The elucidation of miRNAs in response to stress stimuli and its secretion into an oral cavity

2014 Fiscal Year Final Research Report

• Project/Area Number: 25670822
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Prosthodontics/ Dental materials science and
• Research Institution: The University of Tokushima
• Principal Investigator: ICHIKAWA Tetsuo 徳島大学, ヘルスバイオサイエンス研究部, 教授 (90193432)
• Co-Investigator(Kenkyū-buntansha): YOSHIMOTO Katsuhiko 徳島大学, 大学院ヘルスバイオサイエンス研究部, 教授 (90201863) ; TOMOTAKE Yoritoki 徳島大学, 病院, 准教授 (70263853) ; MIZUSAWA Noriko 徳島大学, 大学院ヘルスバイオサイエンス研究部, 助教 (80254746)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: microRNA / メカニカルストレス / 細胞増殖 / MC3T3-E1細胞

Outline of Final Research Achievements

In the present study, we attempted to identify miRNA in response to mechanical stress in MC3T3-E1 cells, a mouse osteoblast-like cell line, and to elucidate its functions.
We identified miRNAs whose expression was changed in MC3T3-E1 cells subjected to compressive force at 294 Pa for 24 h. Treatment with compressive force and overexpression of miR-494-3p, a miRNA up-regulated by compressive force, in MC3T3-E1 cells inhibited the cell proliferation. Furthermore, we demonstrated that Fgfr2 and Rock1 were targets of mi494-3p in MC3T3-E1 cells, and their knockdown inhibited the cell proliferation.
We concluded that compressive force affected expressions of several miRNAs including miR-494-3p in MC3T3-E1 cells. Compressive force might inhibit cell proliferation in MC3T3-E1 cells by up-regulating miR-494-3p followed by Fgfr2 and Rock1 gene repressions. For further study, we will investigate whether these miRNAs induced by compressive force exist in saliva.

Free Research Field

歯科補綴学