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Importantly, this suppressive effect of miR-223-3p was compromised in COPD-derived cultures. In conclusion, we demonstrate that miR-223-3p is increased in lungs of patients with COPD and CS-exposed mice and is associated with neutrophilic inflammation. In vivo data indicate that miR-223 acts as negative regulator of acute CS-induced neutrophilic and monocytic inflammation. In vitro data suggest that miR-223-3p does so by suppressing proinflammatory airway epithelial responses, which is less effective in COPD epithelium.
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Mirjam P. Roffel
Tania Maes
Corry‐Anke Brandsma
AJP Lung Cellular and Molecular Physiology
KU Leuven
University of Groningen
University Medical Center Groningen
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Roffel et al. (Wed,) studied this question.
www.synapsesocial.com/papers/6a0256bbf8e73c25cff60247 — DOI: https://doi.org/10.1152/ajplung.00252.2021