The activity of Nodal signaling can be modulated by microRNAs(miRNAs)as previously reported,but little
is known about which miRNAs are regulated by Nodal during gastrulation.In the present study,we found that the expression of mir206,one of the most abundant miRNAs during zebrafish early embryo development,is regulated by Nodal signaling.Abrogation of Nodal signal activity results in defective convergence and extension(CE)movements,and these cell migration defects can be rescued 有 by supplying an excess of mir206,suggesting that mir206 acts downstream of Nodal signaling to regulate CE movements.Furthermore,in mir206 morphants,the expression of cell adhesion molecule E-cadherin is significantly increased,while the key transcriptional repressor of E-cadherin,snail1a,is depressed.Our study uncovers a novel mechanism by which Nodal-regulated mir206
modulates gastrulation movements in connection with the Snail/E-cadherin 点击此处 pathway.
青光眼是一组以视神经萎缩和视野缺损为共同特征的疾病,病理性眼压增高是主要危险因素。转化生长因子-β(transforming growth factor beta,TGF-β)是一类生物学功能复杂的细胞因子,与很多眼科疾病密切相关。Smad蛋白家族是TGF-β细胞内信号转导的重要因子。本文就TGF-β/Smad信号通路对青光眼产生的机制及术后手术区瘢痕形成的影响进行综述。
Mounting evidence in stem cell biology has shown that microRNAs(miRNAs) play a crucial role in cell fate specification, including stem cell self-renewal, lineagespecific differentiation, and somatic cell reprogramming.These functions are tightly regulated by specific gene expression patterns that involve
miRNAs and transcription factors. To maintain stem cell pluripotency, specific miRNAs suppress transcription factors that 什么 promote differentiation, whereas to initiate differentiation, lineagespecific miRNAs are upregulated via the inhibition of transcription factors that promote self-renewal. Small molecules can be used in a similar manner as natural miRNAs, and a number of natural and synthetic small molecules have been isolated and developed to regulate stem cell fate. Using miRNAs as novel regulators of stem cell fate will provide insight into stem cell biology and aid in understanding the molecular mechanisms and crosstalk between miRNAs and stem cells.