LincRNA-Cox2 Regulates Smoke-induced Inflammation in Murine Macrophages. Academic Article uri icon

Overview

abstract

  • 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 protein-coding 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 lincRNA-Cox2 in regulating immune genes after smoke exposure.

publication date

  • May 1, 2023

Research

keywords

  • Pulmonary Disease, Chronic Obstructive
  • RNA, Long Noncoding

Identity

Scopus Document Identifier

  • 85159247080

Digital Object Identifier (DOI)

  • 10.1165/rcmb.2022-0413OC

PubMed ID

  • 36657060

Additional Document Info

volume

  • 68

issue

  • 5