التفاصيل البيبلوغرافية
| العنوان: |
Localized expression of tenascin in systemic sclerosis-associated pulmonary fibrosis and its regulation by insulin-like growth factor binding protein 3. |
| المؤلفون: |
Brissett, Monique, Veraldi, Kristen L., Pilewski, Joseph M., Medsger, Thomas A., Feghali-Bostwick, Carol A. |
| المصدر: |
Arthritis & Rheumatism; Jan2012, Vol. 64 Issue 1, p272-280, 9p |
| مصطلحات موضوعية: |
BIOMARKERS, ENZYME-linked immunosorbent assay, GLYCOPROTEINS, IMMUNOHISTOCHEMISTRY, PULMONARY fibrosis, RESEARCH funding, STATISTICS, SYSTEMIC scleroderma, T-test (Statistics), WESTERN immunoblotting, DATA analysis, EQUIPMENT & supplies, CONNECTIVE tissue growth factor |
| مصطلحات جغرافية: |
PENNSYLVANIA |
| مستخلص: |
Objective To determine the role of insulin-like growth factor binding protein 3 (IGFBP-3) in mediating the effects of transforming growth factor β (TGFβ) on tenascin-C (TN-C) production and to assess the levels of TN-C in vivo in patients with systemic sclerosis (SSc)-associated pulmonary fibrosis. Methods Human primary lung fibroblasts were stimulated with TGFβ or IGFBP-3 in the presence or absence of specific small interfering RNAs and chemical inhibitors of the signaling cascade. TN-C levels in lung tissue specimens obtained from patients with SSc-associated pulmonary fibrosis were assessed using immunohistochemical analysis and were compared with the levels in specimens obtained from normal donors. TN-C levels were quantified in sera from normal donors and patients with SSc with or without pulmonary fibrosis, using an enzyme-linked immunosorbent assay. Results IGFBP-3 mediated the induction of TN-C by TGFβ. Direct induction of TN-C by IGFBP-3 occurred in a p38 MAP kinase-dependent manner. TN-C levels were abundant in lung tissues from patients with SSc and were localized to subepithelial layers of the distal airways. No TN-C was detectable around the proximal airways. Patients with SSc-associated pulmonary fibrosis had significantly higher levels of circulating TN-C compared with SSc patients without pulmonary fibrosis. Longitudinal samples obtained from patients with SSc before and after the onset of pulmonary fibrosis showed increased levels of TN-C after the onset of pulmonary fibrosis. Conclusion IGFBP-3, which is overexpressed in fibrotic lungs, induces production of TN-C by subepithelial fibroblasts. The increased lung tissue levels of TN-C parallel the levels detected in the sera of SSc patients with pulmonary fibrosis, suggesting that TN-C may be a useful biomarker for SSc-related pulmonary fibrosis. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
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