Air pollution-derived PM2.5 impairs mitochondrial function in healthy and chronic obstructive pulmonary diseased human bronchial epithelial cells

Nrf2 positively regulates autophagy antioxidant response in human bronchial epithelial cells exposed to diesel exhaust particles

“…PAHs and their derivatives are especially important because they are able to generate ROS in tissues 19 .Genes encoding key antioxidant enzymes are important for maintaining intracellular redox homeostasis through the antioxidant response element (ARE) found within the promoter regions of these genes 20 . The transcription factor nuclear factor erythroid-derived 2-like 2 (NFE2L2, also known as Nrf2) induces ARE genes as part of a protective response against oxidative challenge to organelles and macromolecules 21 .Recent in vivo and in vitro models have shown that the oxidative damage caused by PM exposure can activate the Nrf2-antioxidant response element signalling pathway 22,23 . Additionally, A549 cell and murine alveolar macrophage cultures exposed to DEP have shown increased Nrf2 and HO-1 (an Nrf2 target gene) expression levels 24 .There is evidence that some autophagy genes, such as Atg5, Atg4D and SQSTM1/p62, have ARE promoter regions, and these promotors may be regulated through Nrf2 activity 25 .…”

“…Recent in vivo and in vitro models have shown that the oxidative damage caused by PM exposure can activate the Nrf2-antioxidant response element signalling pathway 22,23 . Additionally, A549 cell and murine alveolar macrophage cultures exposed to DEP have shown increased Nrf2 and HO-1 (an Nrf2 target gene) expression levels 24 .…”

Mitochondrial dysfunction in endothelial cells induced by airborne fine particulate matter (<2.5 μm)

“…Mitochondria, a highly dynamic organelle, provides the main source of adenosine triphosphate (ATP) and participates in the regulation of various cellular processes, including redox homeostasis, survival, apoptosis, and signaling responses to frequently changing environmental conditions (Kluge, Fetterman, & Vita, 2013;Leclercq et al, 2018;Li et al, 2003). Besides, they undergo prominent structural changes, including fragmentation and cristae remodeling in response to the intense stimulation (Arnoult, 2007;Jin, Xue, Zhou, Su, & Li, 2018).…”

“…Growing evidence suggests that the alterations in mitochondrial structure and function lead eventually to various human diseases, including aging, cardiovascular diseases and respiratory illness (Kluge et al, 2013;Lemire, Mailloux, & Appanna, 2010;Nunnari & Suomalainen, 2012). Therefore, mitochondria can be used as important biomarkers of pollutants on human health and it is imperative to understand the effect of PM 2.5 on mitochondrial structure and function (Leclercq et al, 2018;Ning, Ji, Li, & Sang, 2019). Recent studies reported that damage to lung mitochondria may be one of the important mechanisms by which PM 2.5 induces lung injury, contributing to respiratory epithelial mitochondria could be used as important biomarkers of pollutants on human health (Leclercq et al, 2018;Li et al, 2015;Meyer et al, 2013).…”

“…Therefore, mitochondria can be used as important biomarkers of pollutants on human health and it is imperative to understand the effect of PM 2.5 on mitochondrial structure and function (Leclercq et al, 2018;Ning, Ji, Li, & Sang, 2019). Recent studies reported that damage to lung mitochondria may be one of the important mechanisms by which PM 2.5 induces lung injury, contributing to respiratory epithelial mitochondria could be used as important biomarkers of pollutants on human health (Leclercq et al, 2018;Li et al, 2015;Meyer et al, 2013). Mitochondria in ECs, which have been ignored due to their small contribution to energy production under normal physiological conditions, play very important regulatory roles in the vascular pathophysiology, considered as "frontline against vascular disease" (Davidson & Duchen, 2007), while its dysfunction would inevitably result in the collapse of endothelial homeostasis (Caja & Enríquez, 2017).…”