Unlocking TB-COPD Pathogenesis: A Biotechnological Approach Targeting the PI3K/Akt Pathway
Jin Dai1,2,3, Zheng Li2,3, Jing Jing2,3
1Xinjiang Medical University, Urumqi 830000, Xinjiang Uygur Autonomous Region; China.
Background:
tuberculosis (tb)-health problems caused by chronic obstructive pulmonary disease (copd), as one of the important problems facing global public health, highlight its far-reaching effects. The pi3k/akt signaling pathway is implicated in inflammatory responses and cellular survival, suggesting its potential role in tb-copd pathogenesis.
Objective:
This study integrated computational and experimental biotechnology approaches to identify key molecular mechanisms linking tb and copd, with a focus on the pi3k/akt signaling pathway.
Materials And Methods:
By analyzing two publicly available gene expression datasets (gse42057, gse83456), weighted network gene coexpression analysis technology was applied to identify differently expressed genes and key coexpression modules to explore their potential biological relevance and functional associations in more depth. Functional enrichment analysis (go/kegg) was performed to assess pathway involvement. Experimentally, a mycobacterium tuberculosis-infected bronchial epithelial cell model (16hbe) was established, and the pi3k/akt inhibitor ly294002 was utilized to evaluate its effects on apoptosis, proliferation, and epithelial-mesenchymal transition (emt) markers.
Results:
Weighted correlation network analysis (Wgcna) identified a key module significantly enriched in pi3k/akt signaling. Experimental validation demonstrated that ly294002 treatment significantly improved cell survival (p < 0.05), reduced apoptosis, and restored epithelial integrity. It was found that an increase in epithelial cadherin expression levels was accompanied by a decrease in neuronal cadherin expression levels. This dynamic change shows that the characteristics and patterns of cell adhesion can significantly adapt to certain physiological or pathological processes. Furthermore, ly294002 suppressed pi3k/akt mrna expression and phosphorylation (p < 0.05), confirming pathway inhibition.
Conclusion:
This study provides a novel biotechnological perspective on the role of pi3k/akt signaling in tb-COPD, highlighting its potential as a therapeutic target. The integrative use of bioinformatics and experimental validation strengthens our understanding of molecular pathogenesis,opens the way to precision medicine strategies in the treatment of respiratory diseases.
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