دورية أكاديمية
Inhibition of microRNA-29a alleviates hyperoxia-induced bronchopulmonary dysplasia in neonatal mice via upregulation of GAB1
| العنوان: | Inhibition of microRNA-29a alleviates hyperoxia-induced bronchopulmonary dysplasia in neonatal mice via upregulation of GAB1 |
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| المؤلفون: | Yu Hu, Liang Xie, Jing Yu, Hongling Fu, Dan Zhou, Hanmin Liu |
| المصدر: | Molecular Medicine, Vol 26, Iss 1, Pp 1-12 (2019) |
| بيانات النشر: | BMC, 2019. |
| سنة النشر: | 2019 |
| المجموعة: | LCC:Therapeutics. Pharmacology LCC:Biochemistry |
| مصطلحات موضوعية: | Bronchopulmonary dysplasia, MicroRNA-29a, GAB1, Apoptosis, Hyperoxia, MLE-12, Therapeutics. Pharmacology, RM1-950, Biochemistry, QD415-436 |
| الوصف: | Abstract Background The main features of bronchopulmonary dysplasia (BPD) are alveolar simplification, pulmonary growth arrest, and abnormal lung function. Multiple studies have highlighted microRNA-29 (miR-29) as a potential biomarker for lung diseases and cancers. Upregulation of miR-29a has been known to downregulate GRB2-associated-binding protein 1 (GAB1), which is often highly expressed in the lung. The current study was designed to investigate the potential role of miR-29a in hyperoxia-induced BPD by targeting GAB1 in a neonatal mouse model. Methods The expression of miR-29a and GAB1 in lung tissues of neonatal mice with hyperoxia-induced BPD and mouse alveolar epithelial cells (MLE-12) was determined using RT-qPCR and western blot analysis. Subsequently, the relationship between miR-29a and GAB1 was verified using in silico analysis. In order to assess the effects of miR-29a or GAB1 on BPD, the pathological characteristics of alveoli, as well as proliferation and apoptosis of cells were measured through gain- and loss-of-function studies. Results Upregulation of miR-29a and downregulation of GAB1 were evident in both lung tissues and MLE-12 cells following BPD modeling. GAB1 was a direct target gene of miR-29a. Inhibition of miR-29a and overexpression of GAB1 were shown to alleviate lung injury, promote cell proliferation and inhibit apoptosis but reduce chord length in lung tissues of neonatal mice following hyperoxia-induced BPD modeling. Conclusion Altogether, down-regulation of miR-29a can potentially elevate GAB1 expression, reducing cell apoptosis and stimulating proliferation, ultimately retarding the development of BPD in mice. This study highlights the potential of a promising new target for preventing BPD. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 1076-1551 1528-3658 |
| العلاقة: | https://doaj.org/toc/1076-1551Test; https://doaj.org/toc/1528-3658Test |
| DOI: | 10.1186/s10020-019-0127-9 |
| الوصول الحر: | https://doaj.org/article/2dc6bc3a93ac457a99940541baffee7cTest |
| رقم الانضمام: | edsdoj.2dc6bc3a93ac457a99940541baffee7c |
| قاعدة البيانات: | Directory of Open Access Journals |
Full Text Finder | تدمد: | 10761551 15283658 |
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| DOI: | 10.1186/s10020-019-0127-9 |