MicroRNA-155 induces differentiation of RAW264.7 cells into dendritic-like cells.
Int J Clin Exp Pathol
; 8(11): 14050-62, 2015.
Article
em En
| MEDLINE
| ID: mdl-26823719
MicroRNA (miRNA, miR)-155 is the most promising pro-inflammatory miRNA molecule. Lipopolysaccharide (LPS) and oxidized low-density lipoprotein (oxLDL) are the most well-known foreign antigens, initiating immune responses against infection and the development of atherosclerosis (AS), respectively. To explore whether miR-155 is involved in regulating LPS- and oxLDL-initiated inflammations, we investigated the level of miR-155 in both LPS- and oxLDL-treated RAW264.7 cells, assessed whether miR-155 induce morphologic changes of the cells and how did it regulate the production of surface markers and cytokines. The results showed that the level of miR-155 was significantly increased by LPS and was modestly increased by oxLDL. Moreover, RAW264.7 cells displayed morphological transformations from macrophage-like cells into DC-like cells when miR-155 was over-expressed. Furthermore, the gain- and loss-of-function studies demonstrated that miR-155 induced the expression of the surface markers (including MHC-II, MHC-I, CD86, and CD83) and pro-inflammatory cytokines (including interleukin (IL)-12, IL-6, and IL-1b) in both LPS- and oxLDL-treated RAW264.7 cells. Additionally, miR-155 induced the expression of CD36 in oxLDL-treated RAW264.7 cells. In conclusion, up-regulated miR-155 is able to induce morphological and phenotypic changes, and the expression of pro-inflammatory cytokines in both LPS- and oxLDL-treated RAW264.7 cells. Therefore, our study suggests that miR-155 is one important regulator involved in enhancing both LPS- and oxLDL-initiated inflammations, which is critical for the progression of immune responses as well as for the development of AS.
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Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Células Dendríticas
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MicroRNAs
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Transdiferenciação Celular
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Macrófagos
Limite:
Animals
Idioma:
En
Revista:
Int J Clin Exp Pathol
Assunto da revista:
PATOLOGIA
Ano de publicação:
2015
Tipo de documento:
Article
País de afiliação:
China