Knockdown of Sfrp4 attenuates apoptosis to protect against myocardial ischemia/reperfusion injury

Zeng, Wenhui; Cao, Yan‐Zhong; Jiang, Wanli; Kang, Ganjun; Huang, Jie; Xie, Songping

doi:10.1016/j.jphs.2019.04.003

Cited by 33 publications

(25 citation statements)

References 24 publications

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“…HBA2 and HBA1 have a key role in hypertension [ 41 ], but these genes might be linked with development HF. SFRP4 was linked with progression of myocardial ischemia [ 42 ]. Emmens et al [ 43 ] and Broch et al [ 44 ] found that PENK (proenkephalin) and IL1RL1 were up regulated in HF.…”

Section: Discussionmentioning

confidence: 99%

Identification of candidate biomarkers and therapeutic agents for heart failure by bioinformatics analysis

Kolur¹,

Vastrad²,

Vastrad

et al. 2021

BMC Cardiovasc Disord

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Introduction Heart failure (HF) is a heterogeneous clinical syndrome and affects millions of people all over the world. HF occurs when the cardiac overload and injury, which is a worldwide complaint. The aim of this study was to screen and verify hub genes involved in developmental HF as well as to explore active drug molecules. Methods The expression profiling by high throughput sequencing of GSE141910 dataset was downloaded from the Gene Expression Omnibus (GEO) database, which contained 366 samples, including 200 heart failure samples and 166 non heart failure samples. The raw data was integrated to find differentially expressed genes (DEGs) and were further analyzed with bioinformatics analysis. Gene ontology (GO) and REACTOME enrichment analyses were performed via ToppGene; protein–protein interaction (PPI) networks of the DEGs was constructed based on data from the HiPPIE interactome database; modules analysis was performed; target gene—miRNA regulatory network and target gene—TF regulatory network were constructed and analyzed; hub genes were validated; molecular docking studies was performed. Results A total of 881 DEGs, including 442 up regulated genes and 439 down regulated genes were observed. Most of the DEGs were significantly enriched in biological adhesion, extracellular matrix, signaling receptor binding, secretion, intrinsic component of plasma membrane, signaling receptor activity, extracellular matrix organization and neutrophil degranulation. The top hub genes ESR1, PYHIN1, PPP2R2B, LCK, TP63, PCLAF, CFTR, TK1, ECT2 and FKBP5 were identified from the PPI network. Module analysis revealed that HF was associated with adaptive immune system and neutrophil degranulation. The target genes, miRNAs and TFs were identified from the target gene—miRNA regulatory network and target gene—TF regulatory network. Furthermore, receiver operating characteristic (ROC) curve analysis and RT-PCR analysis revealed that ESR1, PYHIN1, PPP2R2B, LCK, TP63, PCLAF, CFTR, TK1, ECT2 and FKBP5 might serve as prognostic, diagnostic biomarkers and therapeutic target for HF. The predicted targets of these active molecules were then confirmed. Conclusion The current investigation identified a series of key genes and pathways that might be involved in the progression of HF, providing a new understanding of the underlying molecular mechanisms of HF.

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Section: Discussionmentioning

confidence: 99%

Identification of candidate biomarkers and therapeutic agents for heart failure by bioinformatics analysis

Kolur¹,

Vastrad²,

Vastrad

et al. 2021

BMC Cardiovasc Disord

View full text Add to dashboard Cite

show abstract

“…HBA2 and HBA1 have a key role in hypertension [32], but these genes might be linked with development HF. SFRP4 was linked with progression of myocardial ischemia [33]. Emmens et al [34] and Broch et al [35] found that PENK (proenkephalin) and IL1RL1 were up regulated in HF.…”

Section: Discussionmentioning

confidence: 99%

Identification of candidate biomarkers and therapeutic agents for heart failure by bioinformatics analysis

Vastrad¹,

Tengli

Vastrad³

2021

Preprint

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Heart failure (HF) is a heterogeneous clinical syndrome and affects millions of people all over the world. HF occurs when the cardiac overload and injury, which is a worldwide complaint. The aim of this study was to screen and verify hub genes involved in developmental HF as well as to explore active drug molecules. The expression profiling by high throughput sequencing of GSE141910 dataset was downloaded from the Gene Expression Omnibus (GEO) database, which contained 366 samples, including 200 heart failure samples and 166 non heart failure samples. The raw data was integrated to find differentially expressed genes (DEGs) and were further analyzed with bioinformatics analysis. Gene ontology (GO) and REACTOME enrichment analyses were performed via ToppGene; protein-protein interaction (PPI) networks of the DEGs was constructed based on data from the HiPPIE interactome database; modules analysis was performed; target gene - miRNA regulatory network and target gene - TF regulatory network were constructed and analyzed; hub genes were validated; molecular docking studies was performed. A total of 881 DEGs, including 442 up regulated genes and 439 down regulated genes were observed. Most of the DEGs were significantly enriched in biological adhesion, extracellular matrix, signaling receptor binding, secretion, intrinsic component of plasma membrane, signaling receptor activity, extracellular matrix organization and neutrophil degranulation. The top hub genes ESR1, PYHIN1, PPP2R2B, LCK, TP63, PCLAF, CFTR, TK1, ECT2 and FKBP5 were identified from the PPI network. Module analysis revealed that HF was associated with adaptive immune system and neutrophil degranulation. The target genes, miRNAs and TFs were identified from the target gene - miRNA regulatory network and target gene - TF regulatory network. Furthermore, receiver operating characteristic (ROC) curve analysis and RT-PCR analysis revealed that ESR1, PYHIN1, PPP2R2B, LCK, TP63, PCLAF, CFTR, TK1, ECT2 and FKBP5 might serve as prognostic, diagnostic biomarkers and therapeutic target for HF. The predicted targets of these active molecules were then confirmed. The current investigation identified a series of key genes and pathways that might be involved in the progression of HF, providing a new understanding of the underlying molecular mechanisms of HF.

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“…A more direct role for Sfrp4 in regulating cardiomyocyte apoptosis was shown in a Sfrp4 knockdown study involving ischemia‐reperfusion cardiac injury. Here, loss of Sfrp4 expression reduced injury by preventing the expression of pro‐apoptotic Bax, caspase‐3, and Bcl‐2 genes in cardiomyocytes (Zeng et al, 2019). It is currently unknown if Sfrp3 and Sfrp4 promote cardiomyocyte apoptosis via Wnt dependent pathways.…”

Section: Sfrps and Dkks: Endogenous Wnt Inhibitorsmentioning

confidence: 99%

The role of Sfrp and DKK proteins in cardiomyocyte development

2021

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In this review, we summarize the role of Wnt proteins in cardiomyogenesis. More specifically, we focus on how the development of cardiomyocytes from precursor cells involves a complex interplay between Wnt canonical β‐catenin signaling pathways and Wnt noncanonical signaling pathways involving PCP and JNK. We also describe recent literature which suggests that endogenous Wnt inhibitors such as the Sfrp and DKK proteins play important roles in regulating the cardiomyocyte differentiation.

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Knockdown of Sfrp4 attenuates apoptosis to protect against myocardial ischemia/reperfusion injury

Cited by 33 publications

References 24 publications

Identification of candidate biomarkers and therapeutic agents for heart failure by bioinformatics analysis

Identification of candidate biomarkers and therapeutic agents for heart failure by bioinformatics analysis

Identification of candidate biomarkers and therapeutic agents for heart failure by bioinformatics analysis

The role of Sfrp and DKK proteins in cardiomyocyte development

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