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Updated: Mar 26, 2026
Culture of myeloid dendritic cells from bone marrow precursors
Published on: July 25, 2008
MicroRNA-155 induces differentiation of RAW264.7 cells into dendritic-like cells
Yu-Lan Ma1, Zhi-Jun Ma2, Min Wang3
1Department of Cardiology, General Hospital of Ningxia Medical University Yinchuan 750004, China.
Abstract:
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.
Insights
MicroRNA 155 (miR-155) enhances inflammation triggered by lipopolysaccharide (LPS) and oxidized low-density lipoprotein (oxLDL). Upregulated miR-155 promotes cell changes and cytokine production, impacting immune responses and atherosclerosis development.
Area of Science:
- Immunology
- Molecular Biology
- Cardiovascular Research
Background:
- MicroRNA (miRNA, miR)-155 is a key pro-inflammatory molecule.
- Lipopolysaccharide (LPS) and oxidized low-density lipoprotein (oxLDL) are antigens initiating immune responses and atherosclerosis (AS), respectively.
- The role of miR-155 in LPS- and oxLDL-induced inflammation requires further investigation.
Purpose of the Study:
- To investigate the involvement of miR-155 in LPS- and oxLDL-initiated inflammation.
- To assess miR-155's effect on RAW264.7 cell morphology, surface markers, and cytokine production.
- To determine miR-155's regulatory role in immune responses and AS development.
Main Methods:
- Quantification of miR-155 levels in LPS- and oxLDL-treated RAW264.7 cells.
- Overexpression and knockdown studies of miR-155.
- Assessment of cellular morphology, surface marker expression (MHC-II, MHC-I, CD86, CD83, CD36), and cytokine production (IL-12, IL-6, IL-1b).
Main Results:
- LPS significantly increased miR-155 levels; oxLDL caused a modest increase.
- miR-155 overexpression induced morphological transformation of macrophages into dendritic cell-like cells.
- miR-155 upregulated surface markers and pro-inflammatory cytokines in both LPS- and oxLDL-treated cells.
- miR-155 specifically induced CD36 expression in oxLDL-treated cells.
Conclusions:
- Upregulated miR-155 induces morphological and phenotypic changes, and pro-inflammatory cytokine expression in RAW264.7 cells treated with LPS or oxLDL.
- miR-155 is an important regulator that enhances LPS- and oxLDL-initiated inflammation.
- miR-155 plays a critical role in immune responses and atherosclerosis development.
