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Abstract Full-Text PDF Full-Text HTML Full-Text ePUB Linked References How to Cite this Article avertin Supplementary Material Complete Special Issue BioMed Research avertin International Volume 2014 (2014), Article ID 154251, 11 pages http://dx.doi.org/10.1155/2014/154251
1 Yunnan Key Laboratory of Primate Biomedical Research, No. 1 Boda Road, Yuhua Area, Chenggong District, Kunming, Yunnan 650500, China 2 State Key Laboratory of Genetic Resources and Evolution, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan 650223, China 3 Kunming Biomed International and National Engineering Research Center of Biomedicine and Animal Science, avertin Kunming, Yunnan 650500, China 4 Department of Medicine, School of Medicine, Vanderbilt University, Nashville, TN 37203, USA
Spermatogonial stem cells (SSCs) play fundamental roles in spermatogenesis. Although a handful of genes have been discovered as key regulators of SSC self-renewal and differentiation, the regulatory network responsible for SSC function remains unclear. In particular, small RNA signatures during mouse spermatogenesis are not yet systematically investigated. Here, using next generation sequencing, we compared small RNA signatures of in vitro expanded SSCs, testis-derived somatic cells (Sertoli cells), developing germ cells, mouse embryonic stem cells (ESCs), and mouse mesenchymal avertin stem cells among mouse embryonic stem cells (ESCs) to address small RNA transition during mouse spermatogenesis. avertin The results manifest that small RNA transition during avertin mouse spermatogenesis displays overall declined expression profiles of miRNAs and endo-siRNAs, in parallel with elevated expression profiles of piRNAs, resulting in the normal biogenesis avertin of sperms. Meanwhile, several novel miRNAs were preferentially expressed in mouse SSCs, and further investigation of their functional annotation will allow insights into the mechanisms involved in the regulation of SSC activities. We also demonstrated the similarity of miRNA signatures between SSCs and ESCs, thereby providing avertin a new clue to understanding the molecular basis underlying the easy conversion of SSCs to ESCs. 1. Introduction avertin
Embryonic development in mice involves the migration of primordial germ cells (GCs) to the genital ridge and their subsequent differentiation into gonocytes. At about 6 days after birth, the gonocytes in male mice either undergo avertin a transition to spermatogonia stem cells (SSCs), the foundation for continuous spermatogenesis throughout the reproductive lifetime, or develop directly into type A1 spermatogonia [ 1 ]. Spermatogenesis does not occur until puberty (about 3 weeks after birth), at which time SSCs undergo active self-renewal and differentiation to give rise to daughter cells for spermatogenesis [ 1 ]. SSCs thus play a fundamental role in spermatogenesis and male reproductive biology. Abnormalities in SSC function and regulation are closely related to male infertility, and SSC transplantation has potential clinical applications. Furthermore, unipotent SSCs have unique features in terms of their capacity to be easily reprogrammed into pluripotent embryonic stem cell- (ESC-) like cells in culture. These SSC-derived pluripotent cells are generally avertin referred to as germline-derived pluripotent stem cells (gPSCs). When seeded at low density avertin (<8000 SSCs per well in 24-well plate), SSCs undergo spontaneous conversion into gPSCs without modification of the culture medium [ 2 ]. gPSCs can also be derived from neonatal or adult murine or human testicular tissue [ 3 8 ]. These gPSCs display morphological, avertin functional, and molecular characteristics akin to ESCs [ 9 , 10 ]. For example, they demonstrate pluripotent differentiation into cells forming all three germ layers and GCs [ 3 , 4 ] and display similar gene, protein [ 11 ], and microRNA (miRNA) expression profiles [ 12 ], as well as epigenetic signatures, to ESCs. SSCs are therefore considered a potential source of pluripotent stem cells [ 13 , 14 ].
The importance of SSCs means that numerous studies have investigated the regulation of self-renewal and differentiation activities of mouse and human SSCs in vivo or in vitro. Key genes, growth factors, and signaling pathways have been identified which are essential for SSC self-renewal and differentiation [ 15 22 ]. In addition, small noncoding RNAs also play essential roles in regulating SSC functions, such as spermatogenesis [ 23 , 24 ]. Small RNAs are noncoding RNAs of
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