MiR-574–5p promotes the differentiation of human cardiac fibroblasts via regulating ARID3A

Cui, Jun; Qi, Siyi; Liao, Rongheng; Su, Diansan; Wang, Yong-Yi; Xue, Song

doi:10.1016/j.bbrc.2019.09.107

Cited by 18 publications

(10 citation statements)

References 32 publications

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“…When TGF-β1 was activated, it bounded with the receptor TβRI and TβRII, TβRI bounded with its downstream transcription factor SMAD4, and TβRII phosphorylated SMAD2/3, which combined with SMAD4 and entered into cell nucleus to promote transcription of fibrosis-related genes (Khalil et al, 2017). In our research, we found that after stimulated by TGF-β1, cell viability, fibrosisrelated genes expression, cell proliferation, and migration abilities were all enhanced, which was in line with reports and our previous publication (Cui et al, 2020).…”

Section: Discussionsupporting

confidence: 92%

“…MFA was an organic acid extracted from traditional Chinese herbs (Figure 1A). To elucidate the effect of MFA in HCF differentiation, TGF-β1 was used for inducing the differentiation of HCFs guided by our formal experiences (Cui et al, 2020), 6-level concentrations of TGF-β1 were incubated with HCFs. After 24 h of incubation, the CCK-8 assay was performed to determine the cell viability in different TGF-β1 concentrations.…”

Section: Mfa-attenuated Cell Differentiation In Tgf-β1-stimulated Hcfsmentioning

confidence: 99%

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Methyl Ferulic Acid Attenuates Human Cardiac Fibroblasts Differentiation and Myocardial Fibrosis by Suppressing pRB-E2F1/CCNE2 and RhoA/ROCK2 Pathway

Liao

Qi²,

Tang

et al. 2021

Front. Pharmacol.

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Background: Myocardial fibrosis is a key pathological process after myocardial infarction, which leads to poor outcomes in patients at the end stage. Effective treatments for improving prognosis of myocardial fibrosis are needed to be further developed. Methyl ferulic acid (MFA), a biologically active monomer extracted and purified from the Chinese herbal medicine, is reported as an attenuator in many diseases. In this study, we aim to reveal the role it plays in myocardial fibrosis after myocardial infarction and its possible mechanism.Results: Firstly, we found that MFA attenuated the expression of fibrosis-related proteins and the ability of migration and proliferation in TGF-β1–induced human cardiac fibroblasts (HCFs). Then, myocardial fibrosis after myocardial infarction models on mouse was built to reveal the in vivo affection of MFA. After 28 days of treatments, fibrosis areas, cardiac function, and expression of fibrosis-related proteins were all improved in the MFA-treated group than the myocardial infarction group. Finally, to elucidate the mechanism of phenomenon we observed, we found that MFA attenuated HCF differentiation after myocardial infarction by suppressing the migration and proliferation in HCFs, which was by suppressing the pRB-E2F1/CCNE2 and the RhoA/ROCK2 pathway.Conclusion: Our findings showed that MFA attenuated the expression of fibrosis-related proteins, and the ability of migration and proliferation in HCFs improved the cardiac function of myocardial infarction mice; meanwhile, the mechanism of that was by suppressing the pRB-E2F1/CCNE2 and the RhoA/ROCK2 pathway.

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Section: Discussionsupporting

confidence: 92%

Section: Mfa-attenuated Cell Differentiation In Tgf-β1-stimulated Hcfsmentioning

confidence: 99%

Methyl Ferulic Acid Attenuates Human Cardiac Fibroblasts Differentiation and Myocardial Fibrosis by Suppressing pRB-E2F1/CCNE2 and RhoA/ROCK2 Pathway

Liao

Qi²,

Tang

et al. 2021

Front. Pharmacol.

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“…Moreover, we found that hsa_circ_0001320 was interacted with miR‐574‐5p. Studies had already shown that miR‐574‐5p was related to the proliferation and migration of various tumor cells and the differentiation of fibroblasts 28,34‐37 . The downstream gene of miR‐574‐5p was predicted to be SMAD4 SMAD4 is a transcriptional activator.…”

Section: Discussionmentioning

confidence: 99%

“…Studies had already shown that miR-574-5p was related to the proliferation and migration of various tumor cells and the differentiation of fibroblasts. 28,[34][35][36][37] The downstream gene of miR-574-5p was predicted to be SMAD4 SMAD4 is a transcriptional activator. It is also and an important molecule in the TGF-ß signaling pathway, plays a key role in the transfer of TGF-ß signals from cell surface to the nucleus.…”

Section: Discussionmentioning

confidence: 99%

Identification of differentially expressed circular RNAs in keloid and normal skin tissue by high‐throughput sequencing

Zhang

Liu

et al. 2021

Dermatologic Therapy

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Keloid is a kind of pathological skin scar with unclear molecular pathology. Circular RNAs (circRNAs) are involved in the occurrence and development of many diseases; however, their relationship with keloid is not well understood. To investigate the involvement of dysregulated circRNAs in keloid. Thirty-seven keloids and 37 normal skin tissues were collected, and the changes of circRNAs, microRNAs (miRNAs) and mRNAs in 3 keloids and 3 normal samples by high-throughput sequencing were detected first. Based on the circRNA-miRNA-mRNA interaction network construction, gene ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis combining several signaling pathways associated with keloid formation and progression, the circRNAs required further verification were screened out. The expression levels of the selected circRNAs were verified in 37 keloids and 37 normal skin tissues using quantitative real-time polymerase chain reaction (QPCR). The interaction of candidate circRNA and its predicted binding miRNA was tested by dualluciferase reporter gene experiment. Compared with normal controls, there was an average of 120 and 12 circRNAs, 44 and 63 miRNAs, 656 and 156 mRNAs were upregulated and downregulated, respectively, in keloids. According to the analysis of bioinformation, six circRNAs were picked out. The QPCR validation results of two upregulated circRNAs (hsa_circ_0001320 and circCOL5A1) were consistent with previous sequencing results. The interaction between hsa_circ_0001320 and miR-574-5p was confirmed. This study makes it clear that the abnormal expression of cir-cRNAs may be related to the pathological process of keloid.

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“…Following our previous routines [ 17 ], human cardiac fibroblasts (HCFs) were obtained from Sciencell Research Lab (6300, USA). HCFs were cultured in DMEM/F-12 with 5% FBS (Gibco) 2 mM glutamine and 1% penicillin/streptomycin (Gibco) on condition of 37°C with 5% CO 2 .…”

Section: Methodsmentioning

confidence: 99%

E2F transcription factor 1 (E2F1) promotes the transforming growth factor TGF-β1 induced human cardiac fibroblasts differentiation through promoting the transcription of CCNE2 gene

et al. 2021

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MiR-574–5p promotes the differentiation of human cardiac fibroblasts via regulating ARID3A

Cited by 18 publications

References 32 publications

Methyl Ferulic Acid Attenuates Human Cardiac Fibroblasts Differentiation and Myocardial Fibrosis by Suppressing pRB-E2F1/CCNE2 and RhoA/ROCK2 Pathway

Methyl Ferulic Acid Attenuates Human Cardiac Fibroblasts Differentiation and Myocardial Fibrosis by Suppressing pRB-E2F1/CCNE2 and RhoA/ROCK2 Pathway

Identification of differentially expressed circular RNAs in keloid and normal skin tissue by high‐throughput sequencing

E2F transcription factor 1 (E2F1) promotes the transforming growth factor TGF-β1 induced human cardiac fibroblasts differentiation through promoting the transcription of CCNE2 gene

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