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Cigarette smoke (CS) exposure is a risk factor for many chronic diseases, including chronic obstructive pulmonary disease, but the mechanism by which smoke exposure can alter homeostasis and bring about chronic inflammation is poorly understood. Here, we showcase a novel role for smoke in regulating long noncoding RNAs, showing that it activates lincRNA-Cox2, which we previously characterized as functional in inflammatory regulation. Exposing lincRNA-Cox2 murine models to smoke in vivo confirmed lincRNA-Cox2 as a regulator of inflammatory gene expression in response to smoke both systemically and within the lung. We also report that lincRNA-Cox2 negatively regulates genes in smoked bone marrow-derived macrophages exposed to LPS stimulation. In addition to the effects on long noncoding RNAs, we also report dysregulated transcription and splicing of inflammatory proteincoding genes in the bone marrow niche after CS exposure in vivo. Collectively, this work provides insights into how innate immune signaling from gene expression to splicing is altered after in vivo exposure to CS and highlights an important new role for lincRNACox2 in regulating immune genes after smoke exposure. [ABSTRACT FROM AUTHOR]

An introduction is presented in which author discusses articles on topics including focuses on OLA-1 was first identified by the authors in 2019 as being causally linked to persistent pulmonary hypertension of the newborn via proteostatic down regulation of superoxide dismutase-2.

The article offers several information on Chronic obstructive pulmonary disease (COPD) that is currently the third leading cause of death worldwide. Topics include examines that it led to the exploration of other genetic and environmental factors that contribute to COPD pathogenesis and progression; and reports that regulator of iron metabolism, IREB2 (iron-responsive element–binding protein 2), has emerged from multiple genome-wide association studies as a COPD susceptibility gene.