miR-346 Controls Release of TNF-α Protein and Stability of Its mRNA in Rheumatoid Arthritis
Author Information
Author(s): Semaan Noha, Frenzel Laurent, Alsaleh Ghada, Suffert Guillaume, Gottenberg Jacques-Eric, Sibilia Jean, Pfeffer Sebastien, Wachsmann Dominique
Primary Institution: Laboratoire Physiopathologie des Arthrites, Université de Strasbourg, France
Hypothesis
miR-346 regulates TNF-α synthesis by controlling TTP expression in rheumatoid arthritis fibroblast-like synoviocytes.
Conclusion
miR-346 acts as a negative regulator of TNF-α release in rheumatoid arthritis by inhibiting Btk expression, which stabilizes TNF-α mRNA.
Supporting Evidence
- miR-346 is overexpressed in LPS-activated fibroblast-like synoviocytes.
- Inhibition of miR-346 stabilizes TNF-α mRNA but does not restore TNF-α release.
- Blocking miR-346 reestablishes TNF-α expression in activated fibroblast-like synoviocytes.
- Transfection of miR-346 in THP-1 cells inhibits TNF-α secretion.
- miR-125b and miR-939 do not restore TNF-α release when inhibited.
Takeaway
This study found that a tiny molecule called miR-346 helps control a protein that causes inflammation in arthritis, showing how it can keep the body from getting too inflamed.
Methodology
The study used microarrays and RT-PCR to analyze miRNA expression and ELISA to measure cytokine release in fibroblast-like synoviocytes from rheumatoid arthritis patients.
Limitations
The study does not fully explore the mechanisms behind TNF-α release regulation in rheumatoid arthritis fibroblast-like synoviocytes.
Participant Demographics
Fibroblast-like synoviocytes were isolated from synovial tissues of four rheumatoid arthritis patients.
Statistical Information
P-Value
p<0.01
Statistical Significance
p<0.01
Digital Object Identifier (DOI)
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