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  • Key words: apoptosis, articular chondrocyte, osteoarthritis, rheumatoid arthritis  (1)
  • bullous pemphigoid  (1)
  • gene activation  (1)
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  • 1
    ISSN: 1436-2023
    Schlagwort(e): Key words: apoptosis, articular chondrocyte, osteoarthritis, rheumatoid arthritis
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract: To investigate the relationship of chondrocyte apoptosis and cartilage destruction, we performed in situ nick end labeling (ISNEL), electron microscopy, and im-munohistochemistry against apoptosis-related proteins, p53 and c-myc, in the articular cartilages of patients with rheumatoid arthritis (RA; n = 12) and osteoarthritis (OA; n = 12), and in control articular cartilages from patients with femoral neck fracture (n = 8). The distribution of stained chondrocytes was evaluated semiquantitatively in relation to the degree of cartilage destruction. ISNEL-positive chondrocytes with apoptotic morphological features were identified in a relatively early phase of cartilage destruction, and correlated positively and significantly in a number with the degree of cartilage degeneration. Comparison of RA and OA revealed a significantly greater number of ISNEL-positive chondrocytes in RA cartilage. In contrast, the specimens of normal subjects contained few cells with apoptotic changes. Similarly to the distribution of ISNEL staining, the expression of p53 and c-myc proteins was observed in chondrocytes within the degraded lesions, and showed a positive correlation with the number of ISNEL-stained cells. These results suggest that the degree of chondrocyte apoptosis is closely related to cartilage destruction and that chondrocytes in RA more readily undergo apoptosis than those in OA. The expression of p53 and c-myc proteins in ISNEL-positive areas may reflect the involvement of these proteins in the apoptotic process in articular chondrocytes in inflammatory arthritis.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    Digitale Medien
    Digitale Medien
    New York, NY [u.a.] : Wiley-Blackwell
    Cell Biochemistry and Function 16 (1998), S. 107-116 
    ISSN: 0263-6484
    Schlagwort(e): ultraviolet ; in situ hybridization ; in situ nick translation ; bullous pemphigoid ; gene activation ; Chemistry ; Biochemistry and Biotechnology
    Quelle: Wiley InterScience Backfile Collection 1832-2000
    Thema: Biologie , Medizin
    Notizen: Bullous pemphigoid (BP) is an autoimmune blistering disease and is a photoaggravated dermatosis, but the mechanism of the aggravation is still unknown. Since damage to DNA initiates transcription of some genes, we investigated in epidermis of mouse ears the relationship between DNA damage by ultraviolet (UV) radiation and BP antigen (BP-Ag) gene activation. For this, albino male mice were irradiated with 254 nm wavelength UV for a total dose of 500 J m-2. At fixed times (0·5, 2, 24, 48 and 72 h) post-UV irradiation, mouse ears were cut off, frozen and sectioned. In the sections, it was found that immunohistochemically detectable pyrimidine dimers were observed in nuclei of all epidermal cells at 0·5 h that were almost repaired by 72 h; a frequency of single strand breaks in DNA detected by in situ nick translation started to increase in nuclei of all epidermal cell layers at 0·5 h and the increase continued up to 24 h; mRNA for BP-Ag localized by non-radioactive in situ hybridization appeared in nuclei of basal cells at 0·5 h and in both nuclei and cytoplasm at 2 h; and immunoreactive BP-Ag started to increase in the basal cell cytoplasm and in the basement membrane zone at 2 h. BP-Ag started to accumulate in the basement membrane zone at 2 h. It is suggested that UV radiation increased BP-Ag synthesis through BP-Ag gene activation and that this reaction is a factor which aggravates BP following UV irradiation in BP patients. © 1998 John Wiley & Sons, Ltd.
    Zusätzliches Material: 4 Ill.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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