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miR-19a-3p and miR-19b-3p Promote Microglia Activation Associated With Neuroinflammation
Faezeh Sahebdel1, Ricardo A Battaglino1, Leslie R Morse1
1Department of Rehabilitative Medicine, School of Medicine, University of Minnesota, Minneapolis, Minnesota, USA.
Abstract:
Neuroinflammation, driven by microglia activation and the production of pro-inflammatory cytokines, has been implicated in several neurological diseases and neuropathic pain. MicroRNAs (miRNAs) have emerged as important regulators of neuroinflammatory processes. Prior studies identified elevated levels of circulating miR-19a and miR-19b in individuals living with chronic pain following spinal cord injury (SCI). In this study, we wanted to determine whether miR-19a and miR-19b have a direct effect on microglia activation, specifically pro-inflammatory activation, associated with neuroinflammation. Microglia were activated by inflammatory stimuli in the presence of miR-19a or miR-19b mimics, and assessed for the expression of cytokines, chemokines, and effector molecules. The results show that miR-19a or miR-19b mimics increased the expression of pro-inflammatory cytokines, chemokines, and effector molecules in microglia. The results also showed decreased expression of suppressor of cytokine signaling (SOCS) proteins, namely SOCS1 and SOCS3, in activated microglia with miR-19a and miR-19b mimics. Additionally, enhanced signaling through the NFκB and Jak pathways was observed with increased NFkB-p65 and JAK1 phosphorylation in the presence of miR-19a and miR-19b mimics. Further results show that miR-19a and miR-19b inhibitors reversed these effects on activated microglia. Overall, our results demonstrate that miR-19a or miR-19b increased the expression of pro-inflammatory cytokines, chemokines, and effector molecules in activated microglia. These results indicate that miR-19a and miR-19b can enhance microglia activation and associated inflammatory responses, which may have implications for conditions associated with neuroinflammation.
Insights
MicroRNAs miR-19a and miR-19b amplify neuroinflammation by boosting microglia activation and pro-inflammatory responses. Inhibiting these microRNAs reversed these effects, suggesting therapeutic potential for neurological diseases.
Area of Science:
- Neuroscience
- Molecular Biology
- Immunology
Background:
- Neuroinflammation, involving microglia activation and cytokine release, is linked to neurological disorders and pain.
- MicroRNAs (miRNAs) regulate neuroinflammation, with elevated miR-19a and miR-19b found in chronic pain patients post-spinal cord injury (SCI).
Purpose of the Study:
- To investigate the direct impact of miR-19a and miR-19b on microglia activation and pro-inflammatory responses in neuroinflammation.
Main Methods:
- Microglia were activated with inflammatory stimuli in the presence of miR-19a/miR-19b mimics or inhibitors.
- Assessed expression of cytokines, chemokines, effector molecules, and SOCS proteins (SOCS1, SOCS3).
- Analyzed signaling pathways including NFκB and Jak via phosphorylation of NFkB-p65 and JAK1.
Main Results:
- miR-19a and miR-19b mimics increased pro-inflammatory cytokines, chemokines, and effector molecules in activated microglia.
- Mimics decreased SOCS1 and SOCS3 expression, while enhancing NFκB and Jak pathway signaling.
- miR-19a and miR-19b inhibitors counteracted these pro-inflammatory effects.
Conclusions:
- miR-19a and miR-19b promote microglia activation and enhance neuroinflammatory responses.
- These microRNAs may play a significant role in neurological conditions characterized by neuroinflammation.
