Overexpression of AGT promotes bronchopulmonary dysplasis via the JAK/STAT signal pathway

Song, Lili; Zhang, Tiancheng; Lü, Hongyan

doi:10.18632/oncotarget.21712

Cited by 9 publications

(5 citation statements)

References 36 publications

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“…Angiotensinogen (AGT) is involved in the production of angiotensin II, which is the major mediator of the action of the rennin-angiotensin system (RAS) (51), whereas the RAS mediates the regulation of sodium homeostasis, blood pressure and inflammation (52). Overexpression of AGT activates the Jak2/STAT3 signaling pathway in cells, leading to inflammation (53). Combined with the present results, the above information allows for the speculation that AGT has a role in the pathogenesis of IBD via this signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Identification of differentially expressed genes, associated functional terms pathways, and candidate diagnostic biomarkers in inflammatory bowel diseases by bioinformatics analysis

et al. 2019

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Inflammatory bowel diseases (IBDs), including ulcerative colitis (UC) and Crohn's disease (CD), are chronic inflammatory disorders caused by genetic influences, the immune system and environmental factors. However, the underlying pathogenesis of IBDs and the pivotal molecular interactions remain to be fully elucidated. The aim of the present study was to identify genetic signatures in patients with IBDs and elucidate the potential molecular mechanisms underlying IBD subtypes. The gene expression profiles of the GSE75214 datasets were obtained from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) were identified in UC and CD patients compared with controls using the GEO2R tool. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses of DEGs were performed using DAVID. Furthermore, protein-protein interaction (PPI) networks of the DEGs were constructed using Cytoscape software. Subsequently, significant modules were selected and the hub genes were identified. In the GO and KEGG pathway analysis, the top enriched pathways in UC and CD included Staphylococcus aureus infection, rheumatoid arthritis, complement and coagulation cascades, PI3K/Akt signaling pathway and osteoclast differentiation. In addition, the GO terms in the category biological process significantly enriched by these genes were inflammatory response, immune response, leukocyte migration, cell adhesion, response to molecules of bacterial origin and extracellular matrix (ECM) organization. However, several other biological processes (GO terms) and pathways (e.g., ‘chemotaxis’, ‘collagen catabolic process’ and ‘ECM-receptor interaction’) exhibited significant differences between the two subtypes of IBD. The top 10 hub genes were identified from the PPI network using respective DEGs. Of note, the hub genes G protein subunit gamma 11 (GNG11), G protein subunit beta 4 (GNB4), Angiotensinogen (AGT), Phosphoinositide-3-kinase regulatory subunit 3 (PIK3R3) and C-C motif chemokine receptor 7 (CCR7) are disease-specific and may be used as biomarkers for differentiating UC from CD. Furthermore, module analysis further confirmed that common significant pathways involved in the pathogenesis of IBD subtypes were associated with chemokine-induced inflammation, innate immunity, adapted immunity and infectious microbes. In conclusion, the present study identified DEGs, key target genes, functional pathways and enrichment analysis of IBDs, enhancing the understanding of the pathogenesis of IBDs and also advancing the clarification of the underlying molecular mechanisms of UC and CD. Furthermore, these results may provide potential molecular targets and diagnostic biomarkers for UC and CD.

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Section: Discussionmentioning

confidence: 99%

Identification of differentially expressed genes, associated functional terms pathways, and candidate diagnostic biomarkers in inflammatory bowel diseases by bioinformatics analysis

et al. 2019

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“…Up to now, extensive research has shown that BPD has a multifactorial pathogenesis, especially imbalanced inflammation, 9 which is considered to be a major underlying mechanism. A body of inflammation‐related factors and mediators is involved in the development of BPD, such as IL1β, 27 NLRP3, 28 angiotensinogen (AGT), 29 IL‐6 30 and tumour necrosis factor α (TNF‐α) 31 . Another factor is oxidative stress that may lead to the stimulation of inflammatory cells, activation of pro‐inflammatory cytokines, impairment or apoptosis of respiratory tract epithelium 32,33 …”

Section: Discussionmentioning

confidence: 99%

Long non‐coding RNA MALAT1 targeting STING transcription promotes bronchopulmonary dysplasia through regulation of CREB

Chen

Feng

Chen

et al. 2020

J Cellular Molecular Medi

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Bronchopulmonary dysplasia (BPD) is a severe complication of preterm infants characterized by increased alveolarization and inflammation. Premature exposure to hyperoxia is believed to be a key contributor to the pathogenesis of BPD. No effective preventive or therapeutic agents have been created. Stimulator of interferon gene (STING) is associated with inflammation and apoptosis in various lung diseases. Long non‐coding RNA MALAT1 has been reported to be involved in BPD. However, how MALAT1 regulates STING expression remains unknown. In this study, we assessed that STING and MALAT1 were up‐regulated in the lung tissue from BPD neonates, hyperoxia‐based rat models and lung epithelial cell lines. Then, using the flow cytometry and cell proliferation assay, we found that down‐regulating of STING or MALAT1 inhibited the apoptosis and promoted the proliferation of hyperoxia‐treated cells. Subsequently, qRT‐PCR, Western blotting and dual‐luciferase reporter assays showed that suppressing MALAT1 decreased the expression and promoter activity of STING. Moreover, transcription factor CREB showed its regulatory role in the transcription of STING via a chromatin immunoprecipitation. In conclusion, MALAT1 interacts with CREB to regulate STING transcription in BPD neonates. STING, CREB and MALAT1 may be promising therapeutic targets in the prevention and treatment of BPD.

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“…Increased expression of AGT was demonstrated to be associated with the development and progression of bronchopulmonary dysplasia (BPD) originated from persistent ER stress. In A549 cell system AGT overexpression resulted in the inflammation via the JAK/STAT signal pathway (Shen et al, 2017). Similarly, AGT which is modulated by binding to miR-149-5p, is reported to promote the IL-6-induced inflammatory responses of chondrocytes in osteoarthritis (OA) via JAK2/STAT3 pathway (Wang et al, 2020).…”

Section: The Molecular Signature Of Adverse Reproductive Outcomesmentioning

confidence: 99%

The Secretive Liaison of Particulate Matter and SARS-CoV-2. A Hypothesis and Theory Investigation

et al. 2020

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Overexpression of AGT promotes bronchopulmonary dysplasis via the JAK/STAT signal pathway

Cited by 9 publications

References 36 publications

Identification of differentially expressed genes, associated functional terms pathways, and candidate diagnostic biomarkers in inflammatory bowel diseases by bioinformatics analysis

Identification of differentially expressed genes, associated functional terms pathways, and candidate diagnostic biomarkers in inflammatory bowel diseases by bioinformatics analysis

Long non‐coding RNA MALAT1 targeting STING transcription promotes bronchopulmonary dysplasia through regulation of CREB

The Secretive Liaison of Particulate Matter and SARS-CoV-2. A Hypothesis and Theory Investigation

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