Long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) regulates fibroblast growth factor receptor substrate 2 (FRS2) by targeting microRNA (miR)-29-3p in hypertrophic scar fibroblasts

Wu, Qinghua; Chen, Junjie; Tan, Ziming; Wang, Dehuai; Zhou, Jianwen; Li, Dan; Cen, Ying

doi:10.1080/21655979.2021.1959221

Cited by 8 publications

(3 citation statements)

References 40 publications

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“…In addition, they proposed that miR-29a plays the above functions mainly by directly inhibiting the expression of COL1A1 [ 14 ]. Wu et al found that miR-29a-3p was upregulated in hypertrophic scar (HS) tissue and fibroblasts compared with normal skin tissue and confirmed that miR-29a-3p inhibited the proliferation of hypertrophic scar fibroblasts (HSF) and the production of extracellular matrix (ECM) by directly targeting FRS2 [ 15 ]. Yuan et al found that the expression level of miR-29a in mouse scar tissue was significantly downregulated compared with normal skin tissue and proposed that exosomes from miR-29a modified adipose mesenchymal stem cells could reduce excessive scar formation by inhibiting TGF- β 2/Smad3 signal [ 16 ].…”

Section: Discussionmentioning

confidence: 99%

Identifying miRNAs Associated with the Progression of Keloid through mRNA-miRNA Network Analysis and Validating the Targets of miR-29a-3p in Keloid Fibroblasts

Zhang

Yin

et al. 2022

BioMed Research International

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Background. Keloid has brought great trouble to people and currently has no uniformly successful treatment. It is urgent to find new targets to effectively prevent the progress of keloid. The current research mainly identifies the differentially expressed genes (DEGs) in keloid through high-throughput sequencing technology and bioinformatics analysis technology, to screen new therapeutic targets and potential biomarkers. However, due to the different samples, different control groups, and small sample sizes, the sequencing results obtained from different studies are quite different and lack reliability. It is necessary to analyze the existing datasets in a reasonable way. Methods. Datasets about keloid were filtered in Gene Expression Omnibus (GEO) and ArrayExpress databases according to the inclusion and exclusion criteria. The discovery datasets were used for summarizing significant DEGs, and the validation datasets were to validate the mRNA and miRNA expression levels. The Encyclopedia of RNA Interactomes (ENCORI) online platform was used to predict the interactions between miRNAs and their target mRNAs. Protein-protein interaction network (PPI network) analysis and functional enrichment analysis were conducted. miRNA-mRNA network was established by Cytoscape software and verified in keloid tissue ( n = 8 ) by RT-qPCR. miR-29a-3p mimic and inhibitor were transfected into keloid fibroblasts (KFs) to preliminary verify its targets, the prognostic value of which was estimated by the receiver operating characteristic (ROC) curve. Results. A total of 6 datasets involving 20 patients were included. 15 miRNAs and 12 target mRNAs were identified as potential biomarkers for keloid patients. The RT-qPCR results showed that miR-29a-3p, miR-92a-3p, and miR-143-3p were downregulated, and all their target mRNAs were upregulated in keloid tissue ( P < 0.05 ). The expression of COL1A1, COL1A2, COL3A1, COL5A1, and COL5A2 decreased when miR-29a-3p was overexpressed but increased when miR-29a-3p was knocked down ( P < 0.05 ). And these genes had a good performance in the diagnosis of keloid, especially when using keloid nonlesional skin or normal scar tissues as controls. Conclusion. The miRNA-mRNA network, especially miR-29a-3p and its targets, may provide insights into the underlying pathogenesis of keloid and serve as potential biomarkers for keloid treatment.

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Section: Discussionmentioning

confidence: 99%

Identifying miRNAs Associated with the Progression of Keloid through mRNA-miRNA Network Analysis and Validating the Targets of miR-29a-3p in Keloid Fibroblasts

Zhang

Yin

et al. 2022

BioMed Research International

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“…With the development of biomedical science, increasing evidences have demonstrated that lncRNAs play a regulatory role in the pathogenesis of various diseases including cancer, myocardial infarction, pulmonary fibrosis and hypertrophic scars by regulating key proteins with competing endogenous (ce) RNAs ( 19-21 ). LncRNA NEAT1 regulates FRS2 by targeting miR-29-3p in hypertrophic scar fibroblasts, thereby exacerbating the pathological process of scar formation ( 22 ). The results of the present study indicated that lncRNA NEAT1 serves an important role in hypertrophic scars by mediating miR-488-3p/COL3A1 axis.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of lncRNA‑NEAT1 expression inhibits hypoxia‑induced scar fibroblast proliferation through regulation of the miR‑488‑3p/COL3A1 axis

Xu¹,

Guo²,

Yu³

et al. 2022

Exp Ther Med

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Long non-coding (lnc)RNA nuclear-enriched transcripts 1 (NEAT1) has been demonstrated to be involved in the inhibition of hypoxia-induced scar fibroblast proliferation, but the specific mechanism remains undetermined. The present study found that with the decrease of oxygen concentration, lncRNA NEAT1 was upregulated in hypoxia-induced scar fibroblasts, which promoted the mRNA and protein expression levels of collagen (COL)-I, COL-III and α-smooth muscle actin, thereby suppressing hypoxia-induced scar fibroblasts proliferation. In addition, the microRNA (miR)-488-3p/COL3A1 axis was involved in lncRNA NEAT1's regulation of the proliferation of hypoxia-induced scar fibroblasts. In conclusion, the knockdown of lncRNA-NEAT1 expression can inhibit hypoxia-induced scar fibroblasts proliferation through regulation of the miR-488-3p/COL3A1 axis, which will provide a novel therapeutic target for the treatment of hypertrophic scars.

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“…RT-qPCR was conducted on ABI 7500 real-time PCR system (Thermo Fisher Scientific) with SYBR Green kit. GAPDH or U6 was used as an internal control [ 18 ].…”

Section: Methodsmentioning

confidence: 99%

Long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) promotes the inflammation and apoptosis of otitis media with effusion through targeting microRNA (miR)-495 and activation of p38 MAPK signaling pathway

Dong

Huang

et al. 2021

Bioengineered

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Long non-coding RNA (lncRNA) plays a vital role in human inflammatory diseases. Our study aimed to investigate the function of lncRNA nuclear-enriched abundant transcript 1 (NEAT1) in otitis media with effusion (OME). The mRNA levels of NEAT1 and miR-495 were measured by RT-qPCR. The protein levels of p38 MAPK were detected by western blot. The levels of inflammatory cytokines were examined by ELISA. CCK-8 and flow cytometry assays were used to evaluate the cell viability and apoptosis, respectively. The interaction between NEAT1 and miR-495 was determined by luciferase reporter and RIP assays. NEAT1 was highly expressed in OME, and silencing of NEAT1 facilitated the cell proliferation and suppressed levels of inflammatory cytokines and cell apoptosis in LPS-induced HMEECs. Moreover, miR-495 was confirmed as a downstream target of NEAT1. Functional assays revealed that NEAT1 promoted the OME by targeting miR-495. It was further demonstrated that NEAT1 could activate the p38 MAPK signaling pathway by regulating miR-495, and the p38 MAPK inhibitor restored the effects of NEAT1 overexpression on the inflammation levels, cell proliferation, and apoptosis. Our study revealed that lncRNA NEAT1 served as a ceRNA to activate p38 MAPK signaling by targeting miR-495 in OME, which may offer a new target for OME treatment.

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Long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) regulates fibroblast growth factor receptor substrate 2 (FRS2) by targeting microRNA (miR)-29-3p in hypertrophic scar fibroblasts

Abstract: Cen (2021) Long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) regulates fibroblast growth factor receptor substrate 2 (FRS2) by targeting microRNA (miR)-29-3p in hypertrophic scar fibroblasts,

Cited by 8 publications

References 40 publications

Identifying miRNAs Associated with the Progression of Keloid through mRNA-miRNA Network Analysis and Validating the Targets of miR-29a-3p in Keloid Fibroblasts

Identifying miRNAs Associated with the Progression of Keloid through mRNA-miRNA Network Analysis and Validating the Targets of miR-29a-3p in Keloid Fibroblasts

Knockdown of lncRNA‑NEAT1 expression inhibits hypoxia‑induced scar fibroblast proliferation through regulation of the miR‑488‑3p/COL3A1 axis

Long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) promotes the inflammation and apoptosis of otitis media with effusion through targeting microRNA (miR)-495 and activation of p38 MAPK signaling pathway

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