<p>The Protective Effect of HBO1 on Cigarette Smoke Extract-Induced Apoptosis in Airway Epithelial Cells</p>

• DOI: 10.2147/copd.s234634
• Publication Date: 2020-01-05T19:56:30Z
• Authors: Lin Chen; Lijuan Luo; Naixin Kang; Xue He; Tiao Li; Yan Chen
• Keywords: Terminal deoxynucleotidyl transferase; Pathogenesis

Purpose: Epigenetic modification is one of most important mechanisms underlying the pathogenesis chronic obstructive pulmonary disease (COPD).The purpose this study was to determine whether histone acetyltransferase binding ORC1 (HBO1) can protect against cigarette smoke (CS)-induced cell apoptosis and sustain normal acetylation in COPD.Methods: Human lung tissue samples were obtained from patients who underwent resection.The emphysema mouse model HBO1 overexpressing mice each established by intraperitoneal injection with extract (CSE) or intratracheal lentiviral vectors instillation.TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labeling) assays used assess apoptotic ratio mice.The human bronchial epithelial cells (HBECs) assayed flow cytometry.HBO1, B-cell lymphoma-2 (BCL-2), H3K14ac protein expression detected Western blotting.HBO1 mRNA measured quantitative real-time polymerase chain reaction.Results: Protein decreased significantly COPD CSE-treated models.Overexpression attenuated CSE-induced emphysematous changes, as well lungs mice.In vitro, degraded a time-and dose-dependent course CSE treatment.With cytometry, we proved that could reverse HBECs induced CSE.Furthermore, overexpression promoted antiapoptotic BCL-2 enhanced H3K14 airway cells.Conclusion: These findings demonstrate key modulator plays protective role may shed light on potential therapeutic targets inhibit progress COPD.