LncRNA PICSAR binds to miR-485-5p and activates TGF-β1/Smad to promote abnormal proliferation of hypertrophic scar fibroblasts (HSFs) and excessive deposition of extracellular matrix (ECM)

Xu, Sijia; Dong, Wenxin; Shi, Yu

doi:10.1007/s00795-021-00296-4

Cited by 5 publications

(3 citation statements)

References 24 publications

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“…Xu et al showed that miR-485-5p bound long non-coding RNA PICSAR to activate TGF-β1/ Smad signaling to promote excessive deposition of ECM. 48 This is different from the signaling pathway that miR-485-3p regulates ECM deposition in our study, which may be related to ECM accumulation in different cells. Based on the above evidence, miR-485-3p regulates Wnt/β-catenin signaling by targeting WIF1, thus promoting the inflammatory response and ECM accumulation.…”

Section: Discussioncontrasting

confidence: 82%

MicroRNA-485-3p Promotes the Inflammatory Response and Extracellular Matrix Deposition by Activating Wnt/β-Catenin Signaling in Human Airway Smooth Muscle Cells

Liu

Shu

Gao

et al. 2023

Crit Rev Eukaryot Gene Expr

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The aim of this study was to study the effects of microRNA (miR)-485-3p on the inflammatory response and extracellular matrix deposition of human airway smooth muscle cells (HASMCs). The levels of miR-485-3p and WIF1 in peripheral blood of pediatric asthma (PA) patients and controls were examined by quantitative real-time polymerase chain reaction (qRT-PCR). miR-485-3p inhibitor and mimic, together with negative control (NC) inhibitor/ mimic, were transfected into HASMCs treated with tumor necrosis factor (TNF)-α. The levels of eotaxin, interleukin (IL)-8, and IL-6 were analyzed by enzyme-linked immunosorbent assay (ELISA). Cellular immunofluorescence analysis of fibronectin was also performed. The target genes of miR-485-3p were predicted and validated using TargetScan and dual-luciferase reporter gene assay. The protein levels of IL-6, eotaxin, IL-8, collagen III, collagen I, MMP-9, TIMP-1, MMP-2, axin, β-catenin, phosphorylated β-catenin, GSK3β, p-GSK3β, and WIF1 were tested by Western blot. The level of miR-485-3p was increased, whereas expression of WIF1 was low in PA patients. In TNF-α-induced HASMCs, miR-485-3p overexpression promoted the inflammatory response and the accumulation of extracellular matrix. WIF1 was a direct target of miR-485-3p. Silencing miR-485-3p inhibited activation of Wnt/β-catenin signaling. The reductions in the inflammatory response and ECM accumulation caused by silencing miR-485-3p were induced by blocking Wnt/β-catenin signaling. Thus, miRNA-485-3p targets WIF1 and activates Wnt/β-catenin signaling, facilitating activation of the inflammatory response and ECM accumulation in HASMCs.

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Section: Discussioncontrasting

confidence: 82%

MicroRNA-485-3p Promotes the Inflammatory Response and Extracellular Matrix Deposition by Activating Wnt/β-Catenin Signaling in Human Airway Smooth Muscle Cells

Liu

Shu

Gao

et al. 2023

Crit Rev Eukaryot Gene Expr

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“…HS formation is mainly caused by aberrant proliferation and migration of HSFs as well as excessive ECM deposition. 20 Previously, many studies have reported that HS formation could be alleviated by suppressing the abnormal growth of HSFs and excessive deposition of ECM. For example, miR-519d reduces the proliferation and induces the apoptosis of HSFs, and represses the expression of ECM-related genes, thus inhibiting HS formation.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of ANGPT2 activates autophagy during hypertrophic scar formation via PI3K/AKT/mTOR pathway

Chen

Xu²,

Sun³

et al. 2023

Anais Brasileiros de Dermatologia

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“…The formation of HS is mainly caused by excessive ECM deposition, as well as abnormal proliferation and migration of HSF 19 . Over-production of ECM is a common feature of many fibrotic diseases and may be induced by paracrine signals from activated lymphocytes and macrophages or autocrine factors secreted by fibroblasts 20 , 21 .…”

Section: Discussionmentioning

confidence: 99%

Shikonin promotes hypertrophic scar repair by autophagy of hypertrophic scar-derived fibroblasts

Zhang,

Wang,

Deng

et al. 2023

Acta Cir. Bras.

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To investigate the Shikonin (SHI) induce autophagy of hypertrophic scar-derived fibroblasts (HSFs) and the mechanism of which in repairing hypertrophic scar. Methods: This study showed that SHI induced autophagy from HSFs and repaired skin scars through the AMPK/mTOR pathway. Alamar Blue and Sirius red were used to identify cell activity and collagen.Electron microscopy, label-free quantitative proteomic analysis, fluorescence and other methods were used to identify autophagy. The differences in the expression of autophagy and AMPK/mTOR pathway-related proteins after SHI treatment were quantitatively analyzed by Western blots. A quantitative real-time polymerase chain reaction assay was used to detect the expression of LC3, AMPK and ULK after adding chloroquine (CQ) autophagy inhibitor. Results: After treatment with SHI for 24 hours, it was found that the viability of HSFs was significantly reduced, the protein expression of LC3-II/LC3-I and Beclin1 increased, while the protein expression of P62 decreased. The expression of phosphorylated AMPK increased and expression of phosphorylated mTOR decreased. After the use of CQ, the cell autophagy caused by SHI was blocked. The key genes LC3 and P62 were then reexamined by immunohistochemistry using a porcine full-thickness burn hypertrophic scar model, and the results verified that SHI could induce autophagy in vivo. Conclusion: These findings suggested that SHI promoted autophagy of HSFs cells, and the potential mechanism may be related to the AMPK/mTOR signal pathway, which provided new insights for the treatment of hypertrophic scars.

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LncRNA PICSAR binds to miR-485-5p and activates TGF-β1/Smad to promote abnormal proliferation of hypertrophic scar fibroblasts (HSFs) and excessive deposition of extracellular matrix (ECM)

Cited by 5 publications

References 24 publications

MicroRNA-485-3p Promotes the Inflammatory Response and Extracellular Matrix Deposition by Activating Wnt/β-Catenin Signaling in Human Airway Smooth Muscle Cells

MicroRNA-485-3p Promotes the Inflammatory Response and Extracellular Matrix Deposition by Activating Wnt/β-Catenin Signaling in Human Airway Smooth Muscle Cells

Inhibition of ANGPT2 activates autophagy during hypertrophic scar formation via PI3K/AKT/mTOR pathway

Shikonin promotes hypertrophic scar repair by autophagy of hypertrophic scar-derived fibroblasts

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LncRNA PICSAR binds to miR-485-5p and activates TGF-β1/Smad to promote abnormal proliferation of hypertrophic scar fibroblasts (HSFs) and excessive deposition of extracellular matrix (ECM)

Cited by 5 publications

References 24 publications

MicroRNA-485-3p Promotes the Inflammatory Response and Extracellular Matrix Deposition by Activating Wnt/&beta;-Catenin Signaling in Human Airway Smooth Muscle Cells

MicroRNA-485-3p Promotes the Inflammatory Response and Extracellular Matrix Deposition by Activating Wnt/&beta;-Catenin Signaling in Human Airway Smooth Muscle Cells

Inhibition of ANGPT2 activates autophagy during hypertrophic scar formation via PI3K/AKT/mTOR pathway

Shikonin promotes hypertrophic scar repair by autophagy of hypertrophic scar-derived fibroblasts

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MicroRNA-485-3p Promotes the Inflammatory Response and Extracellular Matrix Deposition by Activating Wnt/β-Catenin Signaling in Human Airway Smooth Muscle Cells

MicroRNA-485-3p Promotes the Inflammatory Response and Extracellular Matrix Deposition by Activating Wnt/β-Catenin Signaling in Human Airway Smooth Muscle Cells