bluuebunny/crossref_metadata_2025_split huggingface dataset:
Predominant integrin ligands expressed by osteoblasts show preferential regulation in response to both cell adhesion and mechanical perturbation
Authors: Carvalho R.S. , Bumann A. , Schaffer J.L. , Gerstenfeld L.C. 
Published: October 2004

AbstractPrevious studies have demonstrated that both mechanical perturbation and cell adhesion induced the expression of osteopontin (opn)by osteoblasts (Carvalho et al. [1998] J. Cell. Biochem. 70:376–390). The present study examined if these same stimuli on osteoblasts would induce the expression of other integrin binding proteins, specifically fibronectin (fn) and bone sialoprotein (bsp). All three genes showed three‐ to four‐fold maximal induction in response to both cell adhesion and a single 2‐h period of an applied spatially uniform, dynamic biaxial strain of 1.3% at 0.25 Hz. Each gene, however, responded with a different time course of induction to mechanical strain, withbsp,fn, andopnshowing their maximal response at 1, 3, and 9 h, respectively, after the perturbation period. In contrast, peak induction to cell adhesion was observed at 24 h forbspandopn, whilefnlevels peaked at 8 h. Interestingly, while bothopnandfnmRNA expression returned to base line after cell adhesion,bspmRNA levels remained elevated. Examination of collagen type I and osteocalcin mRNAs showed unaltered levels of expression in response to either type of perturbation. A common feature of the signal transduction pathways, which mediate the gene expression in response to both cell adhesion and mechanical perturbation, was the activation of specific tyrosine kinases based on the ablation of the induction of these genes by the tyrosine kinase inhibitor genistein. While cycloheximide blocked the induction of all three mRNAs in response cell adhesion, it failed to block the induction of any of these genes in response to mechanical perturbation. Such results suggest that the induction of these genes after mechanical perturbation was mediated by an immediate response to signal transduction, while cell adhesion mediated effects secondary to signal transduction. Depolymerization of microfilaments with cytochalasin D had no effect on the overall expression of any of these genes in response to cell adhesion and only blocked the induction ofopnexpression in response to mechanical perturbation. These results suggest that cytoskeletal integrity is only selectively important in the signal transduction of certain types of stimuli and for the regulation of certain genes. In summary, both mechanical perturbation and cell adhesion stimulated the expression of integrin binding proteins. Furthermore, while there are common features in the signal transduction processes that mediate the induction of these genes in response to both stimuli, specific genes are separately regulated by precise mechanisms that are unique to both forms of stimuli. J. Cell. Biochem. 84: 497–508, 2002. © 2001 Wiley‐Liss, Inc.
Chronic electromagnetic field exposure decreases HSP70 levels and lowers cytoprotection
Authors: Di Carlo Andrea , White Nicole , Guo Fuling , Garrett Peter , Litovitz Theodore 
Published: October 2004

AbstractElectromagnetic field (EMF) exposures have been shown to induce heat shock proteins (HSPs), which help to maintain the conformation of cellular proteins during periods of stress. We have previously reported that short‐term exposure of chick embryos to either 60 Hz (extremely low frequency: ELF), or radio‐frequency (RF: 915 MHz) EMFs induce protection against hypoxia. Experiments presented in the current report are based on a study in which long‐term (4 days), continuous exposure to ELF‐EMFs decreased protection against ultraviolet radiation. Based on this result, it was hypothesized that de‐protection against hypoxia should also occur following long‐term, continuous, or daily, repeated exposures to EMFs. To test this hypothesis, chick embryos were exposed to ELF‐EMFs (8 μT) continuously for 4 days, or to ELF or RF (3.5 mW incident power)‐EMFs repeated daily (20, 30, or 60 min once or twice daily for 4 days). Several of the exposure protocols yielded embryos that had statistically significant decreases in protection against hypoxic stress (continuous and 30 or 60 min ELF twice daily; or 30 or 60 min once daily RF). This is consistent with our finding that following 4 days of ELF‐EMF exposure, HSP70 levels decline by 27% as compared to controls. In addition, the superposition of ELF‐EM noise, previously shown to minimize ELF‐EMF induced hypoxia protection, inhibited hypoxia de‐protection caused by long term, continuous ELF or daily, repeated RF exposures. This EMF‐induced decrease in HSP70 levels and resulting decline in cytoprotection suggests a mechanism by which daily exposure (such as might be experienced by mobile phone users) could enhance the probability of cancer and other diseases. J. Cell. Biochem. 84: 447–454, 2002. © 2001 Wiley‐Liss, Inc.
Small heat shock protein p26 associates with nuclear lamins and HSP70 in nuclei and nuclear matrix fractions from stressed cells
Authors: Willsie Julia K. , Clegg James S. 
Published: October 2004

AbstractThe small heat shock/α‐crystallin protein p26 undergoes nuclear translocation in response to stress in encysted embryos of the brine shrimp Artemia franciscana. About 50% of total p26 translocates to nuclei in embryos treated with heat shock or anoxia, and in embryo homogenates incubated at low pH. Nuclear fractionation shows that the majority of nuclear p26 and a nuclear lamin are associated with the nuclear matrix fraction. To further explore the roles of p26 and other HSPs in stabilizing nuclear matrix proteins (NMPs), nuclear matrices from control, and heat‐shocked embryos were disassembled in urea and evaluated by one and two‐dimensional (2‐D) gel electrophoresis and Western immunoblotting after reassembling. Nuclear lamins were present only in reassembled fractions and, in the case of heat shock, p26 and HSP70 were also present. HSP90 was not detected in any nuclear fraction. Confocal microscopy on isolated nuclei and nuclear matrix preparations from control and heat‐shocked embryos showed that the majority of p26 and a nuclear lamin share similar nuclear distributions. The combination of microscopy and fractionation results suggests that p26 and HSP70 play a role in the protection of nuclear lamins within the nuclear matrix. J. Cell. Biochem. 84: 601–614, 2002. © 2001 Wiley‐Liss, Inc.
Expression of Na+/Ca2+exchanger isoforms (NCX1 and NCX3) and plasma membrane Ca2+ATPase during osteoblast differentiation
Authors: Stains Joseph P. , Weber Janet A. , Gay Carol V. 
Published: October 2004

AbstractThe ability to deliver calcium to the osteoid is critical to osteoblast function as a regulator of bone calcification. There are two known transmembrane proteins capable of translocating calcium out of the osteoblast, the Na+/Ca2+exchanger (NCX) and the plasma membrane Ca2+‐ATPase (PMCA). In this study, we reveal the presence of the NCX3 isoform in primary osteoblasts and examine the expression of NCX1, NCX3, and PMCA1 during osteoblast differentiation. The predominant NCX isoform expressed by osteoblasts is NCX3. NCX1 also is expressed, but at low levels. Both NCX isoforms are expressed at nearly static levels throughout differentiation. In contrast, PMCA expression peaks at 8 days of culture, early in osteoblast differentiation, but declines thereafter. Immunocytochemical co‐detection of NCX and PMCA reveal that NCX is positioned along surfaces of the osteoblast adjacent to osteoid, while PMCA is localized to plasma membrane sites distal to the osteoid. The expression pattern and spatial distribution of NCX support a role as a regulator of calcium efflux from osteoblasts required for calcification. The expression pattern and spatial distribution of PMCA makes its role in the mineralization process unlikely and suggests a role in calcium homeostasis following signaling events. J. Cell. Biochem. 84: 625–635, 2002. © 2001 Wiley‐Liss, Inc.
Divergent regulation by p44/p42 MAP kinase and p38 MAP kinase of bone morphogenetic protein‐4‐stimulated osteocalcin synthesis in osteoblasts
Authors: Kozawa Osamu , Hatakeyama Daijiro , Uematsu Toshihiko 
Published: October 2004

AbstractIn the present study, we investigated whether the mitogen‐activated protein (MAP) kinase superfamily is involved in the bone morphogenetic protein (BMP)‐4‐stimulated synthesis of osteocalcin in osteoblast‐like MC3T3‐E1 cells. BMP‐4 dose‐dependently stimulated osteocalcin synthesis. BMP‐4 markedly induced the phosphorylation of p44/p42 MAP kinase and p38 MAP kinase, while having little effect on SAPK (stress‐activated protein kinase)/JNK (c‐Jun N terminal kinase) phosphorylation. SB203580 and PD169316, specific inhibitors of p38 MAP kinase, significantly reduced the osteocalcin synthesis stimulated by BMP‐4. In contrast, PD98059 and U0126, inhibitors of upstream kinase of p44/p42 MAP kinase, markedly enhanced the BMP‐4‐stimulated osteocalcin synthesis. The BMP‐4‐induced phosphorylation of p44/p42 MAP kinase was suppressed by PD98059, which did not, however, affect the BMP‐4‐induced phosphorylation of p38 MAP kinase. Taken together, our results strongly suggest that p38 MAP kinase takes part in BMP‐4‐stimulated osteocalcin synthesis as a positive regulator in osteoblasts, whereas p44/p42 MAP kinase acts as a negative regulator in the synthesis. J. Cell. Biochem. 84: 583–589, 2002. © 2001 Wiley‐Liss, Inc.
Magnolol suppresses proliferation of cultured human colon and liver cancer cells by inhibiting DNA synthesis and activating apoptosis
Authors: Lin Shyr‐Yi , Liu Jean‐Dean , Chang Hui‐Chiu , Yeh Shauh‐Der , Lin Chien‐Huang , Lee Wen‐Sen 
Published: October 2004

AbstractMagnolol, a hydroxylated biphenyl compound isolated from the Chinese herb Hou p'u of Magnolia officinalis, has been reported to have anti‐cancer activity. In the present study, magnolol at very low concentrations of 3–10 μM inhibited DNA synthesis and decreased cell number in cultured human cancer cells (COLO‐205 and Hep‐G2) in a dose‐dependent manner, but not in human untransformed cells such as keratinocytes, fibroblasts, and human umbilical vein endothelial cells (HUVEC). Magnolol was not cytotoxic at these concentrations and this indicates that it may have an inhibitory effect on cell proliferation in the subcultured cancer cell lines. [3H]thymidine incorporation and flow cytometry analyses revealed that magnolol treatment decreased DNA synthesis and arrested the cells at the G0/G1 phase of the cell cycle. Moreover, the magnolol‐induced cell cycle arrest occurred when the cyclin‐CDK system was inhibited, just as p21 protein expression was augmented. When magnolol concentration was increased to 100 μM, apoptosis was observed in COLO‐205 and Hep‐G2 cells, but not in cultured human fibroblasts and HUVEC. COLO‐205 cells implanted subcutaneously in nude mice formed solid tumors; subsequent daily i.p. injections of magnolol led to profound regression of these tumors of upto 85%. In these tumors, an increase in the expression of p21 protein level and the occurrence of apoptosis were observed. These findings demonstrate for the first time that magnolol can inhibit the proliferation of tumor cells in vitro and in vivo. J. Cell. Biochem. 84: 532–544, 2002. © 2001 Wiley‐Liss, Inc.
Overexpression of murine phosphatidylinositol 4‐phosphate 5‐kinase type Iβ disrupts a phosphatidylinositol 4,5 bisphosphate regulated endosomal pathway
Authors: Galiano Floyd J. , Ulug Emin T. , Davis J. Nathan 
Published: October 2004

AbstractThe type I phosphatidylinositol 4‐phosphate 5‐kinases (PI4P5K) phosphorylate phosphatidylinositol 4‐phosphate [PI(4)P] to produce phosphatidylinositol 4,5‐bisphosphate [PI(4,5)P2]. PI(4,5)P2 has been implicated in signal transduction, receptor mediated endocytosis, vesicle trafficking, cytoskeletal structure, and membrane ruffling. However, the specific type I enzymes associated with the production of PI(4,5)P2 for the specific cellular processes have not been rigorously defined. Murine PI4P5K type Iβ (mPIP5K‐Iβ) was implicated in receptor mediated endocytosis through the isolation of a truncated and inactive form of the enzyme that blocked the ligand‐dependent downregulation of the colony‐stimulating factor‐1 receptor. The present study shows that enforced expression of mPIP5K‐Iβ in 293T cells resulted in the accumulation of large vesicles that were linked to an endosomal pathway. Similar results were obtained after the expression of the PI(4,5)P2‐binding pleckstrin homology (PH) domain of phospholipase‐Cδ (PLC‐δ). Analysis of the conserved domains of mPIP5K‐Iβ led to the identification of dimerization domains in the N‐ and C‐terminal regions. Enforced expression of the individual dimerization domains interfered with the proper subcellular localization of mPIP5K‐Iβ and the PLC‐δ‐PH domain and blocked the accumulation of the endocytic vesicles induced by these proteins. In addition to regulating early steps in endocytosis, these results suggest that mPIP5K‐Iβ acts through PI(4,5)P2 to regulate endosomal trafficking and/or fusion. J. Cell. Biochem. 85: 131–145, 2002. © 2002 Wiley‐Liss, Inc.
Osteocytes inhibit osteoclastic bone resorption through transforming growth factor‐β: Enhancement by estrogen*
Authors: Heino Terhi J. , Hentunen Teuvo A. , Väänänen H. Kalervo 
Published: October 2004

AbstractOsteocytes are the most abundant cells in bone and distributed throughout the bone matrix. They are connected to the each other and to the cells on the bone surface. Thus, they may also secrete some regulatory factors controlling bone remodeling. Using a newly established osteocyte‐like cell line MLO‐Y4, we have studied the interactions between osteocytes and osteoclasts. We collected the conditioned medium (CM) from MLO‐Y4 cells, and added it into the rat osteoclast cultures. The conditioned medium had no effect on osteoclast number in 24‐h cultures, but it dramatically inhibited resorption. With 5, 10, and 20% CM, there was 25, 39, and 42% inhibition of resorption, respectively. Interestingly, the inhibitory effect was even more pronounced, when MLO‐Y4 cells were pretreated with 10−8 M 17‐β‐estradiol. With 5, 10, and 20% CM, there was 46, 51, and 58% of inhibition. When the conditioned medium was treated with neutralizing antibody against transforming growth factor‐β (TGF‐β), the inhibitory effect was abolished. This suggests that osteocytes secrete significant amounts of TGF‐β, which inhibits bone resorption and is modulated by estrogen. RT–PCR and Western blot analysis show that in MLO‐Y4 cells, the prevalent TGF‐β isoform is TGF‐β3. We conclude that osteocytes have an active, inhibitory role in the regulation of bone resorption. Our results further suggest a novel role for TGF‐β in the regulation of communication between different bone cells and suggest that at least part of the antiresorptive effect of estrogen in bone could be mediated via osteocytes. J. Cell. Biochem. 85: 185–197, 2002. © 2002 Wiley‐Liss, Inc.
Nigericin inhibits insulin‐stimulated glucose transport in 3T3‐L1 adipocytes
Authors: Chu Chih‐Ying , Kao Ying‐Shun , Fong Jim C. 
Published: October 2004

AbstractWe used nigericin, a K+/H+ exchanger, to test whether glucose transport in 3T3‐L1 adipocytes was modulated by changes in intracellular pH. Our results showed that nigericin increased basal but decreased insulin‐stimulated glucose uptake in a time‐ and dose‐dependent manner. Whereas the basal translocation of GLUT1 was enhanced, insulin‐stimulated GLUT4 translocation was inhibited by nigericin. On the other hand, the total amount of neither transporter protein was altered. The finding that insulin‐stimulated phosphoinositide 3‐kinase (PI 3‐kinase) activity was not affected by nigericin implies that nigericin exerted its inhibition at a step downstream of PI 3‐kinase activation. At maximal dose, nigericin rapidly lowered cytosolic pH to 6.7; however, this effect was transient and cytosolic pH was back to normal in 20 min. Removal of nigericin from the incubation medium after 20 min abolished its enhancing effect on basal but had little influence on its inhibition of insulin‐stimulated glucose transport. Moreover, lowering cytosolic pH to 6.7 with an exogenously added HCl solution had no effect on glucose transport. Taken together, it appears that nigericin may inhibit insulin‐stimulated glucose transport mainly by interfering with GLUT4 translocation, probably by a mechanism not related to changes in cytosolic pH. J. Cell. Biochem. 85: 83–91, 2002. © 2002 Wiley‐Liss, Inc.
Reduced CpG methylation is associated with transcriptional activation of the bone‐specific rat osteocalcin gene in osteoblasts*
Authors: Villagra Alejandro , Gutiérrez José , Paredes Roberto , Sierra José , Puchi Marcia , Imschenetzky Maria , van Wijnen Andre , Lian Jane , Stein Gary , Stein Janet , Montecino Martin 
Published: October 2004

AbstractChromatin remodeling of the bone‐specific rat osteocalcin (OC) gene accompanies the onset and increase in OC expression during osteoblast differentiation. In osseous cells expressing OC, the promoter region contains two nuclease hypersensitive sites that encompass the elements that regulate basal tissue‐specific and vitamin D‐enhanced OC transcription. Multiple lines of evidence indicate that DNA methylation is involved in maintaining a stable and condensed chromatin organization that represses eukaryotic transcription. Here we report that DNA methylation at the OC gene locus is associated with the condensed chromatin structure found in cells not expressing OC. In addition, we find that reduced CpG methylation of the OC gene accompanies active transcription in ROS 17/2.8 rat osteosarcoma cells. Interestingly, during differentiation of primary diploid rat osteoblasts in culture, as the OC gene becomes increasingly expressed, CpG methylation of the OC promoter is significantly reduced. Inhibition of OC transcription does not occur by a direct mechanism because in vitro methylated OC promoter DNA is still recognized by the key regulators Runx/Cbfa and the vitamin D receptor complex. Furthermore, CpG methylation affects neither basal nor vitamin D‐enhanced OC promoter activity in transient expression experiments. Together, our results indicate that DNA methylation may contribute indirectly to OC transcriptional control in osteoblasts by maintaining a highly condensed and repressed chromatin structure. J. Cell. Biochem. 85: 112–122, 2002. © 2002 Wiley‐Liss, Inc.
DNA replication and nuclear architecture
Authors: Jaunin Françoise , Fakan Stanislav 
Published: October 2004

AbstractThe model of in situ DNA replication provided by immunofluorescence and confocal imaging is compared with observations obtained by electron microscopic studies. Discrepancies between both types of observations call into question the replication focus as a persistent nuclear structure and as a replication entity where DNA replication takes place. Most electron microscopic analyses reveal that replication sites are confined to dispersed chromatin areas at the periphery of condensed chromatin, and the distribution of replication factors exhibits the same localization pattern. Moreover, rapid migration of newly synthesized DNA from the replication sites towards the interior of condensed chromatin regions obviously takes place during S‐phase. It implies modifications of replication domains, hardly detectable by fluorescence microscopy. The confrontation of different observations carried out at light microscopic or electron microscopic levels of resolution lead to a conclusion that a combination of in vivo fluorescence analysis with a subsequent ultrastructural investigation performed on the same cells will represent an optimal approach in future studies of nuclear functions in situ. J. Cell. Biochem. 85: 1–9, 2002. © 2002 Wiley‐Liss, Inc.
Soluble fragment of P‐cadherin adhesion protein found in human milk
Authors: Soler Alejandro Peralta , Russo Jose , Russo Irma H. , Knudsen Karen A. 
Published: October 2004

AbstractClassical cadherins such as E‐ and P‐cadherin are transmembrane proteins that mediate specific cell‐to‐cell adhesion and are important to tissue development and function. Cadherin function can be modulated by various means, including proteolytic cleavage of the extracellular adhesion domain from the cells' surface, yielding large soluble fragments termed (soluble) sE‐ or sP‐cadherin. In people with certain carcinomas, sE‐cadherin can be detected at elevated levels in the serum and sometimes can serve as a prognostic marker. Soluble E‐cadherin also is found in urine of patients with bladder cancer. In addition to being present in bodily fluids of cancer patients, sE‐ and sP‐cadherin are present in the serum of healthy people, suggesting that shedding of cadherins is a normal event. Here, we report high levels of 80 kDa sP‐cadherin in human milk. In the lactating mammary gland tissue, P‐cadherin appears to be a protein secreted by epithelial cells, rather than an adhesion protein. This is in contrast to the non‐lactating mammary gland where P‐cadherin is restricted to myoepithelial cells, and is present at sites of cell–cell contact. J. Cell. Biochem. 85: 180–184, 2002. © 2002 Wiley‐Liss, Inc.
1‐Rotational Steiner triple systems over arbitrary groups
Authors: Buratti Marco 
Published: October 2004

AbstractPhelps and Rosa introduced the concept of 1‐rotational Steiner triple system, that is an STS(ν) admitting an automorphism consisting of a fixed point and a single cycle of length ν − 1 [Discrete Math. 33 (1981), 57–66]. They proved that such an STS(ν) exists if and only if ν ≡ 3 or 9 (mod 24). Here, we speak of a 1‐rotational STS(ν) in a more general sense. An STS(ν) is 1‐rotational over a group G when it admits G as an automorphism group, fixing one point and acting regularly on the other points. Thus the STS(ν)'s by Phelps and Rosa are 1‐rotational over the cyclic group. We denote by 𝒜1r, 𝒞1r, 𝒬1r, 𝒢1r, the spectrum of values of ν for which there exists a 1‐rotational STS(ν) over an abelian, a cyclic, a dicyclic, and an arbitrary group, respectively. In this paper, we determine 𝒜1r and find partial answers about 𝒬1r and 𝒢1r. The smallest 1‐rotational STSs have orders 9, 19, 25 and are unique up to isomorphism. In particular, the only 1‐rotational STS(25) is over SL2(3), the special linear group of dimension 2 over Z3. © 2001 John Wiley & Sons, Inc. J Combin Designs 9: 215–226, 2001
There exists no (15,5,4) RBIBD
Authors: Kaski Petteri , Östergård Patric R. J. 
Published: October 2004

AbstractAn (n, M, d)q code is a q‐ary code of length n, cardinality M, and minimum distance d. We show that there exists no (15,5,4) resolvable balanced incomplete block design (RBIBD) by showing that there exists no (equidistant) (14,15,10)3 code. This is accomplished by an exhaustive computer search using an orderly algorithm combined with a maximum clique algorithm. © 2001 John Wiley & Sons, Inc. J Combin Designs 9: 227–232, 2001
A hole‐size bound for incomplete t‐wise balanced designs
Authors: Kreher Donald L. , Rees Rolf S. 
Published: October 2004

AbstractAn incomplete t‐wise balanced design of index λ is a triple (X,H,ℬ︁) where X is a υ–element set, H is a subset of X called the hole, and B is a collection of subsets of X called blocks, such that, every t‐element subset of X is either in H or in exactly λ blocks, but not both. If H is a hole in an incomplete t‐wise balanced design of order υ and index λ, then |H| ≤ υ/2 if t is odd and |H| ≤ (υ − 1)/2 if t is even. In particular, this result establishes the validity of Kramer's conjecture that the maximal size of a block in a Steiner t‐wise balanced design is at most υ/2 if t is odd and at most (υ−1)/2 when t is even. © 2001 John Wiley & Sons, Inc. J Combin Designs 9: 269–284, 2001