Inhibition of miR-182-5p attenuates pulmonary fibrosis via TGF-β/Smad pathway

Chen, Y; Q, Zhang; Zhou, Yan; Yang, Zehui; Tan, Mingqi

doi:10.1177/0960327119895549

Cited by 25 publications

(17 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, in fibroblasts, the expression of miR-29 was negatively regulated by TGF-β1/Smad3 signal (43)(44)(45). Similarly, Smad7, a negative regulator of TGF-β1, is suppressed by miR-182-5p which is induced by TGF-β1, resulting in the development of IPF (46). TGF-β1 activates Semaphorin (SEMA) 7A and its receptors through a Smad3-independent and Smad 2/3-independent mechanism, respectively, promoting pulmonary fibrosis (47) Activating transcription factor 4 (ATF4) was a pivotal transcriptional regulator for the metabolism of amino acid (48).…”

Section: Tgf-β1: Gentlemanly Orchestrator In Idiopathic Pulmonary Fibrosis (Review)mentioning

confidence: 99%

TGF‑β1: Gentlemanly orchestrator in idiopathic pulmonary fibrosis (Review)

2021

Int J Mol Med

121

View full text Add to dashboard Cite

Idiopathic pulmonary fibrosis (IPF) is a worldwide disease characterized by the chronic and irreversible decline of lung function. Currently, there is no drug to successfully treat the disease except for lung transplantation. Numerous studies have been devoted to the study of the fibrotic process of IPF and findings showed that transforming growth factor-β1 (TGF-β1) plays a central role in the development of IPF. TGF-β1 promotes the fibrotic process of IPF through various signaling pathways, including the Smad, MAPK, and ERK signaling pathways. There are intersections between these signaling pathways, which provide new targets for researchers to study new drugs. In addition, TGF-β1 can affect the fibrosis process of IPF by affecting oxidative stress, epigenetics and other aspects. Most of the processes involved in TGF-β1 promote IPF, but TGF-β1 can also inhibit it. This review discusses the role of TGF-β1 in IPF. Contents1. Introduction 2. TGF-β1-involved pathway in IPF 3. Discussion 4. Conclusion

show abstract

Section: Tgf-β1: Gentlemanly Orchestrator In Idiopathic Pulmonary Fibrosis (Review)mentioning

confidence: 99%

TGF‑β1: Gentlemanly orchestrator in idiopathic pulmonary fibrosis (Review)

2021

Int J Mol Med

121

View full text Add to dashboard Cite

show abstract

“…miRNAs, a class of noncoding small RNAs, are involved in RNA silencing, posttranscriptional regulation, and other biological processes [ 20 ]. It has been confirmed that miRNAs play a critical role in the occurrence and development of various diseases, including IPF [ 21 – 23 ]. As an example, miR-92, miR-210, and miR-let-7d have been confirmed to be associated with IPF [ 24 – 26 ].…”

Section: Introductionmentioning

confidence: 99%

[Retracted] Identification and Validation of Potential Biomarkers and Pathways for Idiopathic Pulmonary Fibrosis by Comprehensive Bioinformatics Analysis

Qian

Cai

Qian

et al. 2021

BioMed Research International

View full text Add to dashboard Cite

Objective. Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, irreversible, high-mortality lung disease, but its pathogenesis is still unclear. Our purpose was to explore potential genes and molecular mechanisms underlying IPF. Methods. IPF-related data were obtained from the GSE99621 dataset. Differentially expressed genes (DEGs) were identified between IPF and controls. Their biological functions were analyzed. The relationships between DEGs and microRNAs (miRNAs) were predicted. DEGs and pathways were validated in a microarray dataset. A protein-protein interaction (PPI) network was constructed based on these common DEGs. Western blot was used to validate hub genes in IPF cell models by western blot. Results. DEGs were identified for IPF than controls in the RNA-seq dataset. Functional enrichment analysis showed that these DEGs were mainly enriched in immune and inflammatory response, chemokine-mediated signaling pathway, cell adhesion, and other biological processes. In the miRNA-target network based on RNA-seq dataset, we found several miRNA targets among all DEGs, like RAB11FIP1, TGFBR3, and SPP1. We identified 304 upregulated genes and 282 downregulated genes in IPF compared to controls both in the microarray and RNA-seq datasets. These common DEGs were mainly involved in cell adhesion, extracellular matrix organization, oxidation-reduction process, and lung vasculature development. In the PPI network, 3 upregulated and 4 downregulated genes could be considered hub genes, which were confirmed in the IPF cell models. Conclusion. Our study identified several IPF-related DEGs that could become potential biomarkers for IPF. Large-scale multicentric studies are eagerly needed to confirm the utility of these biomarkers.

show abstract

“…miRNAs are endogenous, small non-coding RNA that modulate genes at the post-transcription level in various physiological and pathological processes (20). Increasing evidence has indicated that miRNAs drive the onset and progression of PF (21,22).…”

Section: Discussionmentioning

confidence: 99%

Downregulation of miR‑483‑5p inhibits TGF‑β1‑induced EMT by targeting RhoGDI1 in pulmonary fibrosis

et al. 2021

View full text Add to dashboard Cite

Transforming growth factor-β1 (TGF-β1)-induced epithelial-mesenchymal transition (EMT) serves a significant role in pulmonary fibrosis (PF). Increasing evidence indicates that microRNAs (miRNAs or miRs) contribute to PF pathogenesis via EMT regulation. However, the role of miR-483-5p in PF remains unclear. Therefore, the present study investigated the potential effect of miR-483-5p on TGF-β1-induced EMT in PF. It was found that the expression of miR-483-5p was upregulated in both PF tissue and A549 cells treated with TGF-β1, whereas expression of Rho GDP dissociation inhibitor 1 (RhoGDI1) was downregulated. miR-483-5p mimic transfection promoted TGF-β1-induced EMT; by contrast, miR-483-5p inhibitor inhibited TGF-β1-induced EMT. Also, miR-483-5p mimic decreased RhoGDI1 expression, whereas miR-483-5p inhibitor increased RhoGDI1 expression. Furthermore, dual-luciferase reporter gene assay indicated that miR-483-5p directly regulated RhoGDI1. Moreover, RhoGDI1 knockdown eliminated the inhibitory effect of the miR-483-5p inhibitor on TGF-β1-induced EMT via the Rac family small GTPase (Rac)1/PI3K/AKT pathway. In conclusion, these data indicated that miR-483-5p inhibition ameliorated TGF-β1-induced EMT by targeting RhoGDI1 via the Rac1/PI3K/Akt signaling pathway in PF, suggesting a potential role of miR-483-5p in the prevention and treatment of PF.

show abstract

Inhibition of miR-182-5p attenuates pulmonary fibrosis via TGF-β/Smad pathway

Cited by 25 publications

References 39 publications

TGF‑β1: Gentlemanly orchestrator in idiopathic pulmonary fibrosis (Review)

TGF‑β1: Gentlemanly orchestrator in idiopathic pulmonary fibrosis (Review)

[Retracted] Identification and Validation of Potential Biomarkers and Pathways for Idiopathic Pulmonary Fibrosis by Comprehensive Bioinformatics Analysis

Downregulation of miR‑483‑5p inhibits TGF‑β1‑induced EMT by targeting RhoGDI1 in pulmonary fibrosis

Contact Info

Product

Resources

About