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MicroRNA‐29b act as mediators of lipopolysaccharide‐induced bone loss
Author(s) -
Sul OJ,
Choi HyeSeon
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.778.16
Subject(s) - microrna , annexin , endogeny , christian ministry , lipopolysaccharide , apoptosis , chemistry , medicine , microbiology and biotechnology , endocrinology , cancer research , andrology , gene , biology , biochemistry , political science , law
MicroRNAs (miR) play critical roles in osteoclastogenesis, resulting in regulating bone density. Since the expression level of miR‐29b was increased in tibiae from lipopolysaccharide(LPS)‐injected mice and LPS‐induced osteoclasts (OCs). we hypothesized that LPS induces miR‐29b, which enhance OC formation, leading to excessive bone loss. Overexpression of miR‐29b increased OC survival without any change in OC differentiation, whereas inhibition of endogenous miR‐29b induced by LPS decreased it. Increased OC survival upon overexpression of miR‐29b was due to anti‐apoptotic activity evaluated by staining annexin V‐positive cells. We found that a target gene of miR‐29b is Bcl2 modifying factor ( Bmf ), which acts as a proapoptotic factor, and that miR‐29b binds to the 3′‐UTR of Bmf . Our data demonstrate that LPS‐induced miR‐29b increases the number of OC by enhancing OC survival through decreased BMF. Support or Funding Information This work was supported by the Basic Science Research Programs (2018R1A2B6001276;2016R1A6A3A11932375 2014R1A6A1030318) of the NRF and Korea Healthcare Technology R&D Project (HI18C0375) funded by the Ministry of Health. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .