Pathway centrality in protein interaction networks identifies putative functional mediating pathways in pulmonary disease. View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2019-12

AUTHORS

Jisoo Park, Benjamin J Hescott, Donna K Slonim

ABSTRACT

Identification of functional pathways mediating molecular responses may lead to better understanding of disease processes and suggest new therapeutic approaches. We introduce a method to detect such mediating functions using topological properties of protein-protein interaction networks. We define the concept of pathway centrality, a measure of communication between disease genes and differentially expressed genes. Using pathway centrality, we identify mediating pathways in three pulmonary diseases (asthma; bronchopulmonary dysplasia (BPD); and chronic obstructive pulmonary disease (COPD)). We systematically evaluate the significance of all identified central pathways using genetic interactions. Mediating pathways shared by all three pulmonary disorders favor innate immune and inflammation-related processes, including toll-like receptor (TLR) signaling, PDGF- and angiotensin-regulated airway remodeling, the JAK-STAT signaling pathway, and interferon gamma. Disease-specific mediators, such as neurodevelopmental processes in BPD or adhesion molecules in COPD, are also highlighted. Some of our findings implicate pathways already in development as drug targets, while others may suggest new therapeutic approaches. More... »

PAGES

5863

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41598-019-42299-3

DOI

http://dx.doi.org/10.1038/s41598-019-42299-3

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1113355958

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30971743


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51 schema:description Identification of functional pathways mediating molecular responses may lead to better understanding of disease processes and suggest new therapeutic approaches. We introduce a method to detect such mediating functions using topological properties of protein-protein interaction networks. We define the concept of pathway centrality, a measure of communication between disease genes and differentially expressed genes. Using pathway centrality, we identify mediating pathways in three pulmonary diseases (asthma; bronchopulmonary dysplasia (BPD); and chronic obstructive pulmonary disease (COPD)). We systematically evaluate the significance of all identified central pathways using genetic interactions. Mediating pathways shared by all three pulmonary disorders favor innate immune and inflammation-related processes, including toll-like receptor (TLR) signaling, PDGF- and angiotensin-regulated airway remodeling, the JAK-STAT signaling pathway, and interferon gamma. Disease-specific mediators, such as neurodevelopmental processes in BPD or adhesion molecules in COPD, are also highlighted. Some of our findings implicate pathways already in development as drug targets, while others may suggest new therapeutic approaches.
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