented the Ara‐C‐induced down‐regulation of the protooncogene c‐myc. The protooncogene c‐myb was down‐regulated after 15 min of treatment with Ara‐C, and exposure to 1,25(OH)2D3 prior to Ara‐C caused a further down‐regulacion of its expression. The data suggest that the events associated with erythroid differentiation may be separable into at least two groups; one of these may have an influence on the kinetics of the cell cycle traverse, and the other may be related to the expression of the erythroid phenotype. © 1992 Wiley‐Liss, Inc.
Induced thermotolerance to apoptosis in a human T lymphocyte cell line
Authors: Mosser Dick D. , Martin Luis H. 
Published: February 2005

AbstractA brief exposure to elevated temperatures elicits, in all organisms, a transient state of increased heat resistance known as thermotolerance. The mechanism for this thermotolerant state is unknown primarily because it is not clear how mild hyperthermia leads to cell death. The realization that cell death can occur through an active process of self destruction, known as apoptosis, led us to consider whether thermotolerance provides protection against this mode of cell death. Apoptosis is a common and essential form of cell death that occurs under both physiological and pathological conditions. This mode of cell death requires the active participation of the dying cell and in this way differs mechanistically from the alternative mode of cell death, necrosis. Here we show that mild hyperthermia induces apoptosis in a human leukemic T cell line. This is evidenced by chromatin condensation, nuclear fragmentation and the cleavage of DNA into oligonucleosome size units. DNA fragmentation is a biochemical hallmark of apoptosis and requires the activation of an endogenous endonuclease. The extent of DNA fragmentation was proportional to the severity of heat stress for cells heated at 43°C from 30 to 90 minutes. A brief conditioning heat treatment induced a resistance to apoptosis. This was evident as a resistance to DNA fragmentation and a reduction in the number of apoptotic cells after a heat challenge. Resistance to DNA fragmentation developed during a recovery period at 37°C and was correlated with enhanced heat shock protein (hsp) synthesis. This heat‐induced resistance to apoptosis suggests that thermotolerant cells have gained the capacity to prevent the onset of this pathway of self‐destruction. An examination of this process in heated cells should provide new insights into the molecular basis of cellular thermotolerance. © 1992 Wiley‐Liss, Inc.
Regulation of vascular smooth muscle cell integrin expression by transforming growth factor β1 and by platelet‐derived growth factor‐BB
Authors: Janat M. Fouad , Argraves W. Scott , Liau Gene 
Published: February 2005

AbstractWe have examined the ability of transforming growth factor‐β1 (TGF‐β1) and platelet‐derived growth factor‐BB (PDGF‐BB) to regulate the expression of various integrins in cultured rabbit vascular smooth muscle cells (SMC). We found that expression of the αvβ3 integrin complex was induced by both growth factors, although TGF‐β1 appeared to be the more potent inducer. mRNA level of the β3 integrin subunit was undetectable in quiescent cells and enhanced by both growth factors, while the αv integrin subunit mRNA level did not change with growth factor addition. Therefore, appearance of the αvβ3 integrin protein complex after growth factor stimulation was due to increased expression of the β3 integrin subunit mRNA. The TGF‐β1 induced increase in β3 integrin mRNA was delayed, but did not require prior protein synthesis, since cycloheximide was unable to block the increase in β3 mRNA level. By contrast, PDGF‐BB induced a more rapid increase in β3 integrin mRNA level that peaked by 6 h after growth factor addition and no detectable β3 integrin mRNA remained after 24 h. Interestingly, the PDGF‐BB induced elevation of β3 integrin, although more rapid, was completely inhibited by cycloheximide. Expression of the α5 integrin subunit in response to growth factors was very similar to β3. However, in contrast to β3 and α5, neither TGF‐β1 nor PDGF‐BB were able to alter the expression of the β1 integrin subunit in vascular SMC. However, in TGF‐β1 treated cells, there was a large increase in expression of a 190 kDa polypeptide that was associated with the β1 integrin subunit. This 190 kDa polypeptide was not detected in PDGF treated SMC or in TGF‐β1 treated fibroblasts. The α1 integrin subunit has a MW of approximately 190 kDa and is capable of complexing with β1. Analysis of the α1 integrin subunit mRNA level indicated that it was indeed induced by TGF‐β1, but not by PDGF‐BB, suggesting that the 190 kDa polypeptide may be the α1 integrin subunit. These results indicate that TGF‐β1 and PDGF‐BB are potent but distinct activators of integrin expression in vascular SMC. © 1992 Wiley‐Liss, Inc.
Ca2+ accumulation and loss by aberrant endocytic vesicles in sickle erythrocytes
Authors: Williamson Patrick , Puchulu Estela , Penniston John T. , Westerman Maxwell P. , Schlegel Robert A. 
Published: February 2005

AbstractSickle cells contain internal vesicles which accumulate Ca2+. As shown here, the membrane enclosing the vesicles contains the plasma membrane Ca2+‐ATPase, or Ca2+ pump, as judged by staining with an antibody directed against the protein. Moreover, the number of cells containing such vesicles increases upon deoxygenation. These findings argue strongly that the vesicles arise by endocytosis from the plasma membrane, and explain how they accumulate Ca2+. When sickle cells are depleted of ATP Ca2+ is lost from the vesicles, as judged by the disappearance of staining with the Ca2+/membrane probe chlortetracycline (CTC), without a corresponding loss of antibody staining. This loss of Ca2+ can be inhibited by nitrendipine, a Ca2+ channel blocker. These results suggest that the vesicle membrane allows outward passage of Ca2+ by a nitrendipine‐sensitive pathway, which can be overcome by the inward‐directed activity of the Ca2+ pump of the vesicle membrane. If so, the Ca2+ which vesicles contain is in dynamic equilibrium with the cytoplasm of the sickle erythrocyte. © 1992 Wiley‐Liss, Inc.
Effects of acute vs. chronic phorbol ester exposure on transepithelial permeability and epithelial morphology
Authors: Mullin James M. , Snock Kathleen V. , Shurina Robert D. , Noe Jasna , George Kenneth , Misner Lisa , Imaizumi Shotaro , O'Brien Thomas G. 
Published: February 2005

AbstractIn previous experiments we have shown that acute (30 minutes) exposure to phorbol esters or other protein kinase C activators causes increased transepithelial permeability, specifically by the increased paracellular permeability through tight junctions. However, the role of protein kinase C activators in carcinogenesis is predicted upon a chronic exposure of an effective dose at frequent intervals for a prolonged period of time. We therefore sought to determine the effect of chronic phorbol ester exposure on transepithelial permeability by exposing cells of the polar renal epithelial cell line, LLC‐PK1, to phorbol esters for time periods as long as 16 weeks. The following changes ensued: (1) after the initial drop in transepithelial resistance due to phorbol ester exposure, i.e., an increase in transepithelial permeability (in the acute phase of exposure), an adaptive response occurs as transepithelial resistances in chronically exposed cultures recover to approximately 50% of control values, (2) the cell sheets in chronically exposed cultures lose their acute responsiveness of transepithelial permeability to phorbol ester exposure, (3) cell sheet architecture changes as cells occasionally multilayer and actual polyp‐like cell masses appear at high frequency, and (4) cytosolic protein kinase C activity decreases to 50% of control level with acute exposure and then is further decreased to less than 1% of control level in chronically treated cells; membrane‐associated PKC activity is not as sharply decreased. The possible role of transepithelial permeability in carcinogenesis and the value of chronically treated epithelial cell cultures as a model for two‐stage carcinogenesis are discussed. © 1992 Wiley‐Liss, Inc.
Thrombin and histamine rapidly stimulate the phosphorylation of the myristoylated alanine‐rich C‐kinase substrate in human umbilical vein endothelial cells: Evidence for distinct patterns of protein kinase activation
Authors: Jacobson Brian C. , Pober Jordan S. , Fenton John W. , Ewenstein Bruce M. 
Published: February 2005

AbstractHuman α‐thrombin and histamine each stimulates protein phosphorylation in human umbilical vein endothelial cells (HUVEC). We have identified the most prominent of these phosphoproteins by immunoprecipitation as the human homolog of the widely distributed myristoylated alanine‐rich C‐kinase substrate (MARCKS). Stimulation by 0.1–10 U/ml of α‐thrombin produces a time‐dependent, sustained (plateau 3–5 min) level of MARCKS phosphorylation. MARCKS phosphorylation requires thrombin catalytic activity but not receptor binding and is also seen in response to stimulation by a peptide, TR (42–55), that duplicates a portion of the thrombin receptor tethered ligand created by thrombin proteolytic activity. One micromolar histamine, like α‐thrombin, produces sustained phosphorylation of MARCKS (plateau 3–5 min). In contrast, 100 μM histamine results in rapid but transient MARCKS phosphorylation (peak 1–3 min). HUVEC treated with 100 μM histamine for 5 min can be restimulated by α‐thrombin but not fresh histamine, suggesting that the histamine receptor was desensitized. MARCKS phosphorylation can also be induced by several exogenous protein kinase C (PKC) activators and both α‐thrombin‐ and histamine‐induced MARCKS phosphorylation are inhibited by the PKC antagonist staurosporine. However, while prolonged PMA pretreatment ablates histamine‐induced MARCKS phosphorylation, the ability of thrombin to induce MARCKS phosphorylation is retained. These findings provide evidence for agonist‐specific pathways of protein kinase activation in response to thrombin and histamine in HUVEC. © 1992 Wiley‐Liss, Inc.
Calcium alginate beads as a slow‐release system for delivering angiogenic molecules In Vivo and In Vitro
Authors: Downs Elizabeth C. , Robertson Nancy E. , Riss Terry L. , Plunkett Marian L. 
Published: February 2005

AbstractA method previously used in this laboratory for entrapment of tumor cells in alginate beads has been extended to provide a slow release delivery system for growth factors with known in vivo angiogenic activity. Protein growth factors were entrapped in alginate beads in amounts sufficient to cause incorporation of 3H‐thymidine by COMMA‐D cells in vitro, and in vivo neovascularization when injected subcutaneously into Balb/c mice. Entrapment of 125I‐labelled growth factors showed that the amount of molecule entrapped in alginate beads may vary with the charge of the molecule. In vitro cell proliferation studies showed that entrapment in alginate beads may provide a slow‐release system or a stabilizing environment for the protein. In some cases biological activity of the growth factor in solution was increased by the presence of control alginate beads. When alginate‐entrapped growth factors were injected into Balb/c mice, induction of new blood vessels could be monitored qualitatively by macroscopic photography and assessed quantitatively by measuring the pooling of radiolabelled red blood cells at the experimental site. Subcutaneous injection of purified angiogenic factors not entrapped in alginate beads did not cause neovascularization. Diffusion of 125I‐labelled growth factors from alginate beads in the animal showed that release in vivo may depend on the charge of the protein molecule. These results indicate that injection of purified molecules entrapped in alginate beads provides an effective localized and slow‐release delivery of biologically active molecules. This delivery system may extend the time of effectiveness of biologically active molecules in vivo compared to direct injection without alginate entrapment. The method of entrapment and injection has potential for identifying active factors in tumor‐induced angiogenesis and testing new compounds as modulators of neovascularization. © 1992 Wiley‐Liss, Inc.
Ethanol inhibits ligand‐activated Ca2+ channels in human B lymphocytes
Authors: Brodie Chaya , Domenico Joanne , Mazer Bruce D. , Gelfand Erwin W. 
Published: February 2005

AbstractEthanol reportedly is immunosuppressive, interfering with lymphocyte proliferation. To investigate the basis for this immunosuppression, the effects of acute treatment with ethanol were studied on Ca2+ mobilization in tonsillar B lymphocytes and the human lymphoblastoid B‐cell line, Ramos. The level of intracellular Ca2+ was monitored in cells loaded with the fluorescent dye indo‐1 following stimulation with either anti‐lgM antibody or platelet activating factor. The effect of ethanol was also examined on the induction of the early proto‐oncogene c‐fos in these cells. Ethanol inhibited ligand‐activated Ca2+ mobilization due to transmembrane influx but not intracellular store release, in a dose‐and time‐dependent manner. This inhibition was not due to the inability of anti‐lgM to bind to its surface receptor nor to membrane depolarization induced by ethanol. Ethanol also inhibited the Ca2+‐dependent induction by anti‐lgM of c‐fos in these cells. The inhibitory effects of ethanol on ligand‐activated Ca2+ channels and subsequent induction of c‐fos may provide the basis for its immunosuppressive action. © 1992 Wiley‐Liss, Inc.
EGF receptor regulation in normal mouse mammary gland
Authors: Haslam Sandra Z. , Counterman Laura J. , Nummy Katherine A. 
Published: February 2005

AbstractEstrogen (E), progesterone (P), and epidermal growth factor (EGF) are known to regulate growth and development of the normal mammary gland, and it is possible that EGF may interact with E and/or P. Estrogen (ER), progesterone (PR), and EGF receptors (EGF‐R) have been detected in both mammary epithelial and stromal cells, and the relative roles of the various cells types in hormone‐dependent growth regulation are not known. The present studies were undertaken to determine if E and/or P influence EGF action by exerting a regulatory effect on EGF‐R levels and which cell types are affected. The comparative effects of ovariectomy and hormone treatments on EGF‐R levels were examined in immature, pubertal 5‐week‐old and sexually mature 10‐week‐old female mice. EGF‐R were characterized as a single class of high affinity sites and EGF‐R concentration was 2‐fold higher in glands of 5‐week‐old mice. Ovariectomy had no significant effect on EGF‐R concentration in either age group, and treatment with E and/or P had no effect on EGF‐R levels in either epithelial or stromal cells in 5‐week‐old mice. In contrast, E+P treatment caused a 2‐fold increase in receptor concentration in 10‐week‐old mice in the mammary epithelium. Thus it appears that the developmental state of the gland may determine the nature and extent of the interaction of EGF, E, and P. © 1992 Wiley‐Liss, Inc.
Amnion cell biosynthesis of interleukin‐8: Regulation by inflammatory cytokines
Authors: Trautman Michael S. , Dudley Donald J. , Edwin Samuel S. , Collmer Debbie , Mitchell Murray D. 
Published: February 2005

AbstractThe cellular constituents of the placenta are important participants in the recruitment and trafficking of inflammatory cells within the placenta. In infectioninduced labor, gestational tissues synthesize and release a variety of inflammatory cytokines whose effects include increased prostaglandin biosynthesis and the initiation of uterine contractions. Interleukin‐8 (IL‐8), a potent neutrophil chemoattractant, has been recently described as being elevated in the amniotic fluid of mothers with chorioamnionitis. We investigated the biosynthesis of IL‐8 by human amnion cells and its regulation by other inflammatory cytokines. Cultured amnion cells obtained from normal term placentae were found to produce IL‐8 in response to pathophysiologic concentrations of interleukin 1β (IL‐1β) and tumor necrosis factor alpha (TNF‐α). Treatment of amnion cells stimulated by IL‐1β with cycloheximide resulted in increased IL‐8 production, while incubation of IL‐1β treated amnion cells with actinomycin D resulted in a concentration‐dependent decrease in detectable amounts of IL‐8. Northern blot analysis of cultured amnion cells stimulated with IL‐1β demonstrated a rapid increase in IL‐8 mRNA which peaked at 2–4 hr. These in vitro result suggest inflammation of gestational tissues in vivo may result in locally produced IL‐8 and, in association with other inflammatory mediators, may be important in the pathophysiology of infection‐induced labor. © 1992 Wiley‐Liss, Inc.
Neutrophil adhesion to TNFα‐activated endothelial cells potentiates leukotrine B4production
Authors: Ishii Yoshiki , Lo Siu K. , Malik Asrar B. 
Published: February 2005

AbstractSince adhesion of neutrophils (PMN) to endothelial cells may influence PMN activation responses, we examined whether adhesion of PMN to TNFα‐activated human umbilical vein endothelial cells (HUVEC) stimulates leukotriene B4(LTB4) production. Endothelial adhesivity towards PMN increased after HUVEC pretreatment with TNFαfor 4 h. LTB4production increased markedly in response to stimulation with arachidonic acid (20 μM) when PMN were added to the hyperadhesive HUVEC. In contrast, stimulation of PMN in suspension did not potentiate LTB4production. LTB4production persisted when PMN were applied to TNFα‐pretreated HUVEC fixed with 1% paraformaldehyde excluding the possibility that metabolic activity of endothelium participates in this response. PMN adhesion to plastic and gelatin also enhanced LTB4indicating that adhesion was critical event in inducing LTB4production. We used monoclonal antibodies (mAb) to adhesion molecules on endothelial cells (i.e., endothelial leukocyte adhesion molecule‐1 (ELAM‐1) and intercellular adhesion molecule‐1 (ICAM‐1) or on PMN (CD18) to assess the role of PMN adhesion to the activated endothelium on LTB4potentiation. Both anti‐ELAM‐1 mAb and anti‐ICAM‐1 mAb inhibitied PMN adhesion (by 55 and 41% respectively) as well as LTB4production (by 65 and 50% respectively). Anti‐CD18 mAB also reduced the adhesion (65%) and the LTB4production (66%). Furthermore, combination of anti‐ELAM‐1 mAb (H18/7) and anti‐ICAM‐1 mAb (RR1/1) or of anti‐ELAM‐1 mAb (H18/7) and anti‐CD 18 mAb (IB4) had an additive effect in inhibiting both PMN adhesion as well as LTB4production. PMN adherence to immobolized recombinant soluble rELAM‐1 or rlCAM‐1 also increased LTB4production, which was prevented with relevant mAbs. However, neither rELAM‐1 nor rlCAM‐1 stimulated LTB4production of PMN in suspension. We conclude that PMN adhesion to TNFα‐stimualted endothelial cells enhances LTB4production by PMN, a response activated by binding of PMN to expressed endothelial cell surface adhesion molecules. © 1992 Wiley‐Liss, Inc.
Tributyltin is a potent inducer of the heat shock response in human diploid fibroblasts
Authors: Zhang Hua , Liu Alice Y.‐C. 
Published: February 2005

AbstractSubmicromolar concentrations of tributyltin (TBT), a commercially used organotin compound, were found to induce the expression of several stress proteins, most notably HSP89 and HSP70, in IMR‐90 human diploid fibroblats in a time‐ and dose‐dependent manner. This induction can be demonstrated by quantitation of 1) synthesis of the heat shock proteins (HSPs), 2) relative abundance of mRNA of hsp70, and 3) transient expression of a human hsp70 promoter driven reporter gene. TBT also increased the abundance of mRNA of heme oxygenase, whereas heat shock was without effect. Analysis of protein binding to a consensus heat shock element (HSE)by electrophoretic mobility shift assay suggests that the induction of the heat shock response by TBT was attributable to activation of the heat shock transcription factor (HSTF). © 1992 Wiley‐Liss, Inc.
Inhibitory effects of a bacteria‐derived sulfated polysaccharide against basic fibroblast growth factor‐induced endothelial cell growth and chemotaxis
Authors: Nakayama Yutaka , Iwahana Michio , Sakamoto Noritsugu , Tanaka Noriko G. , Osada Yasuaki 
Published: February 2005

AbstractThe effects of sulfated polysaccharides on the growth and chemotaxis of endothelial cells promoted by basic fibroblast growth factor (bFGF), a heparin‐binding growth factor, and epidermal growth factor (EGF), a non‐heparin‐growth factor, were examined. The binding abilities of these two growth factors to D‐gluco‐galactan sulfate (DS‐4152) were the same as to heparin. DS‐4152 inhibited the growth and chemotaxis of the cells stimulated by bFGF, and prevented the binding of bFGF to the cells at both its low and high affinity binding sites: the former and the latter are heparin‐like molecules and receptor proteins for bFGF, respectively. However, DS‐4152 affected neither the binding of EGF to endothelial cells nor the proliferation and chemotaxis of the cells stimulated by the factor. Heparin also inhibited the binding of bFGF to low affinity binding sites to the same degree as DS‐4152, but had little effect on the binding of bFGF to high affinity sites and no effects on bFGF‐induced endothelial cell growth. Chondroitin sulfate A prevented neither the binding of bFGF to both sites of the cells nor bFGF‐induced cell proliferation. We thus concluded that the inhibitory effects of DS‐4152 against the growth and chemotaxis of endothelial cells induced by bFGF might be due to the prevention of bFGF binding to its receptor proteins resulting from the binding of DS‐4152 to bFGF. © 1993 Wiley‐Liss, Inc.