Endoplasmic reticulum stress and apoptosis via PERK-eIF2α-CHOP signaling in the methamphetamine-induced chronic pulmonary injury

Gu, Yijun; Wang, Yun; Bai, Yang; Liu, Ming; Wang, Huailiang

doi:10.1016/j.etap.2017.01.003

Cited by 30 publications

(19 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Cardiomyocytes alleviate ERs through the unfolded protein response (UPR), which is regulated by ER chaperones and folding enzymes, such as GRP78 and CHOP. The GRP78, the major ER-resident chaperone, is well known as a biomarker of ERs in the course of disease [19,20]. If sustained ERs persisted, inflammatory and apoptotic pathways are activated, including the induction of CHOP, PERK, caspase-3, caspase-12 and NF-κB [21][22][23].…”

Section: Discussionmentioning

confidence: 99%

Protective effect of FBXL10 in myocardial ischemia reperfusion injury via inhibiting endoplasmic reticulum stress

Gao

Guo

Liu

et al. 2020

Respiratory Medicine

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Protective effect of FBXL10 in myocardial ischemia reperfusion injury via inhibiting endoplasmic reticulum stress

Gao

Guo

Liu

et al. 2020

Respiratory Medicine

View full text Add to dashboard Cite

“…ERS can activate many signal pathways, PERK-eIF2α-ATF4 signaling pathway (He et al, 2016 ), PI3K-Akt-NOS pathway (Alexaki et al, 2004 ), PERK-eIF2α-CHOP signaling (Gu et al, 2017 ), IRE1α-ASK1-JNK pathway (Kong et al, 2017 ), and IRE1α-ASK1-P38 pathway (Kong et al, 2017 ) have been confirmed to be involved in ERS mediated apoptosis. And Nrf2, plays an important role in oxidative stress, also involved in ERS-mediated apoptosis (Zhang et al, 2016 ; Wang et al, 2017 ).…”

Section: Discussionmentioning

confidence: 99%

Hydrogen Sulfide Inhibits Cigarette Smoke-Induced Endoplasmic Reticulum Stress and Apoptosis in Bronchial Epithelial Cells

et al. 2017

View full text Add to dashboard Cite

Background: Apoptosis of lung structural cells contributes to the process of lung damage and remodeling in chronic obstructive pulmonary disease (COPD). Our previous studies demonstrated that exogenous hydrogen sulfide (H2S) can reduce the lung tissue pathology score, anti-inflammation and anti-oxidation effects in COPD, but the effect of H2S in regulating cigarette smoke (CS) induced bronchial epithelial cell apoptosis and the underlying mechanisms are not clear.Objectives: To investigate the effect of H2S on CS induced endoplasmic reticulum stress (ERS) and bronchial epithelial cell apoptosis.Methods: Male Sprague–Dawley rats randomly divided into four groups for treatment: control, CS, NaHS + CS, and propargylglycine (PPG) + CS. The rats in the CS group were exposed to CS generated from 20 commercial unfiltered cigarettes for 4 h/day, 7 days/week for 4 months. Since the beginning of the third month, freshly prepared NaHS (14 μmol/kg) and PPG (37.5 mg/kg) were intraperitoneally administered 30 min before CS-exposure in the NaHS and PPG groups. 16HBE cells were pretreated with Taurine (10 mM), 5 mmol/L 4-phenylbutyric acid (4-PBA) or NaHS (100, 200, and 400 μM) for 30 min, and then cells were exposed to 40 μmol/L nicotine for 72 h. ERS markers (GRP94, GRP78) and ERS-mediated apoptosis markers 4-C/EBP homologous protein (CHOP), caspase-3 and caspase-12 were assessed in rat lung tissues and human bronchial epithelial cells. The apoptotic bronchial epithelial cells were detected by Hoechst staining in vitro and TUNEL staining in vivo.Results: In CS exposed rats, peritoneal injection of NaHS significantly inhibited CS induced overexpression ERS-mediated apoptosis markers and upregulation of apoptotic rate in rat lungs, and inhibiting the endogenous H2S production by peritoneal injection of PPG exacerbated these effects. In the nicotine-exposed bronchial epithelial cells, appropriate concentration of NaHS and ERS inhibitors taurine and 4-PBA inhibited nicotine-induced upregulation of apoptotic rate and overexpression of ERS-mediated apoptosis markers.Conclusion: H2S inhibited lung tissue damage by attenuating CS induced ERS in rat lung and exogenous H2S attenuated nicotine induced ERS-mediated apoptosis in bronchial epithelial cells.

show abstract

“…Research in the past decade has established a relation between ER stress and lung fibrosis ( 115 ). CHOP, the key player in ER stress, was found to mediate methamphetamine (MA) and thrombin-induced apoptosis of AECs in chronic pulmonary injury or fibrotic lung tissue ( 116 , 117 ). Likewise, analysis of lung tissue from mouse fibrosis models induced by bleomycin (BLM) and from patients with IPF has manifested altered CHOP expression along with ER stress.…”

Section: Chop In Diseasesmentioning

confidence: 99%

Transcription Factor C/EBP Homologous Protein in Health and Diseases

et al. 2017

View full text Add to dashboard Cite

C/EBP homologous protein (CHOP), known also as DNA damage-inducible transcript 3 and as growth arrest and DNA damage-inducible protein 153 (GADD153), is induced in response to certain stressors. CHOP is universally acknowledged as a main conduit to endoplasmic reticulum stress-induced apoptosis. Ongoing research established the existence of CHOP-mediated apoptosis signaling networks, for which novel downstream targets are still being determined. However, there are studies that contradict this notion and assert that apoptosis is not the only mechanism by which CHOP plays in the development of pathologies. In this review, insights into the roles of CHOP in pathophysiology are summarized at the molecular and cellular levels. We further focus on the newest advances that implicate CHOP in human diseases including cancer, diabetes, neurodegenerative disorders, and notably, fibrosis.

show abstract

Endoplasmic reticulum stress and apoptosis via PERK-eIF2α-CHOP signaling in the methamphetamine-induced chronic pulmonary injury

Cited by 30 publications

References 47 publications

Protective effect of FBXL10 in myocardial ischemia reperfusion injury via inhibiting endoplasmic reticulum stress

Protective effect of FBXL10 in myocardial ischemia reperfusion injury via inhibiting endoplasmic reticulum stress

Hydrogen Sulfide Inhibits Cigarette Smoke-Induced Endoplasmic Reticulum Stress and Apoptosis in Bronchial Epithelial Cells

Transcription Factor C/EBP Homologous Protein in Health and Diseases

Contact Info

Product

Resources

About