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Fibulin-1 predicts disease progression in patients with idiopathic pulmonary fibrosis.
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- Author(s): Jaffar J;Jaffar J;Jaffar J;Jaffar J; Unger S; Unger S; Corte TJ; Corte TJ; Keller M; Keller M; Wolters PJ; Wolters PJ; Richeldi L; Richeldi L; Richeldi L; Cerri S; Cerri S; Prêle CM; Prêle CM; Prêle CM; Hansbro PM; Hansbro PM; Argraves WS; Argraves WS; Oliver RA; Oliver RA; Oliver BG; Oliver BG; Oliver BG; Black JL; Black JL; Black JL; Burgess JK; Burgess JK; Burgess JK; Burgess JK
- Source:
Chest [Chest] 2014 Oct; Vol. 146 (4), pp. 1055-1063.- Publication Type:
Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't- Language:
English - Source:
- Additional Information
- Source: Publisher: Elsevier Country of Publication: United States NLM ID: 0231335 Publication Model: Print Cited Medium: Internet ISSN: 1931-3543 (Electronic) Linking ISSN: 00123692 NLM ISO Abbreviation: Chest Subsets: MEDLINE
- Publication Information: Publication: 2016- : New York : Elsevier
Original Publication: Chicago : American College of Chest Physicians - Subject Terms: Biomarkers/*metabolism ; Calcium-Binding Proteins/*metabolism ; Fibroblasts/*metabolism ; Idiopathic Pulmonary Fibrosis/*metabolism; Aged ; Aged, 80 and over ; Australia ; Blotting, Western ; Cell Culture Techniques ; Disease Progression ; Female ; Follow-Up Studies ; Humans ; Immunohistochemistry ; Italy ; Male ; Middle Aged ; United States
- Abstract: Background: The underlying mechanisms of idiopathic pulmonary fibrosis (IPF) are unknown. This progressive disease has high mortality rates, and current models for prediction of mortality have limited value in identifying which patients will progress. We previously showed that the glycoprotein fibulin-1 is involved in enhanced proliferation and wound repair by mesenchymal cells and, thus, may contribute to lung fibrosis in IPF.
Methods: Serum, lung tissue, and lung function values were obtained from four independent locations (Sydney, NSW, and Perth, WA, Australia; San Francisco, CA; and Modena, Italy). Patients with IPF were followed for a minimum of 1 year and progression was defined as a significant decline in lung function or death. Primary parenchymal lung fibroblasts of 15 patients with and without IPF were cultured under nonstimulatory conditions. Fibulin-1 levels in serum, and secreted or deposited by fibroblasts, were measured by western blot and in lung tissue by immunohistochemistry.
Results: Serum fibulin-1 levels were increased in patients with IPF compared with subjects without lung disease (P = .006). Furthermore, tissue fibulin-1 levels were increased in patients with IPF (P = .02) and correlated negatively with lung function (r = -0.9, P < .05). Primary parenchymal fibroblasts from patients with IPF produced more fibulin-1 than those from subjects without IPF (P < .05). Finally, serum fibulin-1 levels at first blood draw predicted disease progression in IPF within 1 year (area under the curve , 0.71; 95% CI, 0.57-0.86; P = .012).
Conclusions: Fibulin-1 is a novel potential biomarker for disease progression in IPF and raises the possibility that it could be used as a target for the development of new treatments. - References: Exp Gerontol. 2007 Oct;42(10):1003-11. (PMID: 17706388)
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N Engl J Med. 2011 Apr 21;364(16):1503-12. (PMID: 21506741) - Grant Information: R01 HL095067 United States HL NHLBI NIH HHS
- Accession Number: 0 (Biomarkers)
0 (Calcium-Binding Proteins)
0 (fibulin) - Publication Date: Date Created: 20140517 Date Completed: 20141204 Latest Revision: 20240508
- Publication Date: 20240508
- Accession Number: PMC4188142
- Accession Number: 10.1378/chest.13-2688
- Accession Number: 24832167
- Source:
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