Type of Submission
Poster
Keywords
MiR-146a, metformin, microRNA, inflammation
Abstract
Sjögren’s Syndrome (SjS) is an autoimmune disorder that affects secretory glands in the human body, restricting their function and causing extreme dryness in areas like the mouth and eyes. miR-146a is an anti-inflammatory microRNA that targets the NFκB activation pathway. Previous studies have shown that SjS patients have increased miR-146a expression, despite having high levels of inflammation. The objective of this study was to investigate whether metformin, a diabetes drug with a wide variety of effects and potential functions, reduces levels of miR-146a expression. Metformin is known to reduce inflammation by inhibiting the activation of NFκB. THP-1 human monocytes were treated with various concentrations of metformin ranging from 12.5uM to 200uM. The cells were treated for 24 hours before total RNA was isolated, and qRT-PCR was utilized to compare miR-146a expression in metformin-treated versus untreated cells. Our results showed a dose-dependent decrease of miR-146a expression in the presence of metformin. These results are reasonable since miR-146a expression is dependent on NFκB activation, and metformin is known to inhibit the activation of NFκB. Further studies will investigate metformin’s ability to suppress inflammation in varying conditions.
Campus Venue
Stevens Student Center
Location
Cedarville, OH
Start Date
4-12-2017 11:00 AM
End Date
4-12-2017 2:00 PM
Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.
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Effect of Metformin on miR-146a Expression
Cedarville, OH
Sjögren’s Syndrome (SjS) is an autoimmune disorder that affects secretory glands in the human body, restricting their function and causing extreme dryness in areas like the mouth and eyes. miR-146a is an anti-inflammatory microRNA that targets the NFκB activation pathway. Previous studies have shown that SjS patients have increased miR-146a expression, despite having high levels of inflammation. The objective of this study was to investigate whether metformin, a diabetes drug with a wide variety of effects and potential functions, reduces levels of miR-146a expression. Metformin is known to reduce inflammation by inhibiting the activation of NFκB. THP-1 human monocytes were treated with various concentrations of metformin ranging from 12.5uM to 200uM. The cells were treated for 24 hours before total RNA was isolated, and qRT-PCR was utilized to compare miR-146a expression in metformin-treated versus untreated cells. Our results showed a dose-dependent decrease of miR-146a expression in the presence of metformin. These results are reasonable since miR-146a expression is dependent on NFκB activation, and metformin is known to inhibit the activation of NFκB. Further studies will investigate metformin’s ability to suppress inflammation in varying conditions.
