A. Blumental-Perry Pages 883 - 898 ( 16 )
Cigarette smoke (CS) is a risk factor for the development of chronic obstructive pulmonary disease (COPD). Oxidative stress is an immediate result of CS exposure and has the ability to modify cellular proteins. The endoplasmic reticulum (ER) is a compartment where early steps of synthesis and folding of membrane and secretory proteins takes place. Oxidative stress has been shown to interfere with protein folding in the ER and elicits the unfolded protein response (UPR). The UPR is a massive endoplasmic reticulum to the nucleus and the cellular kinase cascades signaling pathway. The UPR triggers a series of intracellular events that aim to help cells overcome the consequences of the stress or eliminate rogue cells by altering expression of genes involved in anti-oxidant defense, cell cycle progression, inflammation, and apoptosis. Recent data demonstrate that CS induces the UPR in vitro and in vivo. The timing of UPR induction in smokers and the mechanism of CS-induced UPR are areas of active investigation. The role of UPR in the protection of smoker’s lungs from CS-induced oxidative stress, and its contribution to CS-induced apoptosis and inflammation, is beginning to emerge. This review discusses recent data about UPR in COPD and summarizes findings on UPR that have potential relevance to COPD.
Apoptosis, COPD, cigarette smoking, endoplasmic reticulum, inflammation, oxidative damage, proteostasis network, UPR, chronic obstructive pulmonary disease, emphysema, reactive oxidant species, oxidative stress, tissue repair, proteasome activity, autophagy
Department of Biomedical Sciences, Mercer University School of Medicine (Savannah Campus) and Curtis and Elizabeth Anderson Cancer Institute, Memorial University Medical Center, 4700 Waters Avenue, Savannah, GA 31405, USA.