Role of reciprocal interaction between autophagy and endoplasmic reticulum stress in apoptosis of human bronchial epithelial cells induced by cigarette smoke extract

Abstract

Endoplasmic reticulum stress (ERS)‐induced apoptosis of airway epithelial cells plays an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). Furthermore, autophagy is closely related to ERS under apoptosis. Here, this study aimed to investigate the role of the reciprocal interaction between autophagy and ERS in the cigarette smoke extract (CSE)‐induced apoptosis of human bronchial epithelial (HBE) cells. Cell apoptosis was detected by flow cytometry analysis. Protein expression was examined by Western blot. The mRNA expression was detected using real‐time quantitative reverse transcription PCR (qRT‐PCR). The results showed that CSE treatment induced apoptosis, autophagy, and expression of ERS‐related proteins in HBE cells. Furthermore, autophagy inhibition by 3‐MA significantly decreased protein expression of GRP78, p‐PERK, and p‐eIF2α and increased CHOP, ATF4, and caspase‐4, whereas ERS inhibition by 4‐PBA led to autophagy suppression. Moreover, the CSE‐induced autophagy was diminished by knockdown of GRP78, PERK, or eIF2α but enhanced by knockdown of ATF4 or CHOP; however, the CSE‐induced HBE apoptosis was enhanced by knockdown of GRP78, PERK, or eIF2α but was attenuated by knockdown of ATF4 or CHOP. Additionally, both sodium hydrosulfide (NaHS) and melatonin attenuated the CSE‐induced apoptosis, enhanced the CSE‐induced autophagy, increased GRP78, p‐PERK, and p‐eIF2α, and decreased CHOP, ATF4, and caspase‐4, via SIRT1/ORP150 pathway. Collectively, this study provided evidence about the role of the reciprocal interaction between autophagy and ERS in CSE‐induced apoptosis of HBE cells. © 2018 IUBMB Life, 71(1):66–80, 2019

Alantolactone suppresses inflammation, apoptosis and oxidative stress in cigarette smoke-induced human bronchial epithelial cells through activation of Nrf2/HO-1 and inhibition of the NF-κB pathways

“…4 a and b, p < 0.05). Because of evidence showing that airway epithelial cell apoptosis was implicated in the pathogenesis of COPD [25], we next examined the role of ALT in CSE-induced Beas-2B and NHBE cells apoptosis. As shown in Fig.…”

Exosomes derived from T regulatory cells relieve inflammatory bowel disease by transferring miR‐195a‐3p

“…Exosomes have been proposed as a novel mechanism underlying the action of Tregs. Studies have confirmed that Treg-Exo have therapeutic effects on multiple sclerosis, 17 organ transplantation, 10 and so on. Here, we further demonstrated the therapeutic effects of Treg-Exo on IBD.…”

“…More and more studies have shown that Tregs can produce exosomes to regulate the function of effector T cells, thereby maintaining self-immune tolerance and regulating immune responses. 9,10 Exosomes, the nanosized (30-150 nm) vesicles released from various cell types, have recently emerged as crucial mediators of intercellular communication by transmitting bioactive molecules, such as lipids, proteins, and nucleic acids, from parent to recipient cells. 11,12 Recently, Chen et al reported that exosomes derived from CD4 + CD25 + Treg cells (Treg-Exo) could prolong liver allograft survival.…”

“…11,12 Recently, Chen et al reported that exosomes derived from CD4 + CD25 + Treg cells (Treg-Exo) could prolong liver allograft survival. 10 However, whether Treg-Exo can produce a therapeutic effect on IBD is unclear.…”

Fengbaisan suppresses endoplasmic reticulum stress by up-regulating SIRT1 expression to protect rats with chronic obstructive pulmonary diseases

“…Recent evidence suggests that SIRT1 plays a key role in the control of COPD by regulating ERS and autophagy-mediated apoptosis (He et al 2019a). Hydrogen treatment reduces the expression of CHOP, GRP78 and alleviates hyperoxic acute lung injury related-ERS in rats (Sun et al 2017).…”