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Differential Responses to Targeting Matrix Metalloproteinase 9 in Idiopathic Pulmonary Fibrosis.
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- Author(s): Espindola, Milena S.; Habiel, David M.; Lucia Coelho, Ana; Stripp, Barry; Parks, William C.; Oldham, Justin; Martinez, Fernando J.; Noth, Imre; Lopez, David; Mikels-Vigdal, Amanda; Smith, Victoria; Hogaboam, Cory M.; Coelho, Ana Lucia
- Source:
American Journal of Respiratory & Critical Care Medicine; 2/15/2021, Vol. 203 Issue 4, p458-470, 13p- Subject Terms:
METALLOPROTEINASES; IDIOPATHIC pulmonary fibrosis; TRANSFORMING growth factors-beta; PROTEIN expression; ANIMAL models in research; THERAPEUTIC use of monoclonal antibodies; BIOLOGICAL models; RESEARCH; ANIMAL experimentation; RESEARCH methodology; PROTEOLYTIC enzymes; MONOCLONAL antibodies; MEDICAL cooperation; EVALUATION research; PROTEOMICS; COMPARATIVE studies; GENES; EPITHELIAL cells; MICE - Source:
- Additional Information
- Subject Terms:
- Abstract: Rationale: Aberrant lung remodeling in idiopathic pulmonary fibrosis (IPF) is characterized by elevated MMP9 (matrix metalloproteinase 9) expression, but the precise role of this matrix metalloproteinase in this disease has yet to be fully elucidated.Objectives: To evaluate antifibrotic effects of MMP9 inhibition on IPF.Methods: Quantitative genomic, proteomic, and functional analyses both in vitro and in vivo were used to determine MMP9 expression in IPF cells and the effects of MMP9 inhibition on profibrotic mechanisms.Measurements and Main Results: In the present study, we demonstrate that MMP9 expression was increased in airway basal cell (ABC)-like cells from IPF lungs compared with ABC cells from normal lungs. The inhibition of MMP9 activity with an anti-MMP9 antibody, andecaliximab, blocked TGF-β1 (transforming growth factor β1)-induced Smad2 phosphorylation. However, in a subset of cells from patients with IPF, TGF-β1 activation in their ABC-like cells was unaffected or enhanced by MMP9 blockade (i.e., nonresponders). Further analysis of nonresponder ABC-like cells treated with andecaliximab revealed an association with type 1 IFN expression, and the addition of IFNα to these cells modulated both MMP9 expression and TGF-β1 activation. Finally, the inhibition of MMP9 ameliorated pulmonary fibrosis induced by responder lung cells but not a nonresponder in a humanized immunodeficient mouse model of IPF.Conclusions: Together, these data demonstrate that MMP9 regulates the activation of ABC-like cells in IPF and that targeting this MMP might be beneficial to a subset of patients with IPF who show sufficient expression of type 1 IFNs. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of American Journal of Respiratory & Critical Care Medicine is the property of American Thoracic Society and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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