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  • Cell & Developmental Biology  (8)
  • Mice  (2)
  • 1995-1999  (5)
  • 1990-1994  (5)
  • 1
    Electronic Resource
    Electronic Resource
    Growth-inhibiting effect of tumor necrosis factor on human umbilical vein endothelial cells is enhanced with advancing age in vitro (1990)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 142 (1990), S. 31-38 
    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 examined the effects of in vitro aging on the growth capacity of human umbilical vein endothelial cells (HUVECs) under the influence of tumor necrosis factor (TNF) with or without interferon-γ (IFN-γ). The growth and colony-forming abilities of control cells were impaired with advancing age in vitro, especially at later stages (more than 70-80% of life span completed). It was found that treatment with TNF inhibited growth and colony-forming efficiency at any in vitro age. The effects of TNF were shown to increase with increasing in vitro age, as reflected by a more pronounced increase in doubling times, a decrease in saturation density, and a reduction in colony-forming efficiency. However, the characteristics of TNF receptors, including the dissociation constant, and the number of TNF-binding sites per cell-surface area remained rather constant. The effect of TNF was augmented by IFN-γ at a dose that alone affected growth and colony formation only slightly. The augmentation by IFN-γ was also found to depend on in vitro age; the synergy with TNF in the deterioration of colony-forming ability was observed only in “aged” cells. These results suggest that the intrinsic responsiveness of HUVECs to growth-inhibiting factors, as well as to growth-stimulating factors, changes during aging in vitro.
    Additional Material: 9 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041420105
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  • 2
    Electronic Resource
    Electronic Resource
    Endothelin modulates osteopontin and osteocalcin messenger ribonucleic acid expression in rat osteoblastic osteosarcoma cells (1993)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 53 (1993), S. 176-180 
    Details
    ISSN: 0730-2312
    Keywords: osteoblasts ; endothelin ; osteopontin ; osteocalcin ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Endothelins (ETs) are vasoconstrictive peptides produced mainly by endothelial cells. The ET receptors are expressed in many types of cells including osteoblast-like cells. The purpose of this study was to examine the effects of endothelin on the expression of osteoblastic phenotype-related genes. We found that endothelin-1 (ET-1) enhanced approximately two-fold the mRNA expression of both osteopontin and osteocalcin genes in rat osteoblastic osteosarcoma ROS17/2.8 cells. These effects were dose-dependent, peaking at 10-7 M. The ET-1 enhancement of the abundance of osteopontin and osteocalcin mRNAs was time-dependent, with a maximal effect at 24 h. ET-1 modulation of the expression of the two phenotype-related gene products of osteoblasts suggests that endothelin is one of the cytokines which modulate osteoblastic functions and that this molecule may play a role in the regulation of bone metabolism.
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240530211
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  • 3
    Electronic Resource
    Electronic Resource
    Scleraxis messenger ribonucleic acid is expressed in C2C12 myoblasts and its level is down-regulated by bone morphogenetic protein-2 (BMP2) (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 66-74 
    Details
    ISSN: 0730-2312
    Keywords: scleraxis ; C2C12 myoblasts ; mRNA ; BMP2 ; HLH-type transcription factor ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: We examined the mRNA expression of scleraxis, a non-myogenic helix-loop-helix type transcription factor in C2C12 myogenic cells. Scleraxis mRNA has been shown to be expressed in sclerotome and perichondrium of the embryos. We found that C2C12 cells express 1.2 kb scleraxis mRNA constitutively. Since BMP was reported to induce ectopic bone formation when implanted in muscle, we examined the effects of BMP on scleraxis expression. Scleraxis mRNA expression in C2C12 cells was suppressed by the treatment with BMP2. This suppression was observed at 200 ng/ml but not at the lower concentrations. BMP2 treatment suppressed scleraxis mRNA level within 24 h and lasted at least up to 48 h. Electrophoresis mobility shift assay showed that the proteins in the crude nuclear extracts prepared from C2C12 cells bound to an Scx-E-box sequence, CATGTG, which is preferentially recognized by scleraxis. This binding was competed out by 100-fold molar excess of cold Scx-E-box sequence but not by the one with mutations in the E-box. This band was supershifted by the addition of antiserum raised against scleraxis. BMP2 treatment suppressed the Scx-E binding activity in C2C12 cells. This suppression of the Scx-E-box binding activity was in parallel to the BMP2 suppression of the transcriptional activity of the Scx-E-CAT reporter gene transfected into C2C12 cells. These data indicated that although the default pathway for C2C12 cells is to differentiate into muscle cells, these cells do express non-myogenic transcription factor, scleraxis, whose expression is suppressed by BMP2. J. Cell. Biochem. 67:66-74, 1997. © 1997 Wiley-Liss, Inc.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Fibroblast growth factor downregulates expression of a basic helix-loop-helix-type transcription factor, scleraxis, in a chondrocyte-like cell line, TC6 (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 70 (1998), S. 468-477 
    Details
    ISSN: 0730-2312
    Keywords: scleraxis ; transcription factor ; FGF ; chondrocyte ; bHLH ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Scleraxis is a basic helix-loop-helix-type transcription factor that is expressed in sclerotome. Fibroblast growth factor (FGF) is one of the cytokines produced by the cells in skeletal tissues and is a potent modulator of skeletogenesis. The aim of this study was to examine the effects of FGF on the expression of scleraxis in chondrocyte-like cells, TC6. In these cells, scleraxis mRNA was constitutively expressed as a 1.2kb message at a high level in contrast to its low levels of expression in fibroblast-like cells or osteoblast-like cells. Upon treatment with FGF, scleraxis mRNA level was decreased within 12 h. This effect was at its nadir at 24 h and the scleraxis mRNA level returned to its base line level by 48 h. The FGF effect was maximal at 1 ng/ml. FGF effects on scleraxis were blocked by actinomycin D but not by cycloheximide, suggesting the involvement of transcriptional events that do not require new protein synthesis. The FGF effects on scleraxis were blocked by genistein, suggesting the involvement of tyrosine kinase in the post-receptor signaling. TGFβ treatment of TC6 cells enhanced scleraxis mRNA expression; however, combination of the saturation doses of FGF and TGFβ resulted in suppression of scleraxis mRNA level. BMP2 also suppressed scleraxis mRNA expression in TC6 cells and no further suppression was observed in combination with FGF. These results indicate that scleraxis is expressed in chondrocyte-like TC6 cells and it is one of the targets of FGF action in these cells. J. Cell. Biochem. 70:468-477. © 1998 Wiley-Liss, Inc.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Osteopontin expression and function: Role in bone remodeling (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 72 (1998), S. 92-102 
    Details
    ISSN: 0730-2312
    Keywords: osteopontin ; enhanced cell survival ; inhibition of apoptosis ; bone remodeling ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The cytokine and cell attachment protein osteopontin (OPN) is not necessary for the development and survival of mice in a clean animal facility. The primary role of OPN appears to be that of facilitating recovery of the organism after injury or infection, which generally causes an increase in its expression. It also is essential for some forms of bone remodeling. OPN stimulates cellular signaling pathways via various receptors found on most cell types and can encourage cell migration. OPN modulates immune and inflammatory responses and possibly negatively regulates Ras signaling pathways. Its apparent ability to enhance cell survival by inhibiting apoptosis may explain why the metastatic proficiency of tumor cells increases with increased OPN expression. J. Cell. Biochem. Suppls. 30/31:92-102, 1998. © 1998 Wiley-Liss, Inc.
    Additional Material: 2 Ill.
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  • 6
    Electronic Resource
    Electronic Resource
    Effects of the anabolic steroid nandrolone phenylpropionate on craniofacial growth in rats (1994)
    New York, NY : Wiley-Blackwell
    Journal of Morphology 220 (1994), S. 25-33 
    Details
    ISSN: 0362-2525
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Primary testosterone and its derivatives are anabolic steroids used in the treatment of osteoporosis and Turner syndrome. They also enhance fast-twitch muscle weight in female rats. The present study examines the effect of an anabolic steroid on craniofacial growth and development in rats. Five-week-old female Sprague-Dawley rats (125) were divided into experimental and control groups. The experimental group was injected subcutaneously with 1 mg nandrolone phenylpropionate in the interscapular region on alternate days, whereas those in the control group were injected with a vehicle, arachis oil. Rats were sacrificed at 60 and 120 days of age. Cephalometric analysis of soft X-ray cephalograms showed that chronic administration of the anabolic steroid, nandrolone phenylpropionate, resulted in: (1) about a 20% increase in body weight, (2) an increase in total skull length, (3) elongation of the maxillary and mandibular incisors, (4) an increase in the depth of the antegonial notch, and (5) downward-forward growth of the viscerocranium against the neurocranium. These results suggest that nandrolone phenylpropionate may accelerate craniofacial growth and/or induce high functional activity of the masticatory muscles in female rats. © 1994 Wiley-Liss, Inc.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jmor.1052200104
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  • 7
    Electronic Resource
    Electronic Resource
    Involvement of superoxide radicals in the mouse two-cell block (1991)
    New York, NY [u.a.] : Wiley-Blackwell
    Molecular Reproduction and Development 28 (1991), S. 356-360 
    Details
    ISSN: 1040-452X
    Keywords: Oxygen toxicity ; Superoxide dismutase ; Embryo development ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology
    Notes: The effect of oxygen toxicity on the development of mammalian embryos was asssessed by the use of superoxide dismutase (SOD), a potent scavenger of superoxide radicals. Mouse pronuclear embryos recovered 17 h after human chorionic gonadotropin (hCG) were cultured in medium BWW at 37°C under an atmosphere of 5% CO2 in air. Culture of mouse pronuclear embryos in the presence of Cu ∣ Zn-SOD (500 μg/ml) significantly increased the blastulation rate (44.6%) when compared with the control culture system (4.2%). Essentially the same effects were observed in SOD containing either Mn or Fe in the catalytic center. Heat treatment of the SOD preparation, and the addition of anti-SOD antibodies to the culture medium, significantly reduced the attenuation of the two-cell block by SOD, indicating that this effect is SOD dependent. SOD activity was detected in rabbit oviduct fluid (3,675 ± 3,084 mlU/mg protein) by electron spin resonance. These results suggest that active oxygen is involved in the two-cell block phenomenon in mouse embryos exposed to air and that SOD in the oviduct may play an important role in the protection of embryos from superoxide radicals.
    Additional Material: 4 Tab.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/mrd.1080280408
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  • 8
    Electronic Resource
    Electronic Resource
    Effects of oxygen toxicity on early development of mouse embryos (1992)
    New York, NY [u.a.] : Wiley-Blackwell
    Molecular Reproduction and Development 31 (1992), S. 28-33 
    Details
    ISSN: 1040-452X
    Keywords: Mouse embryo ; Superoxide dismutase ; Low-oxygen culture ; Two-cell block ; Oxygen radical ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology
    Notes: To examine the effects of oxygen toxicity on embryonic development, mouse pronuclear embryos were cultured under low oxygen conditions with or without superoxide dismutase (SOD), and the blastulation rate was compared with that of embryos cultured under standard conditions. The blastulation rate of mouse pronuclear embryos cultured under standard conditions was only 1.5% (2/131). This rate was increased significantly, to 28.5% (43/151), when the embryos were cultured under low oxygen conditions; and to 31.0% (35/113) when SOD (500 μg/ml) was added to the medium under standard conditions; the rate was increased to 75.2% (115/153) when the embryos were cultured under low oxygen conditions in the presence of SOD. The minimum effective concentration of SOD in the culture medium was 50 μg/ml under conditions of 5% O2. The blastulation rate was significantly decreased after 1-hr exposure of pronuclear embryos to room atmospheric oxygen concentration (20% O2), and subsequent culture under 5% O2 with SOD did not result in an improved blastulation rate. Culture with SOD under 5% O2 promoted the development of two-cell stage embryos to the blastocyst stage. When two-cell stage embryos were collected 48 hr after hCG and cultured for 66 hr, their blastulation rate was similar to that of embryos collected from mice 114 hr after hCG. These results suggested that embryonic development in vitro is greatly affected by atmospheric oxygen throughout the early embryonic stages and that this harmful effect can be prevented by culturing embryos under low oxygen conditions and in the presence of SOD.
    Additional Material: 4 Tab.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/mrd.1080310106
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  • 9
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    Altered cochlear fibrocytes in a mouse model of DFN3 nonsyndromic deafness (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-28
    Description: DFN3, an X chromosome-linked nonsyndromic mixed deafness, is caused by mutations in the BRN-4 gene, which encodes a POU transcription factor. Brn-4-deficient mice were created and found to exhibit profound deafness. No gross morphological changes were observed in the conductive ossicles or cochlea, although there was a dramatic reduction in endocochlear potential. Electron microscopy revealed severe ultrastructural alterations in cochlear spiral ligament fibrocytes. The findings suggest that these fibrocytes, which are mesenchymal in origin and for which a role in potassium ion homeostasis has been postulated, may play a critical role in auditory function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Minowa, O -- Ikeda, K -- Sugitani, Y -- Oshima, T -- Nakai, S -- Katori, Y -- Suzuki, M -- Furukawa, M -- Kawase, T -- Zheng, Y -- Ogura, M -- Asada, Y -- Watanabe, K -- Yamanaka, H -- Gotoh, S -- Nishi-Takeshima, M -- Sugimoto, T -- Kikuchi, T -- Takasaka, T -- Noda, T -- New York, N.Y. -- Science. 1999 Aug 27;285(5432):1408-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, The Cancer Institute, Japanese Foundation for Cancer Research, 1-37-1 Kami-ikebukuro, Toshima-ku, Tokyo 170-8455, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10464101" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cochlear Duct/*metabolism/pathology ; *DNA-Binding Proteins ; Deafness/genetics/*metabolism/pathology ; Ear, Inner/metabolism/pathology ; Ear, Middle/pathology ; Endolymph/metabolism ; Evoked Potentials, Auditory, Brain Stem ; Female ; Gene Expression ; Gene Targeting ; Genetic Linkage ; In Situ Hybridization ; Ion Transport ; Male ; Membrane Potentials ; Mice ; Mice, Inbred C57BL ; Mutagenesis ; *Nerve Tissue Proteins ; POU Domain Factors ; Potassium/*metabolism ; Transcription Factors/genetics/*metabolism ; X Chromosome
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 10
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    Rapid colorectal adenoma formation initiated by conditional targeting of the Apc gene (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-06
    Description: Familial adenomatous polyposis coli (FAP) is a disease characterized by the development of multiple colorectal adenomas, and affected individuals carry germline mutations in the APC gene. With the use of a conditional gene targeting system, a mouse model of FAP was created that circumvents the embryonic lethality of Apc deficiency and directs Apc inactivation specifically to the colorectal epithelium. loxP sites were inserted into the introns around Apc exon 14, and the resultant mutant allele (Apc580S) was introduced into the mouse germline. Mice homozygous for Apc580S were normal; however, upon infection of the colorectal region with an adenovirus encoding the Cre recombinase, the mice developed adenomas within 4 weeks. The adenomas showed deletion of Apc exon 14, indicating that the loss of Apc function was caused by Cre-loxP-mediated recombination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shibata, H -- Toyama, K -- Shioya, H -- Ito, M -- Hirota, M -- Hasegawa, S -- Matsumoto, H -- Takano, H -- Akiyama, T -- Toyoshima, K -- Kanamaru, R -- Kanegae, Y -- Saito, I -- Nakamura, Y -- Shiba, K -- Noda, T -- New York, N.Y. -- Science. 1997 Oct 3;278(5335):120-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Cancer Institute, Toshima-ku, Tokyo 170, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9311916" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli/*genetics ; Adenomatous Polyposis Coli Protein ; Adenoviridae/genetics ; Animals ; Colon/metabolism ; Cytoskeletal Proteins/biosynthesis ; Disease Models, Animal ; Exons ; Female ; Frameshift Mutation ; Gene Deletion ; *Gene Targeting ; *Genes, APC ; Genetic Vectors ; Germ-Line Mutation ; Homozygote ; Integrases/genetics/metabolism ; Introns ; Male ; Mice ; Mice, Inbred C57BL ; Recombination, Genetic ; *Viral Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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