The long noncoding RNA GAS5 negatively regulates the adipogenic differentiation of MSCs by modulating the miR-18a/CTGF axis as a ceRNA

Li, Ming; Xie, Zhongyu; Wang, Peng; Li, Jinteng; Liu, Wenjie; Tang, Simin; Liu, Zhenhua; Wu, Xiaohua; Wu, Yanfeng; Shen, Huiyong

doi:10.1038/s41419-018-0627-5

Cited by 71 publications

(61 citation statements)

References 51 publications

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“…Written informed consent was obtained from all subjects included in the study. MSCs were isolated and cultured as previously described [16][17][18]. Briefly, MSCs were isolated and purified from bone marrow using density gradient centrifugation at 12,000 rpm for 30 min.…”

Section: Isolation and Culture Of Mscsmentioning

confidence: 99%

TRAF4 positively regulates the osteogenic differentiation of mesenchymal stem cells by acting as an E3 ubiquitin ligase to degrade Smurf2

Wang

Xie

et al. 2019

Cell Death Differ

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TNF receptor-associated factor 4 (TRAF4), a member of the TRAF family, plays an important role in the embryogenesis and development of the bone system. Mesenchymal stem cells (MSCs), which are the primary origin of osteoblasts in vivo, are key cells in bone development; however, whether TRAF4 modulates the osteogenic capacity of MSCs has never been explored. In this study, we demonstrated that TRAF4 positively regulates the osteogenic process of MSCs both in vitro and in vivo. In addition, we further demonstrated that TRAF4 modulates the osteogenic process of MSCs by acting as an E3 ubiquitin ligase to mediate the K48-linked ubiquitination of Smurf2 at the K119 site and cause degradation. Furthermore, TRAF4 was abnormally decreased in bone sections of ovariectomized rat and osteoporosis patients. Taken together, our findings suggest that TRAF4 positively regulates the osteogenic differentiation of MSCs by acting as an E3 ubiquitin ligase to degrade Smurf2. These results emphasize the critical role of TRAF4 in bone formation and could not only improve the clinical use of MSCs in tissue engineering but also clarify the pathogenesis of bone metabolism disorders.

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Section: Isolation and Culture Of Mscsmentioning

confidence: 99%

TRAF4 positively regulates the osteogenic differentiation of mesenchymal stem cells by acting as an E3 ubiquitin ligase to degrade Smurf2

Wang

Xie

et al. 2019

Cell Death Differ

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“…For instance, L. Liu et al () have proposed that GAS5 sensitizes renal cell carcinoma to sorafenib by modulating the miR‐21/sex determining region Y‐box protein‐5 axis as a ceRNA. Furthermore, M. Li et al () have demonstrated that GAS5 negatively regulates the adipogenic differentiation of mesenchymal stem cells by acting as a ceRNA of miR‐18a, which downregulates its target connective tissue growth factor. Besides, Ye et al () have recently reported that GAS5 aggravates inflammatory response by acting as a sponge of miR‐221 in THP‐1 macrophages.…”

Section: Discussionmentioning

confidence: 99%

lncRNA GAS5 promotes M1 macrophage polarization via miR‐455‐5p/SOCS3 pathway in childhood pneumonia

Chi

Ding

Zhang

et al. 2018

Journal Cellular Physiology

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Objectives We herein aimed to explore whether growth arrest‐specific 5 (GAS5) promotes M1 macrophage polarization in childhood pneumonia and to investigate the underlying mechanism. Methods Relative GAS5 and miR‐455‐5p expression and suppressor of cytokine signaling 3 (SOCS3) messenger RNA level were examined using quantitative reverse transcription polymerase chain reaction. Protein expression of SOCS3 and the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway‐related proteins was detected using western blot analysis. Luciferase activity assay was performed to test whether miR‐455‐5p could bind to GAS5 or SOCS3. The macrophage phenotype was determined using flow cytometry analysis and enzyme‐linked immunosorbent assay. Results The macrophage polarization toward the M2 phenotype was observed in peripheral blood from pneumonia children. Furthermore, GAS5 and SOCS3 expression were upregulated but miR‐455‐5p downregulated in human monocyte‐derived macrophages from pneumonia children compared with the control group. Furthermore, GAS5 acted as a sponge for miR‐455‐5p to facilitate SOCS3 expression. Moreover, miR‐455‐5p mimic and SOCS3 knockdown significantly reversed the GAS5 overexpression‐mediated suppression of the JAK2/STAT3 signaling and promotion of M1 polarization. Conclusion GAS5 promotes M1 macrophage polarization by acting as a competing endogenous RNA of miR‐455‐5p to facilitate SOCS3 expression in childhood pneumonia.

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“…RNA immunoprecipitation (RIP) assay was performed using the Magna RNA‐Binding Protein Immunoprecipitation Kit (Merck KGaA, Darmstadt, Germany) and the Ago2 antibody (ab32381; Abcam, Cambridge, UK) according to the manufacturer's protocols. After the antibody was recovered by protein beads, qRT‐PCR was performed to detect the relative expression level of lncRNA ENST00000413528 and miR‐593 in the precipitates …”

Section: Methodsmentioning

confidence: 99%

“…After the antibody was recovered by protein beads, qRT-PCR was performed to detect the relative expression level of lncRNA ENST00000413528 and miR-593 in the precipitates. 34…”

Section: Rna Immunoprecipitation Assaymentioning

confidence: 99%

Long noncoding RNA ENST00000413528 sponges microRNA‐593‐5p to modulate human glioma growth via polo‐like kinase 1

Zhang

Wei

et al. 2019

CNS Neurosci Ther

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Summary Aims In this study, we examined the expression of lncRNA ENST00000413528 in glioma and determined its role in glioma development. Methods LncRNA ENST00000413528 was detected in glioma tissues by lncRNA microarray. Then, we performed real‐time PCR, CCK‐8, colony formation assay, flow cytometry, caspase‐3/7 assay and animal experiment to detect the function of ENST00000413528 in glioma after ENST00000413528 knockdown. Subsequent bioinformatics analysis, luciferase reporter assays and RNA immunoprecipitation (RIP) assay western blotting indicated possible downstream regulatory molecules. The expression of PLK1 in glioma tissues was also examined by immunohistochemistry staining. Results Expression of ENST00000413528 was significantly increased in glioma tissues and LN229 and U251 cells. PLK1 protein could not be detected in peritumoral brain edema (PTBE) tissues; however, it showed an increasing number of positively cytoplasmic stained from WHO‐Grade II to Grade III gliomas. Knockdown of ENST00000413528 in glioma cells inhibited cell proliferation and colony formation abilities, induced the G0/G1 arrest of the cell cycle, and promoted apoptosis. The dual reporter assay and RNA immunoprecipitation assay verified the interaction between ENST00000413528 and miR‐593. We also demonstrated that polo‐like kinase 1 (PLK1) was regulated by miR‐593; PLK1 messenger RNA lacking 3’UTR partially reversed the effects caused by ENST00000413528 knockdown or miR‐593 upregulation. Conclusion lncRNA ENST00000413528 is closely related to the development of glioma via the miR‐593‐5p/PLK1 pathway.

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The long noncoding RNA GAS5 negatively regulates the adipogenic differentiation of MSCs by modulating the miR-18a/CTGF axis as a ceRNA

Cited by 71 publications

References 51 publications

TRAF4 positively regulates the osteogenic differentiation of mesenchymal stem cells by acting as an E3 ubiquitin ligase to degrade Smurf2

TRAF4 positively regulates the osteogenic differentiation of mesenchymal stem cells by acting as an E3 ubiquitin ligase to degrade Smurf2

lncRNA GAS5 promotes M1 macrophage polarization via miR‐455‐5p/SOCS3 pathway in childhood pneumonia

Long noncoding RNA ENST00000413528 sponges microRNA‐593‐5p to modulate human glioma growth via polo‐like kinase 1

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