The miR-130a-3p/TGF-βRII Axis Participates in Inhibiting the Differentiation of Fibroblasts Induced by TGF-β1

Liu, Yanhong; Ding, Yan; Hou, Yapeng; Yu, Tong; Nie, Hongguang; Cui, Yong

doi:10.3389/fphar.2021.732540

Cited by 5 publications

(5 citation statements)

References 49 publications

(52 reference statements)

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“… 96 miR-130a-3p inhibits the TGF-β–induced EMT via SMAD4. 97 , 98 miR-21 is involved in the TGF-β1 signaling pathway 99 and suppresses the Hippo signaling pathway. 100 miR-23b-3p activates TGF-β signaling by increasing SMAD2 phosphorylation 101 and regulates autophagy by suppressing SIRT1.…”

Section: Discussionmentioning

confidence: 99%

Adipose Mesenchymal Stem Cell-Derived Exosomes Promote the Regeneration of Corneal Endothelium Through Ameliorating Senescence

Ryu,

Hwang,

Bo Noh

et al. 2023

Invest. Ophthalmol. Vis. Sci.

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Purpose Human corneal endothelial cells (hCECs) have been considered unable to regenerate in vivo, resulting in corneal decompensation after significant loss of hCECs. adipose-derived mesenchymal stem cell (ASC)-derived exosomes can regenerate tissues and organs. In this study, we investigated whether ASC-derived exosomes could protect and regenerate CECs. Methods We performed cell viability and cell-cycle analyses to evaluate the effect of ASC-derived exosomes on the regeneration capacity of cultured hCECs. Transforming growth factor-β (TGF-β) and hydrogen peroxide (H 2 O 2 ) were used to induce biological stress in CECs. The effect of ASC-derived exosomes on CECs was investigated in vivo. ASC-derived exosomes were introduced into rat CECs using electroporation, and rat corneas were injured using cryoinjury. Next-generation sequencing analysis was performed to compare the differentially expressed microRNAs (miRNAs) between ASC-derived and hCEC-derived exosomes. Results ASC-derived exosomes induced CEC proliferation and suppressed TGF-β- or H 2 O 2 -induced oxidative stress and senescence. ASC-derived exosomes protect hCECs against TGF-β- or H 2 O 2 -induced endothelial-mesenchymal transition and mitophagy. In an in vivo study, ASC-derived exosomes promoted wound healing of rat CECs and protected the corneal endothelium against cryoinjury-induced corneal endothelium damage. Next-generation sequencing analysis revealed differentially expressed miRNAs for ASC-derived and hCEC-derived exosomes. They are involved in lysine degradation, adherens junction, the TGF-β signaling pathway, the p53 signaling pathway, the Hippo signaling pathway, the forkhead box O (FoxO) signaling pathway, regulation of actin cytoskeleton, and RNA degradation based on Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. Conclusions ASC-derived exosomes promoted wound healing and regeneration of endothelial cells by inducing a shift in the cell cycle and suppressing senescence and autophagy.

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Section: Discussionmentioning

confidence: 99%

Adipose Mesenchymal Stem Cell-Derived Exosomes Promote the Regeneration of Corneal Endothelium Through Ameliorating Senescence

Ryu,

Hwang,

Bo Noh

et al. 2023

Invest. Ophthalmol. Vis. Sci.

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“…Recently, miRNAs have been extensively studied for their essential role in regulating gene expression at the posttranscriptional level and their relationship with various biological processes [103]. It has been shown that miRNAs play a critical role in developing and progressing multiple lung diseases, such as IPF [103,104]. miR-130a-3p has been shown to participate in the regulation of IPF by inhibiting lung fibroblast differentiation by blocking the activation of the TGF-β/Smad signaling pathway [104].…”

Section: Discussionmentioning

confidence: 99%

“…It has been shown that miRNAs play a critical role in developing and progressing multiple lung diseases, such as IPF [103,104]. miR-130a-3p has been shown to participate in the regulation of IPF by inhibiting lung fibroblast differentiation by blocking the activation of the TGF-β/Smad signaling pathway [104]. Additionally, it has been observed that miR-199a-5p is upregulated in patients with IPF.…”

Section: Discussionmentioning

confidence: 99%

Identification of Hub Genes in Idiopathic Pulmonary Fibrosis and Their Association with Lung Cancer by Bioinformatics Analysis

Velázquez-Enríquez,

Reyes-Avendaño,

Santos-Álvarez

et al. 2023

ARM

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Background: Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, and irreversible disease with a high mortality rate worldwide. However, the etiology and pathogenesis of IPF have not yet been fully described. Moreover, lung cancer is a significant complication of IPF and is associated with increased mortality. Nevertheless, identifying common genes involved in developing IPF and its progression to lung cancer remains an unmet need. The present study aimed to identify hub genes related to the development of IPF by meta-analysis. In addition, we analyzed their expression and their relationship with patients’ progression in lung cancer. Method: Microarray datasets GSE24206, GSE21369, GSE110147, GSE72073, and GSE32539 were downloaded from Gene Expression Omnibus (GEO). Next, we conducted a series of bioinformatics analysis to explore possible hub genes in IPF and evaluated the expression of hub genes in lung cancer and their relationship with the progression of different stages of cancer. Results: A total of 1888 differentially expressed genes (DEGs) were identified, including 1105 upregulated and 783 downregulated genes. The 10 hub genes that exhibited a high degree of connectivity from the PPI network were identified. Analysis of the KEGG pathways showed that hub genes correlate with pathways such as the ECM–receptor interaction. Finally, we found that these hub genes are expressed in lung cancer and are associated with the progression of different stages of lung cancer. Conclusions: Based on the integration of GEO microarray datasets, the present study identified DEGs and hub genes that could play an essential role in the pathogenesis of IPF and its association with the development of lung cancer in these patients, which could be considered potential diagnostic biomarkers or therapeutic targets for the disease.

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“…Our previous studies demonstrated that TGF-β1-induced proliferation and differentiation of fibroblasts could be inhibited by miR-130a-3p in the MLG2908 cell line, but whether miR-130a-3p can inhibit the progression of PF in vivo , especially in different phases of PF has not been established ( Liu et al, 2021 ). The aim of the present study was to explore the anti-inflammatory and anti-fibrotic effects of miR-130a-3p by examining the activity of the NF-κB and TGF-β1/Smad signaling pathways, which would provide a new therapeutic approach to prevent and perhaps even partially reverse the occurrence and progression of PF.…”

Section: Introductionmentioning

confidence: 99%

MiR-130a-3p Alleviates Inflammatory and Fibrotic Phases of Pulmonary Fibrosis Through Proinflammatory Factor TNF-α and Profibrogenic Receptor TGF-βRII

et al. 2022

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Pulmonary fibrosis (PF) is a progressive disease characterized by extracellular matrix (ECM) deposition that destroys the normal structure of the lung parenchyma, which is classified into two successive inflammatory and fibrotic phases. To investigate the anti-inflammatory and anti-fibrotic roles of miR-130a-3p in mice with bleomycin (BLM)-induced PF and the underlying mechanism, we performed single-cell RNA-sequencing analysis, which demonstrated that BLM increased/decreased the percentage of macrophages and fibroblasts/epithelial cells in PF lungs, respectively. The differentially expressed genes were enriched in PPAR signaling pathway and lysosome, ECM–receptor interaction and ribosome, and metabolism reaction. Time-course studies demonstrated that the inflammation-related factors increased significantly at day 7 (inflammatory phase), whereas the fibrosis-related factors increased at day 28 (fibrotic phase) after BLM exposure. Meanwhile, miR-130a-3p could ameliorate pulmonary lesions by downregulating the secretion of inflammatory cytokines (IL-1β, IL-6, TNF-α, and TGF-β1) and the deposition of ECM (α-SMA, FN, HYP, and collagen) in the inflammatory and fibrotic phase, respectively. In the LPS-induced inflammatory cell model, the upregulation of miR-130a-3p was mainly achieved by the activation of the NF-κB signaling pathway, which suppressed the proinflammatory factor TNF-α. Comparatively, the TGF-β/Smad signaling pathway was inhibited by miR-130a-3p targeting TGF-βRII in the TGF-β1-deduced fibrotic cell model. The evidence supports that miR-130a-3p exerts an anti-inflammatory and anti-fibrotic effect in BLM-induced PF, implying a potential pharmacological agent in the therapy of PF patients.

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The miR-130a-3p/TGF-βRII Axis Participates in Inhibiting the Differentiation of Fibroblasts Induced by TGF-β1

Cited by 5 publications

References 49 publications

Adipose Mesenchymal Stem Cell-Derived Exosomes Promote the Regeneration of Corneal Endothelium Through Ameliorating Senescence

Adipose Mesenchymal Stem Cell-Derived Exosomes Promote the Regeneration of Corneal Endothelium Through Ameliorating Senescence

Identification of Hub Genes in Idiopathic Pulmonary Fibrosis and Their Association with Lung Cancer by Bioinformatics Analysis

MiR-130a-3p Alleviates Inflammatory and Fibrotic Phases of Pulmonary Fibrosis Through Proinflammatory Factor TNF-α and Profibrogenic Receptor TGF-βRII

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