Key result
CRISPR-mediated miR-155 knockout severely impairs macrophage proinflammatory cytokine production and slightly increases osteoclastogenesis.
Why the study?
MicroRNA 155 is a key proinflammatory regulator in clinical and experimental rheumatoid arthritis, motivating investigation of its genome editing effects.
Does CRISPR/CAS9-mediated miR-155 knockout reduce proinflammatory cytokine production in RAW264.7 macrophage cells?
Does CRISPR/CAS9-mediated miR-155 knockout reduce proinflammatory cytokine production in RAW264.7 macrophage cells?
CRISPR/CAS9-mediated knockout of miR-155 in macrophages reduces proinflammatory cytokine production, suggesting a potential therapeutic strategy for rheumatoid arthritis.
MicroRNA 155 (miR-155) is a key proinflammatory regulator in clinical and experimental rheumatoid arthritis (RA). Here we generated a miR-155 genome knockout (GKO) RAW264.7 macrophage cell line using the clustered regulatory interspaced short palindromic repeat (CRISPR)/CRISPR-associated protein 9 (CAS9) technology. While upregulating the Src homology-2 domain-containing inositol 5-phosphatase 1 (SHIP1), the miR-155 GKO line is severely impaired in producing proinflammatory cytokines but slightly increased in osteoclastogenesis upon treatment with receptor activator of nuclear factor-κB ligand (RANKL). Taken together, our results suggest that genome editing of miR-155 holds the potential as a therapeutic strategy in RA.
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Jing et al. (2015) studied Rheumatoid arthritis. CRISPR/CAS9-mediated genome knockout of miR-155 was evaluated on Proinflammatory cytokine production and osteoclastogenesis. CRISPR/CAS9-mediated genome knockout of miR-155 in RAW264.7 macrophages severely impaired proinflammatory cytokine production and slightly increased osteoclastogenesis.
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