Mangiferin Relieves Lipopolysaccharide-Induced Injury by Up-Regulating miR-181a via Targeting PTEN in ATDC5 Cells

Ma, Yunfei; Liu, Ying; Ma, Yunyan; Jiang, Nan; Wang, Lei; Wang, Bowei; Niu, Wanting; Hu, Yanjun; Lin, Qing; Yu, Bin

doi:10.3389/fphar.2020.00137

Cited by 12 publications

(6 citation statements)

References 49 publications

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“…Col10a1 peaked after 21 days of induction, and Runx2 decreased gradually after 7 days of induction. According to the results of this experiment and relevant literature reports [ 29 , 30 ], we set 14 days as the optimal cartilage induction time (Fig. 1 a).…”

Section: Resultsmentioning

confidence: 99%

Positive feedback regulation between USP15 and ERK2 inhibits osteoarthritis progression through TGF-β/SMAD2 signaling

et al. 2021

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Background The transforming growth factor-β (TGF-β) signaling pathway plays an essential role in maintaining homeostasis in joints affected by osteoarthritis (OA). However, the specific mechanism of non-SMAD and classical SMAD signaling interactions is still unclear, which needs to be further explored. Methods In ATDC5 cells, USP15 overexpression and knockout were performed using the transfected lentivirus USP15 and Crispr/Cas9. Western blotting and immunofluorescence staining were used to test p-SMAD2 and cartilage phenotype-related molecular markers. In rat OA models, immunohistochemistry, hematoxylin and eosin (HE)/Safranin-O fast green staining, and histology were used to examine the regulatory activity of USP15 in TGF-β/SMAD2 signaling and the cartilage phenotype. Then, ERK2 overexpression and knockout were performed. The expressions of USP15, p-SMAD2, and the cartilage phenotype were evaluated in vitro and in vivo. To address whether USP15 is required for ERK2 and TGF-β/SMAD2 signaling, we performed rescue experiments in vitro and in vivo. Immunoprecipitation and deubiquitination assays were used to examine whether USP15 could bind to ERK2 and affect the deubiquitination of ERK2. Finally, whether USP15 regulates the level of p-ERK1/2 was evaluated by western blotting, immunofluorescence staining, and immunohistochemistry in vitro and in vivo. Results Our results indicated that USP15 stimulated TGF-β/SMAD2 signaling and the cartilage phenotype. Moreover, ERK2 required USP15 to influence TGF-β/SMAD2 signaling for regulating the cartilage phenotype in vivo and in vitro. And USP15 can form a complex with ERK2 to regulate ubiquitination of ERK2. Interestingly, USP15 did not regulate the stability of ERK2 but increased the level of p-ERK1/2 to further enhance the TGF-β/SMAD2 signaling pathway. Conclusions Taken together, our study revealed positive feedback regulation between USP15 and ERK2, which played a critical role in TGF-β/SMAD2 signaling to inhibit OA progression. Therefore, this specific mechanism can guide the clinical treatment of OA.

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Section: Resultsmentioning

confidence: 99%

Positive feedback regulation between USP15 and ERK2 inhibits osteoarthritis progression through TGF-β/SMAD2 signaling

et al. 2021

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“…It was also indicated that allicin may inhibit invasion of LUAD by reducing the activity of the PI3K/AKT signaling pathway [69], and baicalein may increase cisplatin sensitivity of A549 cells via the PI3K/Akt/NF-κB pathway [70]. On the other hand, it was reported that mangiferin relieves lipopolysaccharide-induced injury by activating the PI3K/AKT pathway [71]. mangiferin also inhibits the MMP-9 gene in phorbol myristate acetate-stimulated human astroglioma, in which the PI3K/AKT pathway is involved [72].…”

Section: Discussionmentioning

confidence: 99%

Potential Therapeutic Value of Mangiferin for Lung Adenocarcinoma (Luad): A Comprehensive Study Based on in Vitro Experiments and Bioinformatics

Liu

Chi

Meng

et al. 2020

Preprint

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Background: Lung adenocarcinoma (LUAD), which is the most common lung cancer type in never-smokers and primarily occurs in women, requires effective treatment methods. Mangiferin is a polyphenol widely found in mango trees and has been reported to have chemotherapeutic and preventive potential against various types of cancer. Thus, we investigated the potential therapeutic value of mangiferin for LUAD.Methods: Cell lines A549, H2030 and H1299 were processed with mangiferin to detect and screen for differentially expressed lncRNAs and mRNAs. Close associations between extracted common lncRNAs and mRNAs were identified for lncRNA-mRNA network construction. Based on the network and an online database, target lncRNAs, target genes and meaningful lncRNA-mRNA pairs were identified, and signaling pathway analysis was performed.Results: The top 200 lncRNA-mRNA pairs were used to construct the network. We identified 12 target lncRNAs and 18 target genes. Gene nodes in the network were mostly visualized on the PI3K-Akt signaling pathway (P < 0.01). Furthermore, lncRNA-mRNA pairs that contained the genes ARHGAP29, BRIX1, CD109, CDK1, CTNNAL1, DAB2IP, DDIT4L, GPR162, ICAM5, KCNAB3 and MMP7 were considered to be meaningful lncRNA-mRNA pairs affected by mangiferin in LUAD.Conclusions: Our study provided a comprehensive understanding of the potential therapeutic value of mangiferin for LUAD.

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“…Col10a1 peaked after 21 days of induction, and Runx2 decreased gradually after 7 days of induction. According to the results of this experiment and relevant literature reports [29,30], we set 14 days as the optimal cartilage induction time (Fig. 1a).…”

Section: Usp15 Overexpression Can Prevent Cartilage Damage In Vivo and In Vitromentioning

confidence: 99%

Positive feedback regulation between USP15 and ERK2 inhibits osteoarthritis progression through TGF-β/SMAD2 signaling

Wang

Zhu

Sun

et al. 2021

Preprint

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Background: The transforming growth factor-β (TGF-β) signaling pathway plays an essential role in maintaining homeostasis in joints affected by osteoarthritis (OA). However, the specific mechanism of non-SMAD and classical SMAD signaling interactions is still unclear, which needs to be further explored.Methods: In ATDC5 cells, USP15 overexpression and knockout were performed using the transfected lentivirus USP15 and Crispr/Cas9. Western blotting and immunofluorescence staining were used to test p-SMAD2 and cartilage phenotype-related molecular markers. In rat OA models, immunohistochemistry, hematoxylin and eosin (HE)/Safranin-O fast green staining, and histology were used to examine the regulatory activity of USP15 in TGF-β/SMAD2 signaling and the cartilage phenotype. Then, ERK2 overexpression and knockout were performed. The expressions of USP15, p-SMAD2, and the cartilage phenotype were evaluated in vitro and in vivo. To address whether USP15 is required for ERK2 and TGF-β/SMAD2 signaling, we performed rescue experiments in vitro and in vivo. Immunoprecipitation and deubiquitination assays were used to examine whether USP15 could bind to ERK2 and affect the deubiquitination of ERK2. Finally, whether USP15 regulates the level of p-ERK1/2 was evaluated by western blotting, immunofluorescence staining, and immunohistochemistry in vitro and in vivo.Results: Our results indicated that USP15 stimulated TGF-β/SMAD2 signaling and the cartilage phenotype. Moreover, ERK2 required USP15 to influence TGF-β/SMAD2 signaling for regulating the cartilage phenotype in vivo and in vitro. And, USP15 can form a complex with ERK2 to regulate ubiquitination of ERK2. Interestingly, USP15 did not regulate the stability of ERK2 but increased the level of p-ERK1/2 to further enhance the TGF-β/SMAD2 signaling pathway.Conclusions: Taken together, our study revealed positive feedback regulation between USP15 and ERK2, which played a critical role in TGF-β/SMAD2 signaling to inhibit OA progression. Therefore, this specific mechanism can guide the clinical treatment of OA.

show abstract

Mangiferin Relieves Lipopolysaccharide-Induced Injury by Up-Regulating miR-181a via Targeting PTEN in ATDC5 Cells

Cited by 12 publications

References 49 publications

Positive feedback regulation between USP15 and ERK2 inhibits osteoarthritis progression through TGF-β/SMAD2 signaling

Positive feedback regulation between USP15 and ERK2 inhibits osteoarthritis progression through TGF-β/SMAD2 signaling

Potential Therapeutic Value of Mangiferin for Lung Adenocarcinoma (Luad): A Comprehensive Study Based on in Vitro Experiments and Bioinformatics

Positive feedback regulation between USP15 and ERK2 inhibits osteoarthritis progression through TGF-β/SMAD2 signaling

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