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miR-424-5p regulates apoptosis and cell proliferation via targeting Bcl2 in nucleus pulposus cells
Lu Hua-tuo,Xu Yong-qing,Wang Hai,Zhang Xu-lin 한국통합생물학회 2020 Animal cells and systems Vol.24 No.3
Background: miRNAs play an important role in the pathogenesis of intervertebral disc degeneration (IDD). The role and the underlying mechanism of miR-424-5p in human nucleus pulposus (NP) are still unknown. We aimed to explore the role of miR-424-5p in IDD. Methods: Real-time PCR was used to detect the expression of miR-424-5p and Bcl2 in IDD tissues and idiopathic scoliosis tissues. Human NP cells were used in our study. MTT and Hoechst apoptosis assays were used to detect the proliferation and apoptosis of NP cells, respectively. Western blotting assays were used to detect the expression levels of Bcl-2, cleaved caspase-3, cleaved caspase-9, caspase-3 and caspase-9 in degenerative NP cells. A luciferase reporter assay was applied to confirm the relationship between miR-424-5p and Bcl2. Results: Our results showed that the expression of miR-424-5p was increased and Bcl2 was decreased in degenerative NP cells. miR-425-5p expression was negatively correlated with Bcl2 expression in IDD tissues. Suppression of miR-424-5p using an inhibitor increased Bcl2 expression at both the mRNA and protein levels, and it promoted cell viability and inhibited apoptosis. Furthermore, the levels of cleaved caspase-3 and cleaved caspase-9 were downregulated in miR-424-5p-silenced NP cells. Interestingly, we found that silencing miR-424- 5p increased p62 expression at both the mRNA and protein levels. Finally, a luciferase reporter assay verified the binding of the miR-424-5p and the 3’UTR of Bcl2. Conclusion: These results suggested that silencing miR-424-5p suppressed NP cell apoptosis by upregulating Bcl2. Therefore, miR-424-5p might be a novel target for IDD therapies.
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( Wan Xing Yong ),( Xu Cheng Fu ),( Lu Chao ),( Yu Wei Lai ),( Zhu Hua Tuo ),( Yu Chao Hui ),( Li You Ming ) 대한내과학회 2014 대한내과학회 추계학술대회 Vol.2014 No.1
Background: Serum uric acid is strongly associated with nonalcoholic fatty liver disease (NAFLD) and insulin resistance in patients. However, whether this association is causally or coincidentally with NAFLD and insulin resistance remains uncertain, neither the mechanisms behind this association are unclear so far. Methods: We first analyzed the impact of uric acid on development of hepatic steatosis in mice and two cell models (HepG2 and HL7702), and then explored the effect of uric acid on insulin signaling, including phosphorylation of insulin receptor substrate 1 (IRS1) and Akt in HepG2 and HL7702 cells. Further, we studied the role of NLRP3 inflammasome in regulation of hepatic steatosis and insulin signaling. Results: Uric acid directly induced hepatocyte fat accumulation both in vivo and in vitro. Further, uric acid treatment decreased insulin-induced phospho-Akt (ser437) and enhanced the phospho-IRS1(ser307) in HepG2 and HL7702 cells. Then, we found significant increases of NLRP3 inflammasome-related molecules, both mRNA and protein levels, including NLPR3, caspase-1, IL-1ß, and IL-18, in HepG2 and HL7702 cells stimulated with uric acid. We also found that uric acid induced significant elevations of IL-1ß and IL-18 levels in culture supernatants of HepG2 and HL7702 cells. Consistent with in vitro results, mice fed 8 weeks of hyperuricemia-inducing diet resulted in significant up-regulation of hepatic mRNA and protein expressions of NLPR3, caspase-1, IL-1ß and IL-18, and elevation of serum IL-1ß and IL-18 levels. Further experiments indicated that silencing NLRP3 expression significantly alleviated uric acid-induced fat accumulation in vitro. Moreover, inhibition of NLRP3 expression ameliorated uric acid induced insulin signaling impairing, confirmed by increased insulin- induced phospho-Akt (ser437) and reduced the phospho-IRS1(ser307) in vitro. Conclusions: Our results suggest that uric acid contributes to hepatic steatosis and impairs insulin signaling through the NLRP3 inflammasome dependent mechanism.
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