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Träfflista för sökning "WFRF:(Lange U) srt2:(1996-1999)"

Sökning: WFRF:(Lange U) > (1996-1999)

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1.
  • Lange, D, et al. (författare)
  • Expression of TGF-beta related Smad proteins in human epithelial skin tumors.
  • 1999
  • Ingår i: International journal of oncology. - 1019-6439. ; 14:6, s. 1049-56
  • Tidskriftsartikel (refereegranskat)abstract
    • Members of the transforming growth factor (TGF)-beta family regulate cell growth and differentiation activating intracellular Smad proteins. Their role in skin and skin tumorigenesis is not well understood. Therefore we investigated the expression of TGF-beta type I receptor (TbetaR-I) and Smad-proteins involved in the TGF-beta-pathway, e.g. Smad2, Smad3, Smad4, Smad6 and Smad7. We examined the effects of TGF-beta1, -beta2, BMP2, BMP7 on five epithelial cell lines in vitro. TGF-beta1-mediated growth inhibition of HaCaT and HSC4 were observed with half maximal effects at approximately 7 pg ml-1 and 20 pg ml-1, respectively. However, malignant HSC2 and A431 cells were unresponsive to TGF-beta1. A differentiation was seen after 5 days in HaCaT and HSC4 cells only. We compared the reactivity with specific antisera against TbetaR-I and Smad proteins among the different skin tumors: seborrheic keratoses (SK), actinic keratoses (AK), basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). There were statistically significant differences of the ratio between the expression in tumor and that in non-tumorous epithelial cells in each tissue specimen. There was a tendency for the lower level of TbetaR-I expression of SCC compared with SK (p=0.08). This was accompanied by the decreased expression of the TbetaR-I. We found a markedly decreased expression of all antigens in BCC. conversion of normal keratinocytes to tumorigenic cells may in part be due to an acquisition of resistance to TGF-beta and loss of expression of intracellular signalling Smad proteins.
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2.
  • Lange, D, et al. (författare)
  • Autocrine endothelial regulation in brain stem vessels of newborn piglets.
  • 1999
  • Ingår i: Histology and histopathology. - 0213-3911. ; 14:3, s. 821-5
  • Tidskriftsartikel (refereegranskat)abstract
    • Vasoactive intestinal peptide (VIP) is known as a potent regulator for the development of the central nervous system (CNS). The neonatal period of brain development is characterised by rapid cellular proliferation in parallel with neuronal differentiation and angiogenesis. We examined the expression of native VIP and the VIP receptor-associated protein by immunohistochemistry as well as the expression of VIP mRNA by in situ hybridisation in the brain stem of newborn piglets. We found both the mRNA and the protein of VIP as well as the VIP receptor-associated protein in endothelial cells of veins, arteries and capillaries in the marginal zone of brain stem tissue sections, especially in pons and mesencephalon, as well as in pial vessels. The coexpression of native VIP, VIP mRNA and the VIP receptor-associated protein within the endothelium suggests the presence of an autocrine loop, which has been detected so far only in neuroblastoma cells. This expression pattern gives evidence to the immaturity of endothelial cells at birth and the presence of an adaptive response in the VIP-regulated system during the change from intra- to extrauterine life.
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4.
  • Wollina, U, et al. (författare)
  • Expression of transforming growth factor beta isoforms and their receptors during hair growth phases in mice.
  • 1996
  • Ingår i: Histology and histopathology. - 0213-3911. ; 11:2, s. 431-6
  • Tidskriftsartikel (refereegranskat)abstract
    • Transforming growth factor beta (TGF-beta) is a family of potent growth inhibitor proteins, often produced as a precursor and often secreted in a complex with the latent TGF-beta binding protein (LTBP). We investigated the expression of TGF-beta 1, -beta 2, -beta 3, LTBP, TGF-beta receptor proteins type I and type II (T beta R-I and -II) during induced hair growth in C57 BL-6 mice. We here demonstrated that TGF betas and T beta R-I are expressed in hair follicle epithelium and have found a positive reactivity for LTBP and T beta R-I in ++sebocytes. Dermal tissue was weakly stained for LTBP and TGF-beta 3. In early anagen the inner hair root sheath epithelium expressed TGF-beta 1, whereas outer hair root was positive for T beta R-I during anagen/catagen switch. T beta R-II was found in sebaceous glands without significant variations during the hair cycle. We may conclude that in follicle epithelium TGF-beta 1 is not produced in a complex together with LTBP. On the other hand, it is possible that other types of LTBP, like LTBP-2 and LTBP-3, are present, which are not detected by the antibody we used. Furthermore, a very rapid secretion of LTBP from producing cells may prevent immunohistochemical detection. TGF-beta 1 released by inner hair root sheath may regulate outer root sheath growth. A bidirectional interaction of sebocytes and hair follicle epithelium in the TGF-beta/LTBP seems possible. Sebocytes can be considered to be a target for TGFs since they express both T beta R++-I and -II. The general properties of TGF-beta as a growth inhibitor of epithelial cells may suggest a possible involvement in either the abrogation of extensive growth at the end of anagen or the initiation of catagen for the follicle epithelium as well as growth control for sebaceous glands.
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