MiR-135b调控BMPs/Smads信号通路在牙髓细胞成牙本质向分化中的作用及机制研究
项目来源
广（略）技（略）
项目主持人
宋（略）
项目受资助机构
中（略）
立项年度
2（略）
立项时间
未（略）
项目编号
2（略） A030310227
项目级别
省（略）
研究期限
未（略） （略）
受资助金额
1（略）0（略）
学科
临（略）
学科代码
未（略）
基金类别
广（略）然（略）金（略）启（略）
关键词
M（略）1（略） （略）m（略） （略）m（略） （略）胞（略）;（略）本（略） （略）e（略）d（略）e（略）t（略）i（略）;（略）o（略）b（略）t（略）
参与者
未（略）
参与机构
未（略）
项目标书摘要：目的（略）髓细胞(hDPCs（略）的功能。 （略）比较性miRNA微（略）的成牙本质细胞样分（略）达。通过定量实时逆（略）T-PCR)和原位（略）croRNA-13（略）)的丰度。生物信息（略）结合，用于鉴定与m（略）的靶标。进行了mi（略）研究hDPC在成牙（略）和机制。通过单因素（略）学生t检验进行统计（略）结果：鉴定了36种（略）胞样分化中差异表达（略）hDPCs分化过程（略）达明显下调(P （略）观察结果表明miR（略）质细胞样hDPC分（略）抑制miR-135（略）工程的有前途的治疗（略）
Applicati（略）: Aim:To （略） the func（略）NAs in od（略）ike diffe（略）of human （略） cells(hD（略） Methodo（略）ated comp（略）NA microa（略）ing was u（略）rmine the（略）al miRNAs（略） in odont（略） differen（略）hDPCs.The（略）of microR（略）-135b)was（略）y quantit（略）time reve（略）iptase po（略）ain react（略）)and in s（略）zation(IS（略）matic ana（略）ned with （略）assays we（略） to ident（略）gets inte（略）h miR-135（略）ssion of （略）s perform（略）tigate th（略）mechanism（略）last-like（略）ation of （略）stical an（略）performed（略） analysis（略）e(anova)o（略） t-test. （略）lts:Thirt（略）rentially（略）microRNAs（略）last-like（略）ation of （略）identifie（略）expressio（略）ficantly （略）ed during（略）erentiati（略） Conclusi（略）bservatio（略）d a poten（略）f miR-135（略）ing odont（略） differen（略）hDPCs and（略） of miR-1（略）e a promi（略）eutic way（略）ate denti（略）ngineerin（略）
项目受资助省
广（略）
1.MicroRNA 135b通过调节Smad5和Smad4抑制人牙髓细胞成牙本质细胞样分化(MicroRNA-135b inhibits odontoblast-like differentiation of human dental pulp cells by regulating Smad5 and Smad4)
- 关键词：
- MiR-135b、Smad4、Smad5、细胞分化、成牙本质细胞、MiR-135b、Smad4、Smad5、cell differentiation、odontoblasts
- 宋智；
- 《中山大学；》
- 2020年
- 报告
目的：研究miRNA在人牙髓细胞(hDPCs)成牙本质细胞样分化中的功能。 方法：采用集成的比较性miRNA微阵列分析来确定hDPC的成牙本质细胞样分化中的差异miRNA表达。通过定量实时逆转录聚合酶链反应(qRT-PCR)和原位杂交(ISH)测量microRNA-135b(miR-135b)的丰度。生物信息学分析与萤光素酶分析相结合，用于鉴定与miR-135b相互作用的靶标。进行了miR-135b的过表达以研究hDPC在成牙本质细胞样分化中的作用和机制。通过单因素方差分析(方差分析)或学生t检验进行统计分析。 结果：鉴定了36种在hDPC的成牙本质细胞样分化中差异表达的microRNA。在hDPCs分化过程中,MiR-135b表达明显下调(P<0.05)。此外,miR-135b能够与Smad5和Smad4的3'-UTR结合并抑制这两个基因的表达(P<0.05)。此外,miR-135b的过表达抑制了hDPC的成牙本质细胞样分化，并减弱了Smad5和Smad4的表达(P<0.05)。 结论：这些观察结果表明miR-135b在介导成牙本质细胞样hDPC分化中具有潜在作用，并且抑制miR-135b可能是促进牙本质组织工程的有前途的治疗方法。 Aim:To investigate the function of miRNAs in odontoblast-like differentiation of human dental pulp cells(hDPCs). Methodology:Integrated comparative miRNA microarray profiling was used to determine the differential miRNAs expression in odontoblast-like differentiation of hDPCs.The abundance of microRNA-135b(miR-135b)was measured by quantitative real-time reverse transcriptase polymerase chain reaction(qRT-PCR)and in situ hybridization(ISH).Bioinformatic analyses combined with luciferase assays were utilized to identify the targets interacting with miR-135b.Overexpression of miR-135b was performed to investigate the role and mechanism in odontoblast-like differentiation of hDPCs.Statistical analysis was performed by one-way analysis of variance(anova)or Student's t-test. Results:Thirty-six differentially expressed microRNAs in odontoblast-like differentiation of hDPCs were identified.MiR-135b expression was significantly downregulated during hDPCs differentiation(P<0.05).In addition,miR-135b was able to bind to the 3'-UTR of the Smad5 and Smad4 and repressed these two genes expression(P<0.05).Furthermore,overexpression of miR-135b suppressed odontoblast-like differentiation of hDPCs and attenuated the expression of Smad5 and Smad4(P<0.05). Conclusions:These observations indicated a potential role of miR-135b in mediating odontoblast-like differentiation of hDPCs and inhibition of miR-135b might be a promising therapeutic way to facilitate dentine tissue engineering.
...2.Long noncoding RNA PVT1-214 promotes proliferation and invasion of colorectal cancer by stabilizing Lin28 and interacting with miR-128
- 关键词：
- CELL-PROLIFERATION; POOR-PROGNOSIS; GASTRIC-CANCER; UP-REGULATION;PROGRESSION; MECHANISMS; APOPTOSIS; GROWTH; LOOP
- He, Feng;Song, Zhi;Chen, Huacui;Chen, Zhuanpeng;Yang, Ping;Li, Wanglin;Yang, Zhi;Zhang, Tong;Wang, Fei;Wei, Jianchang;Wei, Fang;Wang, Qiang;Cao, Jie
- 《ONCOGENE》
- 2019年
- 38卷
- 2期
- 期刊
Long noncoding RNAs (lncRNAs) are implicated in human cancer, but their mechanisms of action are largely unknown. In this study, we investigated lncRNA alterations that contribute to colorectal cancer (CRC) through microarray expression profiling in CRC patient samples. Here, we report that the CRC-associated lncRNA PVT1-214 is a key regulator of CRC development and progression; patients with high PVT1-214 expression had a shorter survival and poorer prognosis. In vitro and in vivo investigation of the role of PVT1-214 revealed a complex integrated phenotype affecting cell growth, stem-like properties, migration, and invasion. Furthermore, using RNA pull-down and mass spectrometry, we found that Lin28 (also known as Lin28A), a highly conserved RNA-binding protein, is associated with PVT1-214. Strikingly, we found that PVT1-214 not only upregulated Lin28 protein expression in CRC cells by stabilizing Lin28, but also participated in crosstalk with Lin28 mRNA through competition for miR-128 binding, imposing an additional level of post-transcriptional regulation. In addition, we further show that PVT1-214 repressed expression of let-7 family miRNAs, which was abrogated by Lin28 knockdown. Taken together, our findings support a model in which the PVT1-214/Lin28/let-7 axis serves as a critical regulator of CRC pathogenesis, which may simulate a new direction for CRC therapeutic development.
...3.MicroRNA-135b inhibits odontoblast-like differentiation of human dental pulp cells by regulating Smad5 and Smad4
- 关键词：
- cell differentiation; MiR-135b; odontoblasts; Smad4; Smad5;STEM-CELLS; ODONTOGENIC DIFFERENTIATION; FEEDBACK LOOP; PROLIFERATION;EXPRESSION
- Song, Z.;Chen, L. L.;Wang, R. F.;Qin, W.;Huang, S. H.;Guo, J.;Lin, Z. M.;Tian, Y. G.
- 《INTERNATIONAL ENDODONTIC JOURNAL》
- 2017年
- 50卷
- 7期
- 期刊
Aim To investigate the function of miRNAs in odontoblast-like differentiation of human dental pulp cells (hDPCs).Methodology Integrated comparative miRNA microarray profiling was used to determine the differential miRNAs expression in odontoblast-like differentiation of hDPCs. The abundance of microRNA-135b (miR-135b) was measured by quantitative real-time reverse transcriptase polymerase chain reaction (qRT-PCR) and in situ hybridization (ISH). Bioinformatic analyses combined with luciferase assays were utilized to identify the targets interacting with miR-135b. Overexpression of miR-135b was performed to investigate the role and mechanism in odontoblast-like differentiation of hDPCs. Statistical analysis was performed by one-way analysis of variance (ANOVA) or Student's t-test.Results Thirty-six differentially expressed microRNAs in odontoblast-like differentiation of hDPCs were identified. MiR-135b expression was significantly downregulated during hDPCs differentiation (P < 0.05). In addition, miR-135b was able to bind to the 30-UTR of the Smad5 and Smad4 and repressed these two genes expression (P < 0.05). Furthermore, overexpression of miR-135b suppressed odontoblast-like differentiation of hDPCs and attenuated the expression of Smad5 and Smad4 (P < 0.05).Conclusions These observations indicated a potential role of miR-135b in mediating odontoblast-like differentiation of hDPCs and inhibition of miR-135b might be a promising therapeutic way to facilitate dentine tissue engineering.
...4.Role of transient receptor potential channel 6 in the odontogenic differentiation of human dental pulp cells
- 关键词：
- transient receptor potential channel 6; odontoblasts; celldifferentiation; calcium;OPERATED CA2+ ENTRY; CALCIUM HYDROXIDE; STEM-CELLS; OSTEOGENICDIFFERENTIATION; STROMAL CELLS; TRPC6 PROTEIN; ION RELEASE; ACTIVATION;EXPRESSION; DENTINOGENESIS
- Yang, Xiaoting;Song, Zhi;Chen, Lingling;Wang, Runfu;Huang, Shuheng;Qin, Wei;Guo, Jia;Lin, Zhengmei
- 《EXPERIMENTAL AND THERAPEUTIC MEDICINE》
- 2017年
- 14卷
- 1期
- 期刊
Pulp capping is a restorative technique employed in an attempt to maintain pulpal vitality and generate reparative dentin. Ca2+ released from capping materials is suggested to promote reparative dentin formation. Transient receptor potential channel 6 (TRPC6) is a receptor-operated Ca2+ channel that serves an important role in Ca2+ influx in the majority of non-excitable cells, and influences the calcium signaling and cell respond. Therefore, the purpose of the present study was to gain an insight into the role of TRPC6 in the odontoblastic differentiation of human dental pulp cells (HDPCs). Human dental pulp tissues and HDPCs were obtained from healthy third molars. By immunohistochemical staining, TRPC6 was observed to be highly expressed in the dental pulp tissue, particularly in the odontoblast layer. In addition, the protein level of TRPC6 was increased in a time-dependent manner during odontogenic differentiation of HDPCs. Downregulation of TRPC6 by a lentivirus vector containing TRPC6 shRNA inhibited the process of odontogenic differentiation in HDPCs. In conclusion, the current data demonstrated that TRPC6 served a significant role in the odontogenic differentiation of HDPCs, suggesting it may be a promising therapeutic target in regenerative endodontics.
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