MicroRNA-322 inhibits inflammatory cytokine expression and promotes cell proliferation in LPS-stimulated murine macrophages by targeting NF-κB1 (p50)

Abstract

Inflammation is the body’s normal self-protection mechanism to eliminate pathogens and resist pathogen invasion. The excessive inflammatory response may lead to inflammatory lesions. The mechanisms accounting for inflammation remain hazy. miRNAs have been proposed to have crucial effects on inflammation. In the present study, we reported that lipopolysaccharide (LPS)-stimulation increased the expression levels of inflammatory cytokines and the cell-cycle progression was suppressed in RAW264.7 cells. Meanwhile, the expression of miR-322 was significantly down-regulated after LPS treatment. Bioinformatics predictions revealed a potential binding site of miR-322 in 3′-UTR of NF-κB1 (p50) and it was further confirmed by luciferase assay. Moreover, both the mRNA and protein levels of NF-κB1 (p50) were down-regulated by miR-322 in RAW264.7 cells. Subsequently, we demonstrated that miR-322 mimics decrease in the expression levels of inflammatory cytokines and cell-cycle repression can be rescued following LPS treatment in RAW264.7 cells. The anti-inflammatory cytokines expression including IL-4 and IL-10 were significantly up-regulated. Furthermore, miR-322 could also promote RAW264.7 cells proliferation. These results demonstrate that miR-322 is a negative regulator of inflammatory response by targeting NF-κB1 (p50).

Knockdown of long noncoding RNA urothelial carcinoma associated 1 inhibits colorectal cancer cell proliferation and promotes apoptosis via modulating autophagy

“…Although autophagy might allow tumor cells to survive under metabolic stress, the association between autophagy and tumorigenesis and progression of cancer has been suggested genetically (Karantza‐Wadsworth et al, ; Shan et al, ). Moreover, autophagy and cell proliferation might be linked to each other modulating by noncoding RNA and occur simultaneously or sequentially in the development of cancer cells (Shan et al, ; K. Zhang et al, ). Downregulated MEG3 promoted cell proliferation by activating autophagy in bladder cancer.…”

Knockdown of Long Non-Coding RNA GAS5 Increases miR-23a by Targeting ATG3 Involved in Autophagy and Cell Viability

“…It is reported that LPS is involved in cell proliferation and apoptosis [14,36]. To further explore the functional role of GAS5 and miR-23a in 293T cells, we tested whether GAS5 and miR-23a were capable of affecting the cell viability and apoptosis.…”

“…The majority of the remaining transcripts with no protein-coding capacity are transcribed into non-coding RNAs (ncRNAs), especially microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) [12]. MiRNAs have been indicated to be involved in regulating various physiology processes, such as cellular proliferation, differentiation, as well as apoptosis predominantly through base pairing with the 3'-UTR of target mRNA [13,14]. It is well documented that miRNAs function as autophagy regulator via specifically regulating autophagy related genes [2,[15][16][17].…”

IFN-independent G0 arrest and SAMHD1 activation following TLR4 activation in macrophages

“…The effect of LPS on G0 arrest has been shown in mouse primary cells and murine cell lines 31, 32 or in the human cell line, THP-1/U937 33, 34 . Despite these reports, surprisingly little is known about the mechanism how LPS causes G0 arrest.…”