CircABCB10 Promotes the Apoptosis and Inflammatory  Response of 16HBE Cells by Cigarette Smoke Extract by  Targeting miR-130a/PTEN Axis

Changping  Yun; Yuguang  Wang; Dongxu  Wang; Jialin  Zang; Zhen  Lv; Ruinan  Liu; Houyi  Cong

doi:10.18502/ijph.v53i3.15141

Changping Yun Department of Respiration, The Second Affiliated Hospital of Qiqihar Medical University, Qiqihar 161000, China
Yuguang Wang CT Room, the Second Affiliated Hospital of Qiqihar Medical University, Qiqihar 161000, China
Dongxu Wang CT Room, the Second Affiliated Hospital of Qiqihar Medical University, Qiqihar 161000, China
Jialin Zang CT Room, the Second Affiliated Hospital of Qiqihar Medical University, Qiqihar 161000, China
Zhen Lv School of Pharmacy, Qiqihar Medical University, Qiqihar 161000, China
Ruinan Liu CT Room, the Second Affiliated Hospital of Qiqihar Medical University, Qiqihar 161000, China
Houyi Cong CT Room, the Second Affiliated Hospital of Qiqihar Medical University, Qiqihar 161000, China

DOI: https://doi.org/10.18502/ijph.v53i3.15141

Keywords: Apoptosis; Immunology; Cells; Chronic obstructive pulmonary disease

Abstract

Background: Chronic obstructive pulmonary disease (COPD) has become a global public health problem due to its high mortality. So there is an urgent need to find an effective treatment.

Methods: The targeting relationship among circABCB10, miR-130a and PTEN was predicted by the targetscan database (TargetScanHuman 8.0, https://www.targetscan.org/vert_80/). A total of 60 patients which were from the second affiliated hospital of Qiqihar Medical University from 2022 to 2023 were enrolled. The lung condition was detected by CT (Computed Tomography). The expression levels of circABCB10, miR-130a and PTEN in lung tissues were determined by qRT-PCR. The COPD model was established by stimulating normal and silenced 16HBE cells in circABCB10 genes with cigarette smoke extract (CSE) at different concentrations. qRT-PCR was conducted for the expression levels of circABCB10, miR-130a and PTEN, WB for the expression levels of apoptotic proteins, ELISA for the content of inflammatory factors, and CCK8 for the effect of CSE on the proliferation of cells.

Results: CircABCB10 expression increased in lung tissues from patients with COPD and in 16HBE cells treated with CSE. The stimulation on cells with CSE increased the expression of inflammatory factors, while knocking down circABCB10 could reverse this response. The inflammatory response to the knockdown of circABCB10 was reversed by miR-130a inhibitor, which increased the expression of c-caspase 3. The targetscan database predicted the target factor downstream miR-130a was PTEN. Transfecting OE-PTEN reversed the inflammation of knocking down circABCB10, and increased the apoptosis and inflammation.

Conclusion: CircABCB10 can cause the inflammatory response by targeting miR-130a/PTEN axis, which is a mechanism that may lead to the occurrence and development of COPD.