Network modeling predicts personalized gene expression and drug responses in valve myofibroblasts cultured with patient sera.
Jesse D RogersBrian A AguadoKelsey M WattsLivia S A PassosWilliam J RichardsonPublished in: Proceedings of the National Academy of Sciences of the United States of America (2022)
Aortic valve stenosis (AVS) patients experience pathogenic valve leaflet stiffening due to excessive extracellular matrix (ECM) remodeling. Numerous microenvironmental cues influence pathogenic expression of ECM remodeling genes in tissue-resident valvular myofibroblasts, and the regulation of complex myofibroblast signaling networks depends on patient-specific extracellular factors. Here, we combined a manually curated myofibroblast signaling network with a data-driven transcription factor network to predict patient-specific myofibroblast gene expression signatures and drug responses. Using transcriptomic data from myofibroblasts cultured with AVS patient sera, we produced a large-scale, logic-gated differential equation model in which 11 biochemical and biomechanical signals were transduced via a network of 334 signaling and transcription reactions to accurately predict the expression of 27 fibrosis-related genes. Correlations were found between personalized model-predicted gene expression and AVS patient echocardiography data, suggesting links between fibrosis-related signaling and patient-specific AVS severity. Further, global network perturbation analyses revealed signaling molecules with the most influence over network-wide activity, including endothelin 1 (ET1), interleukin 6 (IL6), and transforming growth factor β (TGFβ), along with downstream mediators c-Jun N-terminal kinase (JNK), signal transducer and activator of transcription (STAT), and reactive oxygen species (ROS). Lastly, we performed virtual drug screening to identify patient-specific drug responses, which were experimentally validated via fibrotic gene expression measurements in valvular interstitial cells cultured with AVS patient sera and treated with or without bosentan-a clinically approved ET1 receptor inhibitor. In sum, our work advances the ability of computational approaches to provide a mechanistic basis for clinical decisions including patient stratification and personalized drug screening.
Keyphrases
- aortic valve
- gene expression
- transforming growth factor
- extracellular matrix
- case report
- transcription factor
- dna methylation
- aortic stenosis
- transcatheter aortic valve replacement
- epithelial mesenchymal transition
- reactive oxygen species
- aortic valve replacement
- transcatheter aortic valve implantation
- poor prognosis
- mitral valve
- ejection fraction
- newly diagnosed
- computed tomography
- endothelial cells
- induced apoptosis
- atrial fibrillation
- machine learning
- single cell
- genome wide
- cell proliferation
- electronic health record
- idiopathic pulmonary fibrosis
- big data
- network analysis
- patient safety
- nuclear factor
- emergency department
- artificial intelligence
- toll like receptor
- endoplasmic reticulum stress
- deep learning
- pi k akt