miR-335 is involved in the rat epididymal development by targeting the mRNA of RASA1
- State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 320 Yue Yang Road, Shanghai 200031 (China)
Research highlights: {yields} The expression of miR-335 decreases from postnatal day 7 to 49 in the rat epididymis. {yields} The expression of RASA1 is inversely related to that of miR-335 during the rat epididymal development. {yields} miR-335 targets the mRNA of RASA1 and inhibits its expression, indicating that the downregulation of miR-335 at least in part causes the upregulation of RASA1 in the rat epididymis. -- Abstract: The expression of 350 miRNAs during the rat epididymal development was profiled by a home-made miRNA microarray recently. The results showed that the expression of miR-335 decreased from postnatal day 7 to 49 in the rat epididymis. Few studies on miR-335's roles in the epididymis and its targets have been reported so far. The bioinformatic analysis indicated that one of miR-335's putative targets is RASA1, a known gene related to cell proliferation and anti-apoptosis, which may contribute to the epididymal development. It was found that the overexpression of miR-335 in NIH/3T3 cells caused the suppression of RASA1 expression. The result of luciferase targeting assay confirmed that the mRNA of RASA1 was targeted by miR-335. In addition, it was also found that the temporal expression of RASA1 was inverse to that of miR-335 during the epididymal development in the rat. These results indicated that the reduction of miR-335 at least in part caused the upregulation of RASA1 in the rat epididymis. Therefore, miR-335 can be involved in the epididymal development by affecting the expression of RASA1.
- OSTI ID:
- 22202889
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 402, Issue 2; Other Information: Copyright (c) 2010 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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