http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
- 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
- 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
RISS 인기검색어
- 검색키워드
- 저자 : Guanghua Lei (검색결과 2 건)
- 무료
- 기관 내 무료
- 유료
-
Upregulation of miR-27b Facilitates Apoptosis of TNF-α-Stimulated Fibroblast-Like Synoviocytes
Shangwen Lei,Guanghua Chen,Liang Deng,Jianying He 연세대학교의과대학 2019 Yonsei medical journal Vol.60 No.6
Purpose: The aim of this study was to explore the function of microRNA-27b (miR-27b) in fibroblast-like synoviocytes (FLSs)stimulated by tumor necrosis factor α (TNF-α). Materials and Methods: mRNA expression of miR-27b in FLS cells (MH7A) treated with or without TNF-α was determined by q-PCR. MiR-27b mimics was transfected into MH7A cells to upregulate miR-27b expression. MTT assay and flow cytometry analysiswere performed to investigate the effect of miR-27b on MH7A cell viability and apoptosis. The targets of miR-27b were predictedby TargetScan. The direct regulation of miR-27b on IL-1β expression was verified by luciferase assay. The protein expressionlevels of apoptosis-related proteins, IL-1β, and NF-κB signaling-related proteins were detected by Western blot. Results: We discovered that miR-27b expression was decreased in MH7A cells stimulated by TNF-α. Upregulation of miR-27b bymiR-27b mimics significantly inhibited the proliferation and promoted the apoptosis of TNF-α-stimulated MH7A cells. Consistently,upregulation of miR-27 decreased the level of Bcl-2 and increased Bax and caspase-3 expression in MH7A cells stimulated byTNF-α. Luciferase assay revealed that IL-1β was indeed a target of miR-27b. By quantitative real-time PCR and Western blot, wefound that the expression of IL-1β is negatively regulated by miR-27b. Moreover, the NF-κB signaling pathway was significantlyinhibited by miR-27b. Conclusion: Taken together, our results illustrated that enhanced miR-27b expression results in the suppression of proliferationand the promotion of apoptosis in FLSs stimulated by TNF-α, partially by regulating IL-1β expression and NF-κB signaling.
-
Luxin Liang,Deye Song,Kai Wu,Zhengxiao Ouyang,Qianli Huang,Guanghua Lei,Kun Zhou,Jian Xiao,Hong Wu 한국생체재료학회 2022 생체재료학회지 Vol.26 No.2
Background: Even though the modulatory effects of Magnisum (Mg) and its alloys on bone-healing cells have been widely investigated during the last two decades, relatively limited attention has been paid on their inflammationmodulatory properties. Understanding the activation process of macrophages in response to the dynamic degradation process of Mg as well as the relationship between macrophage phenotypes and their osteogenic potential is critical for the design and development of advanced Mg-based or Mg-incorporated biomaterials. Methods: In this work, a Ti-0.625 Mg (wt.%) alloy fabricated by mechanical alloying (MA) and subsequent spark plasma sintering (SPS) was employed as a material model to explore the inflammatory response and osteogenic performance in vitro and in vivo by taking pure Ti as the control. The data analysis was performed following Student’s t-test. Results: The results revealed that the macrophages grown on the Ti-0.625 Mg alloy underwent sequential activation of M1 and M2 phenotypes during a culture period of 5 days. The initially increased environmental pH (~ 8.03) was responsible for the activation of M1 macrophages, while accumulated Mg2+ within cells contributed to the lateral M2 phenotype activation. Both M1 and M2 macrophages promoted osteoblast-like SaOS-2 cell maturation. In vivo experiment further showed the better anti-inflammatory response, regenerative potentiality and thinner fibrous tissue layer for the Ti-0.625 Mg alloy than pure Ti. Conclusion: The results highlighted the roles of Mg degradation in the Ti-0.625 Mg alloy on the sequential activation of macrophage phenotypes and the importance of modulating M1-to-M2 transition in macrophage phenotypes for the design and development of inflammation-modulatory biomaterials.
연관 검색어 추천
이 검색어로 많이 본 자료
활용도 높은 자료
