Reactivity of scleroderma fibroblasts to lymphoid cell-derived fibroblast growth factor (FGF) was assessed in this study. The fibroblasts from the sclerotic lesion failed to respond to FGF, whereas those from scleroedematous lesions responded equally to normal fibroblast. Response of the fibroblast
Response of scleroderma fibroblasts to various growth factors
β Scribed by K. Takehara; Y. Soma; A. Igarashi; K. Kikuchi; A. Moro; Y. Ishibashi
- Book ID
- 104745606
- Publisher
- Springer-Verlag
- Year
- 1991
- Tongue
- English
- Weight
- 434 KB
- Volume
- 283
- Category
- Article
- ISSN
- 0340-3696
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β¦ Synopsis
Abnormal growth regulation in lesional skin fibroblasts may be related to scleroderma pathogenesis. We report on the abnormal response of cultured fibroblasts derived from sclerotic lesions to various growth factors. We investigated the responses of skin fibroblasts (10 strains) and normal fibroblasts (9 strains) to the growth factors as PDGF, TGF-beta 1, EGF and basic FGF. Experiments were conducted during the proliferation and confluent stages. PDGF, EGF and basic FGF stimulated fibroblast growth during the proliferation and confluent stages, but the response of scleroderma fibroblasts was significantly lower than that of normal fibroblasts. TGF-beta 1 slightly stimulated confluent fibroblast growth and inhibited proliferating fibroblasts, and the response of scleroderma fibroblasts exceeded that of normal fibroblasts. The decreased response to growth-stimulating factors observed in scleroderma fibroblasts suggests that cultured fibroblasts derived from scleroderma lesions were already senescent because they have been activated by growth-stimulating factors and repeatedly divided in vivo. Thus, abnormal growth regulation of skin fibroblasts may be partially related to the pathogenesis of scleroderma.
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## Abstract ## Objective As an initial approach to understanding the basis of the systemic sclerosis (SSc; scleroderma) phenotype, we sought to identify genes in the transforming growth factor Ξ² (TGFΞ²) signaling pathway that are upβregulated in lesional SSc fibroblasts relative to their normal cou