RETRACTED: Amphiregulin promotes cardiac fibrosis post myocardial infarction by inducing the endothelial-mesenchymal transition via the EGFR pathway in endothelial cells

Liu, Liang; Song, Shuai; Zhang, Ya Ping; Wang, Di; Zhou, Zhong’e; Chen, Yu; Jin, Xian; Hu, Cui Fen; Shen, Cheng

doi:10.1016/j.yexcr.2020.111950

Cited by 18 publications

(23 citation statements)

References 51 publications

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“…The experiment with Gefitinib proved such a possibility. The stimulatory effect of EGF on collagen biosynthesis was confirmed by other authors [39][40][41].…”

Section: Discussionsupporting

confidence: 73%

Extracellular Prolidase (PEPD) Induces Anabolic Processes through EGFR, β1-integrin, and IGF-1R Signaling Pathways in an Experimental Model of Wounded Fibroblasts

Baszanowska

Misiura

Ościłowska

et al. 2021

IJMS

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The role of prolidase (PEPD) as a ligand of the epidermal growth factor receptor (EGFR) was studied in an experimental model of wound healing in cultured fibroblasts. The cells were treated with PEPD (1–100 nM) and analysis of cell viability, proliferation, migration, collagen biosynthesis, PEPD activity, and the expressions of EGFR, insulin-like growth factor 1 (IGF-1), and β1-integrin receptor including downstream signaling proteins were performed. It has been found that PEPD stimulated proliferation and migration of fibroblasts via activation of the EGFR-downstream PI3K/Akt/mTOR signaling pathway. Simultaneously, PEPD stimulated the expression of β1-integrin and IGF-1 receptors and proteins downstream to these receptors such as FAK, Grb2, and ERK1/2. Collagen biosynthesis was increased in control and “wounded” fibroblasts under PEPD treatment. The data suggest that PEPD-induced EGFR signaling may serve as a new attempt to therapy wound healing.

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“…The experiment with Gefitinib proved such a possibility. The stimulatory effect of EGF on collagen biosynthesis was confirmed by other authors [39][40][41].…”

Section: Discussionsupporting

confidence: 73%

Extracellular Prolidase (PEPD) Induces Anabolic Processes through EGFR, β1-integrin, and IGF-1R Signaling Pathways in an Experimental Model of Wounded Fibroblasts

Baszanowska

Misiura

Ościłowska

et al. 2021

IJMS

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“…PLA2G2A [61], CCL23 [62], CD53 [63], TREML4 [64], TREM2 [65], CD180 [66], HPSE (heparanase) [67], CELA2A [68], TNFRSF4 [69], AMBP (alpha-1-microglobulin/bikunin precursor) [70], SOX18 [71], PANX2 [72], RSPO2 [73], COMP (cartilage oligomeric matrix protein) [74], ASGR1 [75] and NOXA1 [76] are involved in progression of atherosclerosis. A previous study reported that S100A9 [77], ADORA3 [78], IL1R2 [79], FPR1 [80], CCL20 [81], CD163 [82], S100A8 [83], TLR2 [84], HAS2 [85], PTX3 [86], TIMP4 [87], AREG (amphiregulin) [88], LBP (lipopolysaccharide binding protein) [89], IL18R1 [90], ALOX5AP [91], RETN (resistin) [92], F13A1 [93], FPR2 [94], SAA1 [95], FLT3 [96], AQP4 [97], FCER1G [98], CCL18 [99], HP (haptoglobin) [100], CDK1 [101], SLC7A11 [102], CFTR (CF transmembrane conductance regulator) [103], F8 [104], STC1[44], IL18RAP [90], TIMP3 [105], PDE4D [106], CYP4A11 [107], SCN10A [108], APOB (apolipoprotein B) [109], ACE (angiotensin I converting enzyme) [110], PENK (proenkephalin) [111], HSPB6 [112], TLR9 [113], EGR1 [114], CACNG8 [115], FOXD3 [116], DBH (dopamine beta-hydroxylase) [117], FOXP3 [118], GLP1R [119], IL34 [120], CCN1 [121], ADRA2A [122], BGN (biglycan) [123], NOS2 [124], AGRN (agrin) [125], DRD1 [126], GNB3 [127], EGR2 [128], MDK (midkine) [129], NOTCH3 [130], AZIN2 [131], NOTCH1 [132], LOX...…”

Section: Discussionmentioning

confidence: 99%

Identification and Interaction Analysis of Molecular Markers in Myocardial Infarction by Integrated Bioinformatics Analysis

Vastrad¹,

Vastrad²

2021

Preprint

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Myocardial infarction (MI) is the leading cardiovascular diseases in worldwide, yet relatively little is known about the genes and signaling pathways involved in MI progression. The present investigation aimed to elucidate potential crucial candidate genes and pathways in MI. expression profiling by high throughput sequencing dataset (GSE132143) was downloaded from the Gene Expression Omnibus (GEO) database, which included data from 20 MI samples and 12 normal control samples. Differentially expressed genes (DEGs) were identified using t-tests in the DESeq2 R package. These DEGs were subsequently investigated by Gene Ontology (GO) and pathway enrichment analysis, a protein-protein interaction (PPI) network, modules, miRNA-hub gene regulatory network and TF-hub gene regulatory network were constructed and analyzed. Hub genes were validated by receiver operating characteristic curve (ROC) analysis. In total, 958 DEGs were identified, of which 480 were up regulated and 478 were down regulated. GO and pathway enrichment analysis results revealed that the DEGs were mainly enriched in, immune system, neuronal system, response to stimulus, and multicellular organismal process. A PPI network, modules, miRNA-hub gene regulatory network and TF-hub gene regulatory network was constructed by using Cytoscape software, and CFTR, CDK1, RPS13, RPS15A, RPS27, NOTCH1, MRPL12, NOS2, CCDC85B and ATN1 were identified as the hub genes. Our results highlight the important roles of the genes including CFTR, CDK1, RPS13, RPS15A, RPS27, NOTCH1, MRPL12, NOS2, CCDC85B and ATN1 in MI pathogenesis or therapeutic management.

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“…In contrast, restoration of OGN in OGN-null CMFs resulted in inhibition of cell migration and proliferation through decreased EGFR signaling ( Zuo et al, 2018 ). Stimulation of EGFR/ErbB receptors by amphiregulin (AR), another member of EGF family of ligands, induced cardiac fibrosis after myocardial infarction ( Liu et al, 2018 ; Liu et al, 2020 ) highlighting the detrimental role of EGFR/ErbBs in cardiac pathology. EGFR transactivation was also involved in mediating the non-canonical, cardiomyocyte hypertrophy-promoting, effects of the death receptor 5 that normally mediates apoptosis ( Tanner et al, 2019 ).…”

Section: Diabetes-induced Cardiac Dysfunction: the Dual Role Of Epidermal Growth Factor Receptor Family Of Receptor Tyrosine Kinases And mentioning

confidence: 99%

The Role of Epidermal Growth Factor Receptor Family of Receptor Tyrosine Kinases in Mediating Diabetes-Induced Cardiovascular Complications

et al. 2021

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Diabetes mellitus is a major debilitating disease whose global incidence is progressively increasing with currently over 463 million adult sufferers and this figure will likely reach over 700 million by the year 2045. It is the complications of diabetes such as cardiovascular, renal, neuronal and ocular dysfunction that lead to increased patient morbidity and mortality. Of these, cardiovascular complications that can result in stroke and cardiomyopathies are 2- to 5-fold more likely in diabetes but the underlying mechanisms involved in their development are not fully understood. Emerging research suggests that members of the Epidermal Growth Factor Receptor (EGFR/ErbB/HER) family of tyrosine kinases can have a dual role in that they are beneficially required for normal development and physiological functioning of the cardiovascular system (CVS) as well as in salvage pathways following acute cardiac ischemia/reperfusion injury but their chronic dysregulation may also be intricately involved in mediating diabetes-induced cardiovascular pathologies. Here we review the evidence for EGFR/ErbB/HER receptors in mediating these dual roles in the CVS and also discuss their potential interplay with the Renin-Angiotensin-Aldosterone System heptapeptide, Angiotensin-(1-7), as well the arachidonic acid metabolite, 20-HETE (20-hydroxy-5, 8, 11, 14-eicosatetraenoic acid). A greater understanding of the multi-faceted roles of EGFR/ErbB/HER family of tyrosine kinases and their interplay with other key modulators of cardiovascular function could facilitate the development of novel therapeutic strategies for treating diabetes-induced cardiovascular complications.

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RETRACTED: Amphiregulin promotes cardiac fibrosis post myocardial infarction by inducing the endothelial-mesenchymal transition via the EGFR pathway in endothelial cells

Cited by 18 publications

References 51 publications

Extracellular Prolidase (PEPD) Induces Anabolic Processes through EGFR, β1-integrin, and IGF-1R Signaling Pathways in an Experimental Model of Wounded Fibroblasts

Extracellular Prolidase (PEPD) Induces Anabolic Processes through EGFR, β1-integrin, and IGF-1R Signaling Pathways in an Experimental Model of Wounded Fibroblasts

Identification and Interaction Analysis of Molecular Markers in Myocardial Infarction by Integrated Bioinformatics Analysis

The Role of Epidermal Growth Factor Receptor Family of Receptor Tyrosine Kinases in Mediating Diabetes-Induced Cardiovascular Complications

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