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Published on: January 10, 2015
CircABCB10 Promotes the Apoptosis and Inflammatory Response of 16HBE Cells by Cigarette Smoke Extract by Targeting
Changping Yun1, Yuguang Wang2, Dongxu Wang2
1Department of Respiration, The Second Affiliated Hospital of Qiqihar Medical University, Qiqihar 161000, China.
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.
Insights
Circular RNA ABCB10 (circABCB10) promotes chronic obstructive pulmonary disease (COPD) by targeting the miR-130a/PTEN axis, driving inflammation and apoptosis. This finding offers a potential therapeutic target for COPD treatment.
Area of Science:
- Molecular Biology
- Cell Biology
- Pulmonology
Background:
- Chronic obstructive pulmonary disease (COPD) presents a significant global health challenge due to high mortality rates.
- Effective therapeutic strategies for COPD remain urgently needed.
Purpose of the Study:
- To investigate the role of circABCB10 in the pathogenesis of COPD.
- To elucidate the molecular mechanism involving circABCB10, miR-130a, and PTEN in COPD development.
Main Methods:
- Predicted the circABCB10, miR-130a, and PTEN targeting relationship using the TargetScan database.
- Analyzed circABCB10, miR-130a, and PTEN expression in lung tissues of COPD patients and CSE-treated 16HBE cells via qRT-PCR.
- Assessed inflammatory factors, apoptotic proteins, and cell proliferation using ELISA, Western Blot, and CCK8 assays, respectively.
Main Results:
- CircABCB10 expression was elevated in COPD lung tissues and CSE-exposed 16HBE cells.
- Knockdown of circABCB10 reduced CSE-induced inflammation, an effect reversed by miR-130a inhibition.
- Overexpression of PTEN counteracted the effects of circABCB10 knockdown, modulating inflammation and apoptosis.
Conclusions:
- CircABCB10 exacerbates inflammatory responses in COPD by targeting the miR-130a/PTEN axis.
- The circABCB10/miR-130a/PTEN pathway represents a potential therapeutic target for managing COPD.
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