bluuebunny/crossref_metadata_2025_split huggingface dataset:
Relationship between c‐Kit expression and proliferation in acute myeloblastic leukemia cell lines
Authors: Tohda S. , Yang G. S. , Ashman L. K. , McCulloch E. A. , Minden M. D. 
Published: February 2005

AbstractWe have proposed that the transmembrane receptor encoded by the c‐Kit protooncogene and its ligand play an important role in regulating the proliferation of blasts cells in acute myeloblastic leukemia (AML). To test this hypothesis, immunobeads were used to separate blasts from three Kit‐expression positive cell lines into strongly Kit‐protein positive and weakly Kit‐protein positive fractions. The strongly positive fraction had greater proliferative potential than the weakly positive fraction as assessed both by colony‐formation in methylcellulose and growth of clonogenic cells in suspension. The reproducibility of the percentage of each blast population found in the strongly and weakly positive fractions provided evidence that Kit‐protein expression is regulated. Kinetic experiments provided evidence for reversible transitions between strong and weak Kit protein expression. Thus regulated expression of the Kit receptor may be a mechanism for controlling blast cell growth in culture. © 1993 Wiley‐Liss, Inc.
K+ fluxes mediated by Na+‐K+‐Cl− cotransport and Na+‐K+‐ATPase pumps in renal tubule cell lines transformed by wild‐type and temperature‐sensitive strains of simian virus 40
Authors: Vandewalle A. , Vuillemin T. , Teulon J. , Baudouin B. , Wahbe F. , Bens M. , Cassingéna R. , Ronco P. 
Published: February 2005

AbstractThe relative contributions of Na+‐+‐pumps and Na+‐+‐− contransport to total rubidium (Rb+) influx into primary cultures of renal tubule cells (PC.RC) and cells transformed either with the wild‐type or a temperature‐sensitive mutant of the simian virus 40 (SV40), were measured under various growth conditions. The Na+‐+‐mediated component represented 74% and 44–48% of total Rb+ influx into PC.RC and SV40‐transformed cells, respectively. Proliferating transformed cells showed substantial ouabain‐resistant bumetanide‐sensitive (Or‐Bs) Rb+ influx (41–45% of total) which indicated the presence of Na+‐+‐− contransport. The Or‐Bs component of Rb+ influx was greatly reduced when temperature‐sensitive transformed renal cells (RC.SVtsA58) grown in Petri dishes or on permeable filters were shifted from the permissive (33°C) to the restrictive temperature (39.5°C) to arrest cell growth. The ouabain‐sensitive Rb+ influx mediated by the Na+‐+‐, the total and amiloride‐sensitive Na+ uptakes were not modified following inhibition of cell proliferation. A similar fall in the Or‐Bs influx was obtained when renal tubule cells transformed by the wild‐type SV40 (RC.SV) were incubated with the K+ channel blocker, tetraethylammonium (TEA) ion, which we had previously shown to arrest cell growth without affecting cell viability (Teulon et al.: J. Cell. Physiol., 151:113–125, 1992). Reinitiation of cell growth by removal of TEA or return to 33°C of the temperature‐sensitive cells restored the Or‐Bs component of Rb influx. Taken together, these results indicate that the Na+‐+‐− cotransport activity is critically dependent on cell growth con ditions. © 1993 Wiley‐Liss, Inc.
Stimulation of DNA synthesis and protooncogene expression in primary rat hepatocytes in long‐term DMSO culture
Authors: Serra Rosa , Isom Harriet C. 
Published: February 2005

AbstractWe have previously described the use of a chemically defined medium (CDM) supplemented with epidermal growth factor (EGF) and dimethylsulfoxide (DMSO) to maintain long‐term cultures of rat hepatocytes in a highly differentiated state. In this study, conditions necessary to stimulate high levels of DNA synthesis in hepatocytes in long‐term DMSO culture were defined. Hepatocytes were maintained in culture for 20 days in CDM containing DMSO and EGF, insulin, and glucagon. EGF, insulin, and glucagon were then removed for 7 days. Readdition of EGF, insulin, and glucagon at day 27 (shiftup) was accompanied by a three‐ to sixfold increase in labeling index. If DMSO or dexamethasone (dex) + DMSO were removed at time of shiftup, the labeling index increased by 18‐ to 54‐fold. TGFβ inhibited DNA synthesis stimulated by EGF shiftup, TGFα shiftup, or EGF shiftup in combination with removal of dex + DMSO. Stimulation of DNA synthesis was accompanied by a specific, sequential induction of protooncogene mRNA levels; c‐fos mRNA was induced 23‐fold at 0.5 h after readdition of EGF; c‐myc mRNA was induced three‐ to fourfold by 0.5 h; TGFα mRNA was induced sevenfold by 8 h; K‐ras mRNA was induced fourfold by 26 h. Changes in protooncogene expression paralleled changes seen in regenerating liver. When DMSO was removed for greater than 48 h, the cells flattened and spread out, chords of cells were no longer well defined, albumin mRNA levels decreased, and fibronectin, β1 integrin, and TGFβ transcripts increased. © 1993 Wiley‐Liss, Inc.
Long‐term culture of disaggregated rat osteoclasts: Inhibition of bone resorption and reduction of osteoclast‐like cell number by calcitonin and PTHrP[107‐139]
Authors: Fenton A. J. , Martin T. J. , Nicholson G. C. 
Published: February 2005

AbstractThe islated osteoclast bone resorption assay has proved to be a useful means of examining the response of mammalian and avian osteoclasts to a variety of stimuli. The assay has traditionally been performed over a period of 24 hours. By extending the duration of the osteoclast bone resorption assay, we have been able to assess the long‐term effects of carboxyl‐terminal parathyroid hormone‐related protein (hPTHrP[107‐139]), salmon calcitonin (sCT) and hPTH[1‐34] on bone resorption and TRACP‐positive osteoclast‐like cell number. We found that, in control cultures over a period of up to 144 hours, the osteoclast‐like cells not only remained viable but their numbers also increased. The number of mononucleated and multinucleated osteoclast‐like cells doubled in the first 48 hours before stabilizing over the remainder of the incubation period. Osteoblasts also proliferated, resulting in a resorption response to hPTH [1‐34] being evident from 48 hours onward. hPTHrP[107‐139] persistently inhibited basal and PTH‐stimulated bone resorption for at least 96–144 hours. Where as “escape” from the inhibijtory effect of sCT was seen after 48–72 hours. Decreased numbers of bothe mononucleated and multinucleated TRACP‐positive osteoclast‐like cells were seen by 48 hours in cultures treated with sCT. In contrast, hPTHrP[107‐139] reduced the number of mononuclear TRACP‐positive cells with only a late effect on multinucleated cells. Furthermore, the incsreased number of osteoclast‐like cells seen in response to hPTH[1‐34] was inhibited by carboxyl‐terminal PTHrP. In summary, this study indicates that the extended bone resorption assay system is a complex one where bothe osteoclastic resorption and osteoclast maturation are evident. Using this syste, we have shown that hPTHrP[107‐139] acts as a potent long‐term inhibitor of osteoclastic bone resorption, without evidence of escape from its effect. Its action to reduce the number of mononucleated osteoclst‐like cells suggests that it affects several aspects of osteoclast activity. © 1993 Wiley‐Liss, Inc.
Cyclic AMP‐induced inhibition of collagen lattice contraction by fibroblasts may be attenuated by both cyclic AMP dependent and independent mechanisms
Authors: Chen Jan‐Kan , Li Shing‐Rong , Tsai Ray Jui‐Fung 
Published: February 2005

AbstractThe contraction of collagen lattices made with forskin fibroblasts in medium containing 1% fetal bovine serum was inhibited by intracelluar cyclic AMP raising drugs including cholera toxin (CT), forskolin, and dibutyryl‐cAMP. The inhibition by CT was attenuated by insulin, acidic fibroblast growth factor (aFGF), and transforming growth factor‐β (TGF‐β). All three peptide factors have previously been reported to promote collagen lattice contraction by arterial smooth muscle cells and/or fibroblasts. Incubation of cells suspended in collagen gels with CT and forskolin resulted in a transient rise of the intracellular cyclic AMP levels, which peaked at 2 hr and 30 min, respectively, after drug exposure. Cholera toxin‐induced intracellular cyclic AMP increase was attenuated by TGF‐β, but not by aFGF and insulin, when added simultaneously. Thus, TGF‐β may attenuate CT's inhibition on collagen lattice contraction by attenuating CTinduced intracellualr cyclic AMP increse, whereas the attenuation by insulin and aFGF on the inhibition of lattice contraction may be mediated by a cyclic AMPindependent mechannism. © 1993 Wiley‐Liss, Inc.
Differential effects of transforming growth factor‐β1 and bone morphogenetic protein 4 on gene expression and differentiated function of preosteoblasts
Authors: Zhou Hong , Hammonds R. Glenn , Findlay David M. , Martin T. John , Ng Kong Wah 
Published: February 2005

AbstractTransforming growth factor‐β (TGF‐β) and bone morphogenetic protein 4 (BMP 4) are both able, under certain circumstances, to induce endochondral bone formation in vivo. This study compared the effects of TGF‐β and BMP 4 on the gene expression of a retinoic acid (RA) responsive rat clonal preosteoblast cell line, UMR 201, as well as the way in which these proteins interact with RA in these cells. Both similarities as well as differences between the effects and mechanism of action of TGF‐β1 and BMP 4 were demonstrated. TGF‐β1 (0.1 ng/ml) strongly induced matrix gla protein (MGP) mRNA and increased the steady state osteonectin (ON) mRNA level. Cotreatment with TGF‐β1 and RA did not result in a further increase in MGP mRNA expression. In contrast, BMP 4 alone had no influence on MGP or ON mRNA expression but it significantly enhanced the RA induction of MGP mRNA. Pro‐α(1) (l) collagen mRNA was increased by TGF‐β1 (1 ng/ml) and BMP 4 (50 ng/ml). The addition of either TGF‐β1 or BMP 4 together with RA resulted in a further increase in pro‐α1(l) collagen mRNA levels. Both RA and TGF‐β1, but not BMP 4, increased the transcriptional rate of the pro‐α 1(l) collagen gene. TGF‐β1 reduced the constitutive as well as RA‐induced expression of osteopontin (OP) mRNA while BMP 4 reduced only the constitutive expression of OP mRNA. RA increased the transcriptional rate of the OP gene. Since the responses of UMR 201 cells to these structurally related factors were not identical, the results lend support to the concept that the coordinated expression of members of the TGF‐β1 superfamily may be necessary to control the progression of specific cell types through their differentiation pathways. © 1993 Wiley‐Liss, Inc.
Secretion of α‐amylase in human parotid gland epithelial cell culture
Authors: Chopra Dharam P. , Xue‐Hu Iris C. 
Published: February 2005

AbstractThe secretions of the salivary gland system are essential for the maintenance of oral health. The nature of cell‐specific secretions of the various glands and their regulation is not completely understood. The objective of this study was to establish epithelial cell cultures from the human parotid gland that exhibit the tissue‐specific function of α‐amylase secretion. A specimen of normal human parotid gland was obtained at surgery and used to obtain primary cultures by the explant/outgrowth procedure. The cultures were maintained in keratinocyte basal medium, supplemented with insulin (5 μg/ml), EGF (10 ng/ml), hydrocortisone (0.5 μg/ml), bovine pituitary extract (25 μg/ml), and antibiotics. The cultures were passaged using 0.125% trypsin to dissociate the cells. Phase contrast and ultrastructural observations showed that the cells were polygonal and exhibited desmosomes. Their cytoplasm contained tonofilament bundles and abundant rough endoplasmic reticulum and Golgi complexes. Immunofluorescence studies showed that all cells were positive for cytokeratins. Immunoblot analysis revealed keratins with molecular weights of 58, 56, 52, 50, 48, 46, and 40 KD, which are characteristic of secretory epithelia. The cells have been passaged 35 times so far, undergoing a cumulative 120–140 population doublings. The serially passaged epithelial cell cultures produced and secreted α‐amylase, a major component of parotid gland acinar cell secretion. The β‐adrenergic agonist, isoproterenol (ISP), stimulated α‐amylase secretion, which was accompanied by increased intracellular concentrations of cAMP. ISP‐induced stimulation of amylase and cAMP was blocked by the β‐adrenergic antagonist, propranolol. Further, dibutryl cAMP also enhanced the secretion of amylase. Thus we have established a long‐term epithelial cell culture model of human parotid gland epithelial cells that exhibits differentiated function and retains the intact β‐adrenergic receptor system. © 1993 Wiley‐Liss, Inc.
Serum‐stimulated cell cycle progression and stress protein synthesis in C3H10T1/2 fibroblasts treated with sodium arsenite
Authors: Van Wijk Roeland , Welters Marij , Souren Jan E. M. , Ovelgonne Hans , Wiegant Fred A. C. 
Published: February 2005

AbstractIn this work, we demonstrate that a nonlethal dose of arsenite administered to quiescent C3H10T1/2 fibroblasts can enhance the mitogenic effect of suboptimal concentrations of serum. The mitogenic effect was dependent on the serum concentration and on the time interval between the administration of arsenite and that of serum. This suggests that mitogen sensitivity changes in time after arsenite treatment. It is shown that the concentrations of arsenite that enhance the mitogenic effect of serum also increase the mRNA levels of c‐fos, HSP68, and HSP84 and induce the specific synthesis of Heat Shock Proteins (HSPs). The physiological significance of this phenomenon is most likely to counteract the long‐term toxic effect of arsenite by early induction of compensation for cell loss. © 1993 Wiley‐Liss, Inc.
CSF‐1 control of C‐FMS expression in normal human bone marrow progenitors
Authors: Panterne Béatrice , Zhou Yi‐Quing , Hatzfeld Jacques , Li Ma‐Lin , Levesque Jean‐Pierre , Clark Steven C. , Hatzfeld Antoinette 
Published: February 2005

AbstractWe have previously shown (Zhou et al: Blood, 72:1870, 1988) that IL3, added with low concentrations of CSF‐1 (1 ng/ml) to normal human CD34+ enriched cells, promoted the development of various types of colonies including those containing immature monocytes. However, when high concentrations of CSF‐1 (20 ng/ml) were added alone or together with IL3, smaller colonies with mature macrophages were found. Here we show by in situ hybridization that IL3 allows the development, from CD34+ cells, of a subpopulation of immature progenitors which express the CSF‐1 receptor (c‐fms) mRNA. The expression of c‐FMS protein was also substantiated by immunocytochemical studies using anti‐c‐fms antibody. The percentage of c‐fms positive cells peaked at day 7 and began to decrease thereafter. When anti‐CSF‐1 antibodies were included in the culture, the decrease in c‐fms mRNA after day 7 was abrogated. This indicated that endogenous CSF‐1 was produced as CD34+ cells developed into monocytes or progenitors of monocytes and that CSF‐1 modulates c‐fms expression. We further demonstrated that when a high dose of CSF‐1 (20 ng/ml) was added at day 7 to IL3‐stimulated CD34+ cells, a rapid down‐regulation of c‐fms mRNA and protein was seen. No down‐regulation was observed with low concentration of CSF‐1 (1 ng/ml). The possibility that different concentrations of CSF‐1 could modulate the development of monocytic progenitors is discussed. © 1993 Wiley‐Liss, Inc.
IPG (inositolphosphate glycan) as a cellular signal for TGF‐β1 modulation of chondrocyte cell cycle
Authors: Vivien Denis , Petitfrère Emmanuelle , Martiny Laurent , Sartelet Hervè , Galéra Philippe , Haye Bernard , Pujol Jean‐Pierre 
Published: February 2005

AbstractThe knowledge of transforming growth factor (TGF)‐β receptors has greatly progressed in the recent years. TGF‐β receptors type I and II have been implicated in the modulation of cell proliferation, whereas type III (betaglycan) may act as a component presenting TGF‐β to its signaling receptors. In addition, four other proteins that bind TGF‐β1 or TGF‐β2 have been recently identified in some cell lines, three being anchored to the membrane through a glycosylphosphatidylinositol (GPI). Despite this knowledge, the molecular mechanism of signal transduction through the TGF‐β receptors remain an enigma. TGF‐β family does not signal via any of the classical pathways. As GPI anchors of membrane proteins have been implicated in the transduction of some hormonal effects, we investigated the putative role of GPI in signaling the TGF‐β effects on the proliferation of rabbit articular chondrocytes (RAC). We previously showed that TGF‐β1 increased DNA replication rate of RAC, with a recruitment of cells in G2/M followed by a subsequent mitosis wave. Here, we find that the factor causes specific GPI hydrolysis, with correlated increase of inositolphosphate glycan (IPG). This effect was specifically inhibited by antibodies that bind TGF‐β1. Using [3H]‐inositol labeling and Triton X‐114 extraction, we demonstrate that a hydrophobic material from the membrane is cleaved by treatment of cell cultures with phosphatidylinositol specific phospholipase C (PI‐PLC) or by exposure to TGF‐β, supporting that a PI‐anchored molecule gives rise to IPG by TGF‐β‐induced hydrolysis. The biological relevance of this hydrolysis was demonstrated by the enhancing effect of purified IPG on the DNA synthesis rate, which mimicked the TGF‐β action. These results demonstrate that IPG could be an early messenger in the cellular signaling that mediates the effect of TGF‐β on RAC growth. © 1993 Wiley‐Liss, Inc.
Hydrogen peroxide‐induced oxidative stress to the mammalian heart‐muscle cell (cardiomyocyte): Nonperoxidative purine and pyrimidine nucleotide depletion
Authors: Janero David R. , Hreniuk David , Sharif Haamid M. 
Published: February 2005

AbstractHydrogen peroxide (H2O2) overload may contribute to cardiac ischemia‐reperfusion injury. We report utilization of a previously described cardiomyocyte model (J. Cell. Physiol., 149:347, 1991) to assess the effect of H2O2‐induced oxidative stress on heart‐muscle purine and pyrimidine nucleotides and high‐energy phosphates (ATP, phosphocreatine). Oxidative stress induced by bolus H2O2 elicited the loss of cardiomyocyte purine and pyrimidine nucleotides, leading to eventual de‐energization upon total ATP and phosphocreatine depletion. The rate and extent of ATP and phosphocreatine loss were dependent on the degree of oxidative stress within the range of 50 μM to 1.0 mM H2O2. At the highest H2O2 concentration, 5 min was sufficient to elicit appreciable cardiomyocyte highenergy phosphate loss, the extent of which could be limited by prompt elimination of H2O2 from the culture medium. Only H2O2 dismutation completely prevented ATP loss during H2O2‐induced oxidative stress, whereas various freeradical scavengers and metal chelators afforded no significant ATP preservation. Exogenously‐supplied catabolic substrates and glycolytic or tricarboxylic acidcycle intermediates did not ameliorate the observed ATP and phosphocreatine depletion, suggesting that cardiomyocyte de‐energization during H2O2‐induced oxidative stress reflected defects in substrate utilization/energy conservation. Compromise of cardiomyocyte nucleotide and phosphocreatine pools during H2O2‐induced oxidative stress was completely dissociated from membrane peroxidative damage and maintenance of cell integrity. Cardiomyocyte de‐energization in response to H2O2 overload may constitute a distinct nonperoxidative mode of injury by which cardiomyocyte energy balance could be chronically compromised in the post‐ischemic heart. © 1993 Wiley‐Liss, Inc.
1,25‐dihydroxy vitamin D3 and 12‐O‐tetradecanoyl phorbol‐13‐acetate synergistically induce monocytic cell differentiation: FOS and RB expression
Authors: Yen Andrew , Coles Mark , Varvayanis Susi 
Published: February 2005

Abstract1,25‐dihydroxy vitamin D3 and 12‐O‐tetradecanoyl phorbol‐13‐acetate (TPA) interact synergistically to induce monocytic differentiation of U937 histiocytic lymphoma cells. Addition of TPA causes an otherwise ineffective dose of 1,25‐dihydroxy vitamin D3 to induce differentiation. The induced differentiation depends on the simultaneous (vs. sequential) presence of both agents. The kinetics of induced differentiation are consistent with a G1 specific cellular response to initiate the metabolic cascade culminating in cell differentiation. The induced differentiation occurs with down‐regulation of c‐fos protein and an accompanying up‐regulation of RB protein expression, consistent with a possible need for up‐regulated RB expression to maintain a given differentiated phenotype and suppress transcriptional activators that might typically be associated with proliferation. © 1993 Wiley‐Liss, Inc.
Type IV collagenase(s) and TIMPs modulate endothelial cell morphogenesis in vitro
Authors: Schnaper H. William , Grant Derrick S. , Stetler‐Stevenson William G. , Fridman Rafael , D'Orazi Gabriella , Murphy Anne N. , Bird Robert E. , Hoythya Matti , Fuerst Thomas R. , French Deborah L. , Quigley James P. , Kleinman Hynda K. 
Published: February 2005

AbstractIt has been proposed that proteases are important in endothelial cell behavior. We examined the contribution of the gelatinase/type IV collagenase system in an in vitro model of endothelial differentiation. Human umbilical vein endothelial cells rapidly align and form networks of tubes when cultured on a basement membrane preparation, Matrigel. Zymograms of culture supernates demonstrate a 72‐kD and a 92‐kD gelatinase activity; the cells produce most of the 72‐kD gelatinase, whereas the 92‐kD activity is derived entirely from the Matrigel. Addition of antibodies against type IV gelatinase/collagenase decreases the area of the tube network. Both tissue inhibitors of metalloproteinases, TIMP‐1 and TIMP‐2, similarly decrease tube formation when added to cultures. Conversely, exogenous recombinant 72‐kD gelatinase increases tube‐forming activity. The effects of the anti‐gelatinase antibodies and the TIMPs are not additive. Inhibition by either antibodies or TIMPs is greatest when they are added at culture initiation, suggesting that the protease activity is important in the early steps of morphogenesis. However, culture of the cells on Matrigel does not increase early expression of mRNA for the 72‐kD gelatinase. Expression of message for the enzyme actually decreases during the course of the assay, while transcription of mRNA for TIMPs increases, further supporting the concept that collagenases facilitate an early event in tube formation. These data demonstrate that gelatinase/type IV collagenase activity is important in endothelial cell morphogenesis on Matrigel, and suggest a role for collagenases in formation of new capillaries in vivo. © 1993 Wiley‐Liss, Inc.