Revealing hub pathway cross-talk for premature newborns with bronchopulmonary dysplasia by the integration of pathway analysis and Monte Carlo Cross-Validation

Wang,Chengbin; Zhu,Bin; Chen,Ming; Chen,Gaoyan; Xu,Muzhen; Pan,Rui

doi:10.3892/etm.2019.7257

Revealing hub pathway cross-talk for premature newborns with bronchopulmonary dysplasia by the integration of pathway analysis and Monte Carlo Cross-Validation

Authors:
- Chengbin Wang
- Bin Zhu
- Ming Chen
- Gaoyan Chen
- Muzhen Xu
- Rui Pan
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Affiliations: Department of Pediatrics, Xiangyang Central Hospital, Hubei University of Arts and Science, Xiangyang, Hubei 441021, P.R. China
Published online on: February 12, 2019 https://doi.org/10.3892/etm.2019.7257
Pages: 2715-2719

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Abstract

The objective of this study was to reveal hub pathway cross‑talk for premature newborns with bronchopulmonary dysplasia (BPD) based on the pathway enrichment analysis and Monte Carlo Cross‑Validation (MCCV) method. The inference of key pathway cross‑talk consisted of four parts: i) Identifying differentially expressed genes (DEGs); ii) detecting differentially expressed pathways (DEPs); iii) computing discriminating score (DS) for each pair of DEPs or cross‑talk and investigating seed cross‑talk through the random forest (RF) algorithm and iv) extracting hub cross‑talk dependent on the MCCV method. The results showed that a total of 132 DEGs and 137 DEPs were obtained across BPD patients and normal controls. Using the DS and RF algorithm, 10 seed DEP cross‑talk were detected. By conducting the MCCV on seed cross‑talk, 3 hub cross‑talk for BPD were uncovered: i) The pair of pathways role of interleukin‑17F (IL‑17F) in allergic inflammatory airway diseases and role of IL‑17A in psoriasis; ii) the pair of pathways role of IL random forest 17A in psoriasis and IL‑17A signaling in fibroblasts and ii) the pair of pathways IL‑17A signaling in airway cells and role of hypercytokinemia/hyperchemokinemia in the pathogenesis of influenza. These 3 hub cross‑talk among DEPs might give an insight to reveal the molecular mechanism underlying the premature newborns with BPD.

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