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  • 1
    Call number: YY Diss Clau/Mag
    Keywords: DKFZ-publications / academic dissertations
    Pages: 117 p.
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    YY Diss Clau/Mag departmental collection or stack – please contact the library
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  • 2
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    Basel : Birkhäuser Verlag
    Call number: 08-AlMed
    Keywords: Neovascularization, Pathologic ; Neovascularization, Physiologic
    Pages: xiv, 307 p. : ill. (some col.)
    ISBN: 3764364599
    Signatur Availability
    08-AlMed departmental collection or stack – please contact the library
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  • 3
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1058-8388
    Keywords: Angiogenesis ; flt-1 ; flk-1 ; Mouse embryo ; Placenta ; Vasculogenesis ; VEGF ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Vascular endothelial growth factor (VEGF) is a candidate regulator of blood vessel growth during embryonic development and in tumors. To evaluate the role of VEGF receptor-1/flt-1 (VEGFR1/flt-1) in the development of the vascular system, we have characterized the murine homolog of the human flt-1 gene and have analyzed its expression pattern during mouse embryogenesis. Receptor binding studies using transfected COS cells revealed that the murine flt-1 gene encodes a high affinity receptor for VEGF. The apparent Kd for VEGF binding, as determined by Scatchard analysis, was 114 pM, demonstrating that VEGFR1/flt-1 has a higher affinity to VEGF than VEGF receptor-2/flk-1 (VEGFR2/flk-1). By in situ hybridization, VEGFR1/flt-1 was detected in the yolk sac mesoderm already at the early stages of vascular development, while the receptor ligand was expressed in the entire endoderm of 7.5-day mouse embryos. A comparison with VEGFR2/flk-1 showed that the two receptors shared a common expression domain in the yolk sac mesoderm, but were expressed at different sites in the ectoplacental cone. The differential expression of the two VEGF receptors persisted in the developing placenta, where VEGFR1/flt-1 mRNA was detected in the spongiotrophoblast layer, whereas VEGFR2/flk-1 transcripts were present in the labyrinthine layer which is the site of VEGF expression. In the embryo proper, VEGFR1/flt-1 mRNA was specifically localized in blood vessels and capillaries of the developing organs, closely resembling the pattern of VEGFR2/flk-1 transcript distribution. In the developing brain, the expression of VEGF receptors in the perineural capillary plexus and in capillary sprouts which have invaded the neuroectoderm correlated with endothelial cell proliferation and brain angiogenesis. The data are consistent with the hypothesis that VEGF and its receptors have an important function both in the differentiation of the endothelial lineage and in the neovascularization of developing organs, and act in a paracrine fashion. © 1995 wiley-Liss, Inc.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Apoptosis 5 (2000), S. 141-151 
    ISSN: 1573-675X
    Keywords: Brain ; EMAP II ; immunosurveillance ; monocytes ; tRNA multi-synthetase complex
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Endothelial monocyte-activating polypeptide II (EMAP II) is a chemoattractant for monocytes and granulocytes. EMAP II is translated as a precursor protein, proEMAP II, and is proteolytically cleaved to become the mature, biologically active cytokine. In this study we show that the EMAP II mRNA and the EMAP II precursor protein are constitutively expressed by all cell types analyzed in vitro, whereas the mature cytokine is only present in the supernatant of apoptotic cells. During mouse embryogenesis we found widespread expression of the EMAP II mRNA with transcripts being abundant in areas of tissue remodeling, where a large number of apoptotic cells could be detected by TUNEL staining. In the adult mouse, strong expression of the EMAP II mRNA is restricted to the brain, testis and thymus. Interestingly, prominent signals for EMAP II mRNA are found in local correlation with sites of apoptosis in thymus and testis but not in the brain. We propose that during development, the generation and release of the mature EMAP II may provide a mechanism for the recruitment of phagocytic cells to sites of programmed cell death. In the adult brain, the generation of mature EMAP II may contribute to the recruitment of monocytes and the immunosurveillance of this tissue.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Epidermal G1-chalone and transforming growth factor-β (TGFβ), two endogenous inhibitors of epidermal cell proliferation, were compared with regard to several effects on epidermis in vivo and in vitro. Both factors inhibited DNA labeling in a rat tongue epithelial cell line, with similar kinetics and half-maximal effects at approximately 1 pg/ml (enriched chalone) and 1 ng/ml (TGFβ). For primary neonatal mouse keratinocytes, (TGFβ) was found to be a rather strong inhibitor of cell proliferation, whereas chalone showed only a weak effect on cells grown in medium containing 1.2 mM Ca2+ and no effect at all in the presence of 0.06 mM Ca2+. Vice versa, upon i.p. injection, only chalone was able to inhibit mouse epidermal DNA synthesis in vivo, whereas TGFβ had no effect at all. A moderate increase of transglutaminase activity in neonatal primary mouse keratinocytes was induced by both factors at concentrations of about 300 pg TGFβ/ml and 10 pg chalone fraction/ml. Chalone did not compete with [125]TGFβ for specific binding sites on primary murine keratinocytes. A polyclonal "chalone antiserum" did not interact with TGFβ, and a neutralizing TGFβ antibody that inhibited the effect of TGFβ on cell proliferation could not block the inhibitory effect of chalone on RTE2 cells. In contrast to TGFβ, epidermal G1-chalone did not induce proliferation of NIH-3T3 cells. These results indicate that epidermal G1-chalone and TGFβ are two different inhibitors of epidermal cell proliferation.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
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