Expression and regulation of miR-17a and miR-430b in zebrafish ovarian follicles

被引:23
作者
Abramov, Rina [1 ]
Fu, Guodong [1 ]
Zhang, Yong [1 ]
Peng, Chun [1 ]
机构
[1] York Univ, Dept Biol, Toronto, ON M3J 1P3, Canada
关键词
miR-17a; miR-430b; Gonadotropin; Maturation inducing hormone; Oocyte maturation; Zebrafish; ACTIVIN-BETA-A; BONE MORPHOGENETIC PROTEIN-15; MESSENGER-RNA EXPRESSION; OOCYTE MATURATION; POTENTIAL ROLE; 20-BETA-HYDROXYSTEROID DEHYDROGENASE; II RECEPTOR; GONADOTROPIN; MICRORNAS; CLONING;
D O I
10.1016/j.ygcen.2013.02.012
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
MicroRNAs (miRNAs) are small noncoding RNAs that post-transcriptionally regulate gene expression and control many developmental and physiological processes. Oocyte maturation in fish is mainly regulated by luteinizing hormone (LH) and maturation-inducing hormone (MIH). In addition, growth factors, including members of the transforming growth factor beta (TGF-beta) superfamily, have also been shown to play important roles in regulating oocyte maturation. In this study, we determined the expression and regulation of two miRNAs, miR-17a and miR-430b, which potentially target signalling molecules in the TGF-beta pathway, in zebrafish ovarian follicles. Using real-time PCR, we observed that miR-17a and miR-430b levels in follicular cells were significantly lower in late vitellogenic and full grown follicles than in early vitellogenic follicles. Treatment with a LH analog, human chorionic gonadotropin, significantly down-regulated miR-17a and miR-430b expression in follicular cells but had no effect on their expression in oocytes. Forskolin also inhibited follicular cell miR-430b expression; however, no significant changes in miR-17a levels were observed after Forskolin treatment. Finally, MIH did not affect the expression of these miRNAs either in follicular cells or oocytes at the time points tested. These findings suggest that miR-17a and miR-430b may be involved in the regulation of follicle development and oocyte maturation in zebrafish. (C) 2013 Elsevier Inc. All rights reserved.
引用
收藏
页码:309 / 315
页数:7
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