Proteomic Architecture of Valvular Extracellular Matrix

Bouchareb, Rihab; Guauque-Olarte, Sandra; Snider, Justin; Zaminski, Devyn; Anyanwu, Anelechi C.; Stelzer, Paul; Lebeche, Djamel

doi:10.1016/j.jacbts.2020.11.008

Cited by 34 publications

(9 citation statements)

References 40 publications

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“…Geng et al 34 demonstrated that T allele of rs2392989, the SNP locus of FNDC1, was more prone to acute otitis media, and may be associated with lower methylation level of CG05678571 and higher expression of FNDC1 gene. In 2021, Bouchareb et al 35 found that as the degree of calcification of aortic valve became more severe, the expression of FNDC1 in the extracellular matrix was increased. More interestingly, the metabolic enzymes of aortic valve were also down-regulated, leading to significant destruction of metabolic pathways.…”

Section: Discussionmentioning

confidence: 99%

FNDC1 Polymorphism (rs3003174 C > T) Increased the Incidence of Coronary Artery Aneurysm in Patients with Kawasaki Disease in a Southern Chinese Population

Lin¹,

Zhang²,

Wang³

et al. 2021

JIR

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Background A large number of studies demonstrated that the key to the occurrence and development of Kawasaki disease (KD) is the over-activation of immune cells and the generation of various inflammatory factors, leading to the imbalance of the immune system. Recently, mutations in the FNDC1 gene have been shown to be associated with inflammatory responses. However, there have been no reports on the relationship between FNDC1 gene and KD so far. Methods We enrolled 1611 controls and 1459 patients with KD, including 372 patients with coronary artery aneurysm (CAA) and 179 patients with coronary artery lesion (CAL). The relationship between FNDC1 rs3003174 polymorphism and KD with CAA or without CAA was investigated. Results This study showed no evidence that the association between FNDC1 rs3003174 C>T polymorphism and KD susceptibility was statistically significant (CT versus CC: adjusted odds ratio (OR) =0.897, 95% confidence interval (CI) =0.769–1.045, P=0.162; TT versus CC: adjusted OR=0.995, 95% CI=0.786–1.260, P=0.968; dominant model: adjusted OR=0.916, 95% CI=0.792–1.059, P=0.235; and recessive model: adjusted OR=1.055, 95% CI=0.845–1.316, P=0.638). However, our further stratified analysis in the control and KD group bore out that the incidence of TT genotype of FNDC1 rs3003174 C > T polymorphism was higher than that of CC/CT genotype in KD patients stratified by CAA (adjusted OR=1.437, 95% CI=1.034–1.996, P=0.031). Moreover, a stratified analysis of age and gender in KD patients indicated that the rs3003174 TT genotype increased the risk of CAA formation in aged ≦60 months (CC/CT vs TT: adjusted OR=1.580, 95% CI=1.106–2.259, P=0.012) and male (CC/CT vs TT: adjusted OR=1.653, 95% CI=1.101–2.481, P=0.015) KD patients. Conclusion The results of this study demonstrated that the FNDC1 rs3003174 C>T polymorphism may be a hazard factor in the formation of CAA in KD patients that was not disclosed before.

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Section: Discussionmentioning

confidence: 99%

FNDC1 Polymorphism (rs3003174 C > T) Increased the Incidence of Coronary Artery Aneurysm in Patients with Kawasaki Disease in a Southern Chinese Population

Lin¹,

Zhang²,

Wang³

et al. 2021

JIR

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“…Furthermore, MXRA5 is a new ECM biomarker for calcified aortic valves, and its increased expression level leads to aortic stenosis, which in turn induces the development of HF. [22] Lumican (LUM) is a proteoglycan secreted by the ECM that regulates collagen fibril formation and is highly expressed in HF patients and mice. NF-κB-mediated inflammation induces LUM production by cardiac fibroblasts, and increased LUM promotes raised levels of TGF-β1, exacerbates fibrosis in cardiac fibroblasts and promotes cell adhesion through the TGF-β2/Smad 2 signaling cascade promoting cell adhesion, which in turn exacerbates HF.…”

Section: Discussionmentioning

confidence: 99%

Construction and analysis of heart failure diagnosis model based on random forest and artificial neural network

Boyang

Yiping

et al. 2022

Medicine

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Heart failure is a global health problem and the number of sufferers is increasing as the population grows and ages. Existing diagnostic techniques for heart failure have various limitations in the clinical setting and there is a need to develop a new diagnostic model to complement the existing diagnostic methods. In recent years, with the development and improvement of gene sequencing technology, more genes associated with heart failure have been identified. We screened for differentially expressed genes in heart failure using available gene expression data from the Gene Expression Omnibus database and identified 6 important genes by a random forest classifier (ASPN, MXRA5, LUM, GLUL, CNN1, and SERPINA3). And we have successfully constructed a new heart failure diagnostic model using an artificial neural network and validated its diagnostic efficacy in a public dataset. We calculated heart failure-related differentially expressed genes and obtained 24 candidate genes by random forest classification, and selected the top 6 genes as important genes for subsequent analysis. The prediction weights of the genes of interest were determined by the neural network model and the model scores were evaluated in 2 independent sample datasets (GSE16499 and GSE57338 datasets). Since the weights of RNA-seq predictions for constructing neural network models were theoretically more suitable for disease classification of RNA-seq data, the GSE57338 dataset had the best performance in the validation results. The diagnostic model derived from our study can be of clinical value in determining the likelihood of HF occurring through cardiac biopsy. In the meantime, we need to further investigate the accuracy of the diagnostic model based on the results of our study.

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“…The sample size of n = 12 per group (n = 24 total) was selected based on similar prior studies on heart valves ( 52 , 53 ). This is further confirmed by power analysis showing that with regards to discovery-based proteomic analysis, N = 12/group reaches sufficient power when the confidence is set at 0.05 and fold change is over 1.2 ( 54 ).…”

Section: Methodsmentioning

confidence: 99%

Bioprosthetic heart valve structural degeneration associated with metabolic syndrome: Mitigation with polyoxazoline modification

Abramov

Xue

Zakharchenko

et al. 2022

Proc. Natl. Acad. Sci. U.S.A.

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Bioprosthetic heart valves (BHV), made from glutaraldehyde-fixed xenografts, are widely used for surgical and transcatheter valve interventions but suffer from limited durability due to structural valve degeneration (SVD). We focused on metabolic syndrome (MetS), a risk factor for SVD and a highly prevalent phenotype in patients affected by valvular heart disease with a well-recognized cluster of comorbidities. Multicenter patient data (N = 251) revealed that patients with MetS were at significantly higher risk of accelerated SVD and required BHV replacement sooner. Using a next-generation proteomics approach, we identified significantly differential proteomes from leaflets of explanted BHV from MetS and non-MetS patients (N = 24). Given the significance of protein infiltration in MetS-induced SVD, we then demonstrated the protective effects of polyoxazoline modification of BHV leaflets to mitigate MetS-induced BHV biomaterial degeneration (calcification, tissue cross-linking, and microstructural changes) in an ex vivo serum model and an in vivo with MetS rat subcutaneous implants.

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Proteomic Architecture of Valvular Extracellular Matrix

Cited by 34 publications

References 40 publications

FNDC1 Polymorphism (rs3003174 C > T) Increased the Incidence of Coronary Artery Aneurysm in Patients with Kawasaki Disease in a Southern Chinese Population

FNDC1 Polymorphism (rs3003174 C > T) Increased the Incidence of Coronary Artery Aneurysm in Patients with Kawasaki Disease in a Southern Chinese Population

Construction and analysis of heart failure diagnosis model based on random forest and artificial neural network

Bioprosthetic heart valve structural degeneration associated with metabolic syndrome: Mitigation with polyoxazoline modification

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