Author(s)

Mo Liang^1#, LiLe Wang^1#, Mo Xiao², Bo Chen¹, Jie Li¹, RuiCheng Hu^1*

Affiliation(s)

¹Hunan Provincial People's Hospital (The First Affiliated Hospital of Hunan Normal University), changsha 410005, Hunan, China.

²Ningxiang People's Hospital, Ningxiang 410600, Hunan, China.

Corresponding Author

RuiCheng Hu

ABSTRACT

Objective: To determine whether cigarette smoke promotes apoptosis of human pulmonary artery endothelial cells (HPAECs) via the CCAAT/enhancer-binding protein homologous protein (CHOP) signaling pathway, and whether 4-phenylbutyric acid (4-PBA) has an inhibitory effect on this apoptosis. Methods: CHOP gene expression in HPAECs was silenced by lentiviral transfection of recombinant RNA. Both wild-type and CHOP-silenced HPAECs were divided into four groups: control group (Col group), cigarette smoke extract group (CSE group, with 10% CSE added to the medium), PBA group (PBA group, with 5 mmol/L PBA added to the medium), and CSE + PBA group (with both 10% CSE and 5 mmol/L PBA added to the medium). Cells were treated for 6, 12, and 24 hours. Endoplasmic reticulum morphology was observed by transmission electron microscopy, and cell apoptosis was analyzed by flow cytometry. CHOP protein and mRNA expression levels were detected by Western blot and real-time PCR, respectively. Results: CSE induced apoptosis in HPAECs, and the mechanism was associated with the CHOP-mediated apoptosis signaling pathway. 4-PBA reduced CSE-induced apoptosis in HPAECs. Conclusion: Cigarette smoke extract can induce apoptosis in HPAECs through the CHOP signaling pathway, and 4-PBA can attenuate this effect.

KEYWORDS

Human pulmonary artery endothelial cells; Endoplasmic reticulum stress; ER stress-induced apoptosis; CCAAT/enhancer-binding protein homologous protein; 4-phenylbutyric acid

CITE THIS PAPER

Mo Liang, LiLe Wang, Mo Xiao, Bo Chen, Jie Li, RuiCheng Hu. Cigarette smoke extract promotes apoptosis of human pulmonary arterial endothelial cells via the ER stress CHOP signaling pathway. Journal of Pharmaceutical and Medical Research. 2025, 7(1): 57-64. DOI: https://doi.org/10.61784/jpmr3034.

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