Cardiac fibroblast miR‐27a may function as an endogenous anti‐fibrotic by negatively regulating Early Growth Response Protein 3 (EGR3)

Teng, Lifeng; Huang, Yong; Guo, Jun; Li, Bin; Jin, Lin; Ma, Lining; Wang, Yudai; Ye, Cong; Chen, Qianqian

doi:10.1111/jcmm.15814

Cited by 12 publications

(8 citation statements)

References 28 publications

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“… 43 In addition, cardiac fibrosis significantly upregulates EGR3, which suggests the involvement of EGR3 in cardiac fibrosis. 44 , 45 Although previous results show that a 4-hour TGF-β treatment induces EGR3 expression in adult skin fibroblasts 46 our data show no change of EGR3 expression in NRCFs under TGF-β treatment. It might be due to the different types of cell lines and the different duration of TGF-β treatment.…”

Section: Discussioncontrasting

confidence: 74%

Inhibition of HIPK2 protects stress-induced pathological cardiac remodeling

Zhou

Meng

et al. 2022

eBioMedicine

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Section: Discussioncontrasting

confidence: 74%

Inhibition of HIPK2 protects stress-induced pathological cardiac remodeling

Zhou

Meng

et al. 2022

eBioMedicine

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“…CENPA encodes a centromere protein and is necessary for maintaining proliferation, inhibiting senescence, and promoting survival following differentiation of cardiac progenitor cells [ 46 ]. Cardiac fibroblast miR-27a-5p may function as an inhibitor of pathological myocardial fibrosis and hypertrophy by negatively regulating Egr3 expression [ 47 ]. The predicted target genes of miR-27a-5p are SGOL1, NUF2, CDK1 and ASF1B.…”

Section: Discussionmentioning

confidence: 99%

Identification and validation of the miRNA–mRNA regulatory network in fetoplacental arterial endothelial cells of gestational diabetes mellitus

Wang

Jin

et al. 2021

Bioengineered

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Gestational diabetes mellitus (GDM) increases the risk of fetal heart malformations, though little is known about the mechanism of hyperglycemia-induced heart malformations. Thus, we aimed to reveal the global landscape of miRNAs and mRNAs in GDM-exposed fetoplacental arterial endothelial cells (dAECs) and establish regulatory networks for exploring the pathophysiological mechanism of fetal heart malformations in maternal hyperglycemia. Gene Expression Omnibus (GEO) datasets were used, and identification of differentially expressed miRNAs (DEMs) and genes (DEGs) in GDM was based on a previous sequencing analysis of dAECs. A miRNA-mRNA network containing 20 DEMs and 65 DEGs was established using DEMs altered in opposite directions to DEGs. In an in vivo study, we established a streptozotocin-induced pregestational diabetes mellitus (PGDM) mouse model and found the fetal cardiac wall thickness in different regions to be dramatically increased in the PGDM grouValidation of DEMs and DEGs in the fetal heart showed significantly upregulated expression of let-7e-5p, miR-139-5p and miR-195-5p and downregulated expression of SGOL1, RRM2, RGS5, CDK1 and CENPA. In summary, we reveal the miRNA-mRNA regulatory network related to fetal cardiac development disorders in offspring, which may shed light on the potential molecular mechanisms of fetal cardiac development disorders during maternal hyperglycemia.

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“…These findings are consistent with studies demonstrating that fibrosis and myocardial ion channel dysregulation provide a mechanistic substrate for ventricular arrhythmias across multiple etiologies of heart failure [ 45 , 46 ]. Taken together, these findings suggest that the let-7 family as well as miRs-92a, 130, 27 and 29, which have shown promise as candidate biomarkers in other forms of heart failure, may also be helpful for predicting morbidity in chronically paced children [ 47 – 51 ].…”

Section: Discussionmentioning

confidence: 99%

miR Profile of Chronic Right Ventricular Pacing: a Pilot Study in Children with Congenital Complete Atrioventricular Block

Navarre

Clouthier

et al. 2022

J. of Cardiovasc. Trans. Res.

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Chronic ventricular pacing can lead to pacing-induced cardiomyopathy (PICM). Clinical data alone is insufficient to predict who will develop PICM. Our study aimed to evaluate the circulating miR profile associated with chronic right ventricular pacing in children with congenital complete AV block (CCAVB) and to identify candidate miRs for longitudinal monitoring. Clinical data and blood were collected from chronically paced children (N = 9) and compared with non-paced controls (N = 13). miR microarrays from the buffy coat revealed 488 differentially regulated miRs between groups. Pathway analysis predicted both adaptive and maladaptive miR signaling associated with chronic pacing despite preserved ventricular function. Greater profibrotic signaling (miRs-92a, 130, 27, 29) and sodium and calcium channel dysregulation (let-7) were seen in those paced > 10 years with the most dyregulation seen in a patient with sudden death vs. those paced < 10 years. These miRs may help to identify early adverse remodeling in this population. Graphical abstract

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Cardiac fibroblast miR‐27a may function as an endogenous anti‐fibrotic by negatively regulating Early Growth Response Protein 3 (EGR3)

Cited by 12 publications

References 28 publications

Inhibition of HIPK2 protects stress-induced pathological cardiac remodeling

Inhibition of HIPK2 protects stress-induced pathological cardiac remodeling

Identification and validation of the miRNA–mRNA regulatory network in fetoplacental arterial endothelial cells of gestational diabetes mellitus

miR Profile of Chronic Right Ventricular Pacing: a Pilot Study in Children with Congenital Complete Atrioventricular Block

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