The Journal of rheumatology · 2002
Enhanced expression of the receptor for granulocyte macrophage colony stimulating factor on dermal fibroblasts from scleroderma patients.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Postiglione Loredana, Montagnani Stefania, Riccio Antonio, Montuori Nunzia, Sciorio Salvatore, Ladogana Paolo, Spigna Gaetano Di, Castaldo Clotilde, Rossi Guido
Аннотация
OBJECTIVE: To elucidate events that initiate the involvement and stimulation of fibroblasts in systemic sclerosis (SSc).
METHODS: We examined 15 patients with SSc diffuse form, 15 with CREST syndrome, and 5 healthy subjects. Cultured fibroblasts obtained from skin biopsies in SSc involved and non-involved areas and norrmal skin fibroblasts were cultured with different doses of granulocyte macrophage colony stimulating factor (GM-CSF) to study the effects of this factor on the expression of GM-CSF receptor (GM-CSFR) on fibroblast proliferation and cellular adhesion structures.
RESULTS: Cultured fibroblasts obtained from biopsies of normal and SSc skin areas express GM-CSFR and such expression is increased in SSc fibroblasts. GM-CSF stimulation in vitro did not increase SSc fibroblast growth, in spite of a strongly increased expression of the GM-CSFR. The adhesion structures are always more abundant in SSc fibroblasts as compared to healthy cells and GM-CSF seems able to increase cell adhesion plaques.
CONCLUSION: We suggest that shift of fibroblasts toward a more adhesive differentiated pattern, due to or accompanied by an increased expression of GM-CSFR, may be an important event in the pathogenesis of SSc.
METHODS: We examined 15 patients with SSc diffuse form, 15 with CREST syndrome, and 5 healthy subjects. Cultured fibroblasts obtained from skin biopsies in SSc involved and non-involved areas and norrmal skin fibroblasts were cultured with different doses of granulocyte macrophage colony stimulating factor (GM-CSF) to study the effects of this factor on the expression of GM-CSF receptor (GM-CSFR) on fibroblast proliferation and cellular adhesion structures.
RESULTS: Cultured fibroblasts obtained from biopsies of normal and SSc skin areas express GM-CSFR and such expression is increased in SSc fibroblasts. GM-CSF stimulation in vitro did not increase SSc fibroblast growth, in spite of a strongly increased expression of the GM-CSFR. The adhesion structures are always more abundant in SSc fibroblasts as compared to healthy cells and GM-CSF seems able to increase cell adhesion plaques.
CONCLUSION: We suggest that shift of fibroblasts toward a more adhesive differentiated pattern, due to or accompanied by an increased expression of GM-CSFR, may be an important event in the pathogenesis of SSc.