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  • 1
    Electronic Resource
    Electronic Resource
    Modulation of keratin intermediate filament distribution in vivo by induced changes in cyclic AMP-dependent phosphorylation (1990)
    New York, NY : Wiley-Blackwell
    Cell Motility and the Cytoskeleton 17 (1990), S. 291-300 
    Details
    ISSN: 0886-1544
    Keywords: PtK1 keratin filaments ; electrophoresis ; autoradiography ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Treatment of PtK1 cells with 5 mM acrylamide for 4 hr induces reversible de-phosphorylation of keratin in concert with reversible aggregation of intermediate filaments (Eckert and Yeagle, Cell Motil. Cytoskeleton 11:24-30, 1988). We have examined this phenomenon by 1) in vitro phosphorylation of isolated PtK1 keratin filaments and 2) combined treatments of PtK1 cells with both acrylamide and agents which elevate intracellular cAMP levels. PtK1 keratins were incubated in gamma-32P-ATP in the presence or absence of cAMP-dependent kinase (A-kinase) and cAMP. Levels of phosphorylation were analyzed by electrophoresis and autoradiography. Phosphorylation of keratin polypeptides (56 kD, 53 kD, 45 kD, 40 kD) occurred without added kinase, suggesting the presence of an endogenous kinase which remains with intermediate filaments in residues of Triton X-100 extracted cells. Phosphorylation levels were increased by A-kinase but not by cAMP alone, indicating the presence of cAMP-dependent phosphorylation sites in addition to sites phosphorylated by the endogenous kinase. To study the possible role of cAMP-dependent phosphorylation in acrylamide-induced aggregation of keratin filaments, we treated cells with acrylamide in the presence of 8-bromo-cAMP (brcAMP), pertussis toxin (PT), isobutylmethylxanthine (IBMX), or forskolin, which increase intracellular cAMP levels. The distribution and phosphorylation levels of keratin filaments, as well as intracellular cAMP levels, were determined for each of these treatments. In addition to aggregation and dephosphorylation of keratin filaments reported previously, treatment of cells with acrylamide alone also results in reduced levels of intracellular cAMP. 8-bromo-cAMP, IBMX, and forskolin prevent acrylamide-induced aggregation of keratin filaments and result in both normal levels of keratin phosphorylation and normal intracellular cAMP levels. PT was apparently ineffective. These observations suggest that 1) PtK1 keratins are phosphorylated by cAMP-dependent kinase and an endogenous, cAMP-independent kinase and 2) alteration of levels of cAMP-dependent phosphorylation may be involved in aggregation of keratin filaments in response to acrylamide.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/cm.970170404
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  • 2
    Electronic Resource
    Electronic Resource
    Organization of cortical microfilaments in dividing root cells (1992)
    New York, NY : Wiley-Blackwell
    Cell Motility and the Cytoskeleton 23 (1992), S. 252-264 
    Details
    ISSN: 0886-1544
    Keywords: Allium ; Tradescantia ; actin ; cell cortex ; division plane determination ; immunocytochemistry ; mitosis ; microtubules ; preprophase band ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: In order to assess the possible role of microfilaments (Mfs) in events preceding plant cell division, actin was localized in root cells of Allium cepa and Tradescantia virginiana by immunofluorescence microscopy. The distribution of Mfs was compared to that of microtubules (Mts) by means of dual localizations employing both antiactin and antitubulin. Cycling interphase cells contain Mfs that extend into all regions of the cytoplasm in random fashion. Prior to the rearrangement of the cortical Mt array into the initial broad preprophase band (PPB), the number of Mfs in the cytoplasm decreases, while a new population appears in the cortex. The cortical Mfs, which usually occupy the entire cell surface, are aligned parallel to the cortical Mts. When the initial PPB appears, these Mfs still cover the cortex or are arranged as a broad band encompassing the PPB. As the PPB narrows, the Mfs are also confined to an increasingly restricted zone usually wider than the PPB.than the PPB. When the PPB reaches its narrowest, densest configuration, aligned Mfs are excluded from the band proper, while others appear in flanking regions of the cortex. From prometaphase through anaphase, cortical Mfs are largely restricted to the ends of the cell overlying the spindle poles; they also tend to become more randomly oriented. Little or no actin is present in the spindle. During telophase, the two zones of aligned cortical Mfs over the ends of the cell gradually disappear and are replaced by new interphase networks. These changes provide additional data on the possible control of PPB organization by actin, and in addition indicate that the cortex may be the origin of the actin that aggregates at the spindle poles during cytochalasin treatment. © 1992 Wiley-Liss, Inc.
    Additional Material: 10 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/cm.970230405
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  • 3
    Electronic Resource
    Electronic Resource
    Microtubule reorganization during the cell cycle in synchronized BY-2 tobacco suspensions (1991)
    New York, NY : Wiley-Blackwell
    Cell Motility and the Cytoskeleton 18 (1991), S. 94-106 
    Details
    ISSN: 0886-1544
    Keywords: Nicotiana tabacum ; microfilament ; nuclear envelope ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Tobacco BY-2 suspension cultures were synchronized with aphidicolin in order to assess the relationship between microtubules (MTs), microfilaments (MFs), and the nuclear envelope (NE) at different stages of the cell cycle. Using immunofluorescence techniques, ordered MT arrays were found in the cortex in G1; few MTs are evident deeper in the cytoplasm or near the nucleus. However, MTs radiate from the surface of the nucleus during S and G2 as the interphase cortical array is replaced by the preprophase band. Perinuclear fluorescence is also visible at the end of cytokinesis but does not overlap with new ordered cortical arrays early in G1. When isolated nuclei are examined, associated MTs are again evident in S and G2, but not in G1. Microfilaments are colocalized with the MTs in the radiating arrays, as ascertained by dual staining of cells with rhodamine phalloidin. Propyzamide treatment leads to the loss of MTs at all stages, while cytoplasmic and perinuclear MF networks persist. Conversely, cytochalasin D disrupts MFs, including those radiating from the nucleus during S and G2, without any apparent effect on MTs. The results cast doubt on a proposed role for the NE in the generation of cortical MTs in plants. A universal role for MFs in the deployment of MTs is also in question.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/cm.970180204
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  • 4
    Electronic Resource
    Electronic Resource
    Effect of cytochalasins on actin in dividing root tip cells of Allium and Triticum: A comparative immunocytochemical study (1991)
    New York, NY : Wiley-Blackwell
    Cell Motility and the Cytoskeleton 18 (1991), S. 107-112 
    Details
    ISSN: 0886-1544
    Keywords: cell division ; cytoskeleton ; root cell ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: A collaborative effort was initiated to resolve differences in two recent papers on the effects of cytochalasins in root cells. While both studies reported similar effects on interphase cells (i.e., replacement of microfilaments by many small specks and rods), Palevitz (Cell Motil. Cytoskeleton 9:283-298, 1988) maintained that cytochalasins B and D induce actin aggregation at the poles of dividing Allium root cells at a concentration of 10 μM with rhodamine phalloidin as a reporter probe, whereas McCurdy and Gunning (Cell Motil. Cytoskeleton 15:76-87, 1990) could not find these aggregates following antiactin immunocytochemistry in Triticum roots treated with CB at 50 μM. Employing identical methods and materials in the same laboratory, we found that CD induces polar actin aggregates in dividing cells of both species. However, the aggregates in Triticum are smaller and occur less frequently than those in Allium. A similar pattern is seen with CB.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/cm.970180205
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  • 5
    Electronic Resource
    Electronic Resource
    Cytoskeletal alterations in cultured cardiomyocytes following exposure to the lipid peroxidation product, 4-hydroxynonenal (1994)
    New York, NY : Wiley-Blackwell
    Cell Motility and the Cytoskeleton 28 (1994), S. 119-134 
    Details
    ISSN: 0886-1544
    Keywords: microtubules ; vinculin ; desmin ; sarcolemmal damage ; free radicals ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Damage to the cardiac myocyte sarcolemma following any of several pathological insults such as ischemia (anoxia) alone or followed by reperfusion (reoxygenation), is most apparent as progressive sarcolemmal blebbing, an event attributed by many investigators to a disruption in the underlying cytoskeletal scaffolding. Scanning electron microscopic observation of tissue cultured rat neonatal cardiomyocytes indicates that exposure of these cells to the toxic aldehyde 4-hydroxynonenal (4-HNE), a free radical--induced, lipid peroxidation product, results in the appearance of sarcolemmal blebs, whose ultimate rupture leads to cell death. Indirect immunofluorescent localization of a number of cytoskeletal components following exposure to 4-HNE reveals damage to several, but not all, key cytoskeletal elements, most notably microtubules, vinculin-containing costameres, and intermediate filaments. The exact mechanism underlying the selective disruption of these proteins cannot be ascertained at this time. Colocalization of actin indicated that whereas elements of the cytoskeleton were disrupted by increasing length of exposure to 4-HNE, neither the striated appearance of the myofibrils nor the lateral register of neighboring myofibrils was altered. Monitoring systolic and diastolic levels of intracellular calcium ([Ca2+]i) indicated that increases in [Ca2+]i occurred after considerable cytoskeletal changes had already taken place, suggesting that damage to the cytoskeleton, at least in early phases of exposure to 4-HNE, does not involve Ca2+ -dependent proteases. However, 4-HNE-induced cytoskeletal alterations coincide with the appearance of, and therefore suggest linkage to, sarcolemmal blebs in cardiac myocytes.Although free radicals produced by reperfusion or reoxygenation of ischemic tissue have been implicated in cellular damage, these studies represent the first evidence linking cardiomyocyte sarcolemmal damage to cytoskeletal disruption produced by a free radical product. © 1994 Wiley-Liss, Inc.
    Additional Material: 9 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/cm.970280204
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  • 6
    Electronic Resource
    Electronic Resource
    Activation of serpins and their cognate proteases in muscle after crush injury (1994)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 159 (1994), S. 11-18 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Direct muscle injury was induced in rats in order to evaluate alterations in the balance of serine proteases and inhibitors (serpins) as a response to tissue damage. It was previously found that certain proteases, specifically urokinase-like plasminogen activator (uPA) and others, required activation in order to effect regeneration. We hypothesized that the magnitude and temporal sequence of serpin activation would follow, pari passu, activation of their cognate proteases. In addition to uPA, tissue PA (tPA) and tissue kallikrein were the proteases studied. The serpins we analyzed were protease nexin I (PNI), PA inhibitor 1 (PAI-1), and the kallikrein-binding protein (KBP). uPA nearly doubled 48 h after injury, while there was no change in amidolytic activity after addition of fibrin monomer as an estimation of tPA activity. Tissue kallikrein activity, barely detectable in normal muscle, slowly increased, nearly tripling at 7 days after injury. Greater magnitude and more rapid changes in muscle serpins occurred over the same post-injury time course. By 24 h PNI increased threefold, while PAI-1 increased more slowly, reaching double the control values by 5 days after injury. Surprisingly, KBP, the serpin-class inhibitor of tissue kallikrein, had the most robust response, increasing tenfold over control 48 h after crush injury of muscle. These results further implicate the serpin:protease balance in tissue injury. Participation of complex receptors, such as the α2-macroglobulin receptor/low density lipoprotein receptor-related protein (LRP), various growth factors, cytokines, and other molecules, in regulating this balance is implicated by these data. © 1994 wiley-Liss, Inc.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041590103
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  • 7
    Electronic Resource
    Electronic Resource
    Regulation of Cu,Zn-superoxide dismutase in bovine pulmonary artery endothelial cells (1992)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 153 (1992), S. 491-497 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: To evaluate the regulation of endothelial cell Cu,Zn-SOD, we have exposed bovine pulmonary artery endothelial cells in culture to hyperoxia and hypoxia, second messengers or related agonists, hormones, free radical generating systems, endotoxin, and cytokines and have measured Cu,Zn-SOD protein of these cells by an ELISA developed in our laboratory. Control preconfluent and confluent cells in room air contained 196 ± 18 ng Cu,Zn-SOD/106 cells. A23187 (0.33 μM), for skolin (10 μM), isobutylmethylxanthine (0.1 mM), dexamethasone (1 μM), triiodothyronine (1 μM) and retinoic acid (1 μM) failed to alter this level of Cu,Zn-SOD. Exposure to anoxia and hyperoxia both elevated the level -1.5-2.0-fold over 20% oxygen-exposed controls at 48-72 hr. Similarly, exposures to glucose oxidase (0.0075 units/ml), menadione (12.5 μM), xanthine-xanthine oxidase (10 μM, 0.03 units/ml) and H2O2 (0.0005%) increased the level up to two-threefold over controls at 24-48 hr. Lipopolysaccharide, TGFβ1, TNFα, and II-1 also increased levels of cellular Cu,Zn-SOD, but only in proliferating cells. II-2, II-4, interferon-γ, and GM-CSF had no effect on Cu,Zn-SOD. All treatments that elevated SOD resulted in inhibition of cellular growth, but decreased growth of cells at confluence alone was not associated with increased Cu,Zn-SOD. We propose from these studies that Cu,Zn-SOD of endothelial cells is not under conventional second messenger or hormonal regulation, but that up-regulation of the enzyme is associated with (and perhaps stimulated by) free-radical or oxidant production that also may be influenced by availability of certain cytokines under replicating conditions. © 1992 Wiley-Liss, Inc.
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041530308
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  • 8
    Electronic Resource
    Electronic Resource
    Critical role for intracellular calcium in tight junction biogenesis (1994)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 159 (1994), S. 423-433 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Using the Madin Darby canine kidney (MDCK) cell “calcium switch,” we have previously demonstrated that, as MDCK cells establish contact and ultimately form tight junctions, there are marked global and localized changes in intracellular calcium at the sites of cell-cell contact (Nigam et al., 1992, Proc. Natl. Acad. Sci. USA, 89:6162-6166). We have now examined whether intracellular Ca++ is critical to the biogenesis of tight junctions by chelating this ion and monitoring the formation of junctions by electrical, immunocytochemical, and biochemical criteria. Intracellular Ca++ was chelated with the cell-permeant chelators, dimethyl-BAPTA-AM and BAPTA-AM. By digital imaging of fura-2 loaded cells, it was demonstrated that both agents efficiently chelated Ca++ during the “switch” in a dose-dependent manner which paralleled their respective in vitro affinities for Ca++. Chelation of Ca++ during the switch markedly attenuated the development of transepithelial electrical resistance (TER), a measure of tight junction assembly. Immunofluorescent staining of the tight junctional protein, zonula occludens-1 (ZO-1), revealed that chelation of intracellular Ca++ retarded the movement of ZO-1 from intracellular sites to the plasma membrane during the switch. During the development of tight junctions, a fraction of ZO-1 redistributed from the Triton X-100 soluble to the Triton X-100 insoluble pool; chelation of Ca++ during the induction of cell-cell contact prevented this stabilization into the Triton X-100 insoluble fraction. Taken together, these data indicate an important role for intracellular Ca++ in tight junction biogenesis and suggest a specific role for calcium in the early sorting and possible cytoskeletal association of tight junction components. © 1994 wiley-Liss, Inc.
    Additional Material: 7 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041590306
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  • 9
    Electronic Resource
    Electronic Resource
    Cell cycle regulation of an exogenous human poly(ADP-ribose) polymerase cDNA introduced into murine cells (1990)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 144 (1990), S. 345-353 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: We have evaluated the regulation of expression of the poly(ADP-ribose) polymerase gene during cell growth and replication. In a synchronized population of HeLa cells or in serum-stimulated WI-38 cells, steady-state levels of the polymerase mRNA were highest at late S and S-G2 phases and negligible in early S phase. Transcription did not solely account for the significant increase in the mRNA levels observed in late S phase by Northern analysis. The stability of the mRNA was dependent upon the percent proliferating cells in the culture. Accordingly, polymerase mRNA from cells in early exponential phase was significantly more stable than from cells in stationary phase of asynchronous growth. To clarify these observations, we utilized a novel heterologous expression system that involved murine 3T3 cells transfected with a human poly(ADP-ribose) polymerase cDNA under the control of a non-cell cycle-specific promoter. Cells were synchronized, and a comparison was made of the endogenous (murine) and exogenous (human) polymerase mRNA levels. Both the endogenous and the exogenous mRNA were specifically stabilized by the same mechanisms and only during late S phase; therefore, we concluded that mRNA pools for the polymerase are regulated at the post-transcriptional level. The heterologous expression system confirmed that the post-transcriptional regulation system in the mouse cells can recognize and faithfully regulate the human cDNA in response to the murine cell cycle signals. More importantly, the presence of extra copies (human) of the polymerase gene did not provide an increased amount of the total polymerase mRNA or protein and, in fact, the sum of the endogenous and exogenous mRNA in the transfected cells was approximately the same as the level of endogenous transcript in the control cells. This suggested that there might be a limit to the amount of polymerase protein accumulating in the cellular pool and thus levels of poly(ADP-ribose) polymerase may be autoregulated.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041440221
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  • 10
    Electronic Resource
    Electronic Resource
    Modulation of expression of insulin and IGF-I receptor by Epstein-Barr virus and its gene products LMP and EBNA-2 in lymphocyte cell lines (1993)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 154 (1993), S. 486-495 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The receptors for insulin and insulin-like growth factor I (IGF-I) are two closely related integral membrane glycoproteins involved in signalling of cell growth and metabolism. We have used the unique paradigm of pairs of Burkitt lymphoma cell lines (BLO2, BL30, BL41) with or without Epstein-Barr Virus (EBV) infection and cells transfected with EBV-related genes to examine effects of EBV on expression of these receptors at the gene and protein functional level. In BL30 and BL41 cells, EBV infection increased surface insulin binding and total receptor number by 2-and 18-fold, respectively. By contrast, EBV infection decreased total IGF-I receptors by 29 to 87% in all three cell lines. In general, there was a correlation between total receptor concentration and the level of insulin or IGF-I receptor mRNAs, although in one cell line insulin binding increased while receptor mRNA levels decreased slightly, suggesting posttranslational effects. BL41 cells transfected with a vector expressing the EBV latent membrane protein (LMP) exhibited a 2.6- to 3.2-fold increase in insulin receptor expression, whereas cells transfected with EBNA-2 (one of the EBV nuclear antigens) alone exhibited no effect. However, EBNA-2 appears to be required for the EBV effect on insulin receptor expression since cells infected with a mutant virus, P3JHRI, which lacks the EBNA-2 gene failed to show an increase in insulin receptor number. These data indicate that EBV infection of lymphocytes increases expression of insulin receptors while simultaneously decreasing expression of IGF-I receptors. The magnitude and sometimes even the direction of change, depends on host cell factors. A maximal increase in insulin receptors appears to require the coordinate action of several of the EBV proteins including LMP and EBNA-2. © 1993 Wiley-Liss, Inc.
    Additional Material: 9 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041540306
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