Denbinobin upregulates miR-146a expression and attenuates IL-1β-induced upregulation of ICAM-1 and VCAM-1 expressions in osteoarthritis fibroblast-like synoviocytes

Yang, Congrong; Shih, Kao-Shang; Liou, Jing‐Ping; Wu, Yiwen; Hsieh, I-Ni; Lee, Hsueh Yun; Lin, Tzu-Cheng; Wang, Jyh-Horng

doi:10.1007/s00109-014-1192-8

Cited by 51 publications

(29 citation statements)

References 23 publications

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“…In the present study, it was shown that PDGF-BB stimulation significantly increased the levels of phosphorylated p38 MAPK and Erk1/2 in VSMCs, which was inhibited by evodiamine treatment. These findings were in accordance with previous studies involving tumor cells, and suggested that the inhibition of mitogenesis and p-38/p-Erk activity may serve as the molecular basis for the functions of evodiamine (21,27,28). However, the regulation of p38 and Erk activity by evodiamine is cell type-dependent and may be negative or positive.…”

Section: Discussionsupporting

confidence: 93%

“…Therefore, the observation that PDGF-BB increased and evodiamine decreased the expression of p21 in the present study was not unusual. Of note, the inhibitory effects of evodiamine on cell cycle progression have been previously observed in various human tumor cell lines, including small-cell lung cancer cells (20), gastric cancer cells (11), breast cancer cells (21), gastric adenocarcinoma cells (22) and cervical carcinoma HeLa cells (23), and are considered to be important in the antitumor action of evodiamine. The data obtained in the present study extends the current recognition of evodiamine, and suggested that the regulation of cell cycle progression by evodiamine may be general and function in a broader range of cell types, including tumor cells and vascular cells.…”

Section: Discussionmentioning

confidence: 97%

“…Of note, evodiamine exhibits antitumor properties by inhibiting the proliferation of various cancer cell lines. The molecular mechanisms through which evodiamine suppresses proliferation rates involve cell cycle progression arrest (G2/M phase) and the induction of apoptosis (11). Of note, evodiamine has a beneficial effect in cardiovascular diseases.…”

Section: Introductionmentioning

confidence: 99%

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Evodiamine inhibits PDGF-BB-induced proliferation of rat vascular smooth muscle cells through the suppression of cell cycle progression and oxidative stress

Ge¹,

Chen²,

Liu³

et al. 2016

Molecular Medicine Reports

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Vascular smooth muscle cell (VSMC) proliferation is a key event in the development of in-stent restenosis. Evodiamine is an indole alkaloid extracted from the Chinese medicine, evodia, and has been shown to inhibit tumor cell proliferation and protect the cardiovascular system. However, whether evodiamine affects VSMC proliferation remains to be elucidated. Therefore, the present study examined the effects and the mechanisms of action of evodiamine on the proliferation of rat VSMCs. The cells were treated with evodiamine alone or in combination with platelet-derived growth factor-BB (PDGF-BB) stimulation. It was found that evodiamine inhibited PDGF-BB-induced VSMC proliferation in a dose-dependent manner, without inducing cell death. Evodiamine also retarded cell cycle progression, evidenced by the suppression of the expression of cell cycle-promoting cyclin proteins and cyclin-dependent kinases. In addition, evodiamine attenuated the PDGF-BB-induced phosphorylation of mitogen-activated protein kinases p38 and extracellular signal-regulated kinases 1/2, however, it had no effect on the phosphorylation of Akt. Evodiamine also inhibited the increase of reactive oxygen species generation and upregulated the mRNA expression levels of genes encoding antioxidant enzymes. These findings provide important insights into the mechanisms underlying the vasoprotective actions of evodiamine and suggest that it may be a useful therapeutic agent for the treatment of vascular occlusive disease.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

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Evodiamine inhibits PDGF-BB-induced proliferation of rat vascular smooth muscle cells through the suppression of cell cycle progression and oxidative stress

Ge¹,

Chen²,

Liu³

et al. 2016

Molecular Medicine Reports

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“…MicroRNAs are small noncoding RNAs with lengths of 21-25 nucleotides, which regulate gene expression at the posttranscriptional level [32][33][34]. Aberrant expressions of microRNAs have been found in various types of cancers [35].…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA GIHCG promotes hepatocellular carcinoma progression through epigenetically regulating miR-200b/a/429

et al. 2016

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Long noncoding RNAs (lncRNAs) have been reported to play pivotal roles in a variety of cancers. However, lncRNAs involved in hepatocellular carcinoma (HCC) initiation and progression remain largely unclear. In this study, we identified an lncRNA gradually increased during hepatocarcinogenesis (lncRNA-GIHCG) using publicly available microarray data. Our results further revealed that GIHCG is upregulated in HCC tissues in comparison with adjacent non-tumor tissues. High GIHCG expression is correlated with large tumor size, microvascular invasion, advanced BCLC stage, and poor survival of HCC patients. Functional experiments showed that GIHCG promotes HCC cells proliferation, migration, and invasion in vitro, and promotes xenografts growth and metastasis in vivo. Mechanistically, we demonstrated that GIHCG physically associates with EZH2 and the promoter of miR-200b/a/429, recruits EZH2 and DNMT1 to the miR-200b/a/429 promoter regions, upregulates histone H3K27 trimethylation and DNA methylation levels on the miR-200b/a/429 promoter, and dramatically silences miR-200b/a/429 expression. Furthermore, the biological functions of GIHCG on HCC are dependent on the silencing of miR-200b/a/429. Collectively, our results demonstrated the roles and functional mechanisms of GIHCG in HCC, and indicated GIHCG may act as a prognostic biomarker and potential therapeutic target for HCC. KEY MESSAGE: lncRNA-GIHCG is upregulated in HCC and associated with poor survival of patients. GIHCG significantly promotes tumor growth and metastasis of HCC. GIHCG physically associates with EZH2. GIHCG upregulates H3K27me3 and DNA methylation levels on the miR-200b/a/429 promoter. GIHCG epigenetically silences miR-200b/a/429 expression.

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“…In other inflammatory diseases, miRNA-155 can also indirectly promote the production of IL-1β [33,34]. There are also several miRNAs which can indirectly inhibit the production of IL-1β, such as miR-146a miR-223, and miRNA-146b-5p [30,[35][36][37][38][39].…”

Section: Mirnas and Inflammatory Cytokinesmentioning

confidence: 99%

Could MicroRNAs be Regulators of Gout Pathogenesis?

Wang¹,

Xu²,

Wang³

et al. 2015

Cell Physiol Biochem

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MicroRNAs (miRNAs) are a class of noncoding RNAs that mainly negatively regulate gene expression. miRNAs have important roles in many diseases, including inflammatory diseases. Gout is a common arthritis caused by deposition of monosodium urate crystals within joints. Recent studies suggested that miRNAs may be involved in the development of inflammatory arthritis, including acute gouty arthritis. In the present review, we systemically discuss relevant publications in order to provide a better understanding on the possible role of miRNAs in gout. miRNAs may act as regulators of gout pathogenesis via several pathways. Targeting miRNAs may be a promisingstrategy in the treatment of gout.

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Denbinobin upregulates miR-146a expression and attenuates IL-1β-induced upregulation of ICAM-1 and VCAM-1 expressions in osteoarthritis fibroblast-like synoviocytes

Abstract: Denbinobin inhibited IL-1β-induced ICAM-1/VCAM-1 expression and monocyte adhesion to OA-FLS. It was due to denbinobin increased miR-146a level, which in turn inhibited NF-κB signaling. Our overall findings suggest that denbinobin can be used as a potent anti-inflammatory agent.

Cited by 51 publications

References 23 publications

Evodiamine inhibits PDGF-BB-induced proliferation of rat vascular smooth muscle cells through the suppression of cell cycle progression and oxidative stress

Evodiamine inhibits PDGF-BB-induced proliferation of rat vascular smooth muscle cells through the suppression of cell cycle progression and oxidative stress

Long noncoding RNA GIHCG promotes hepatocellular carcinoma progression through epigenetically regulating miR-200b/a/429

Could MicroRNAs be Regulators of Gout Pathogenesis?

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