2017 Conference Archive (Archived)
Session Format
Conference Session (20 minutes)
Session Format
Presentation Session (45 minutes)
Target Audience
K12 Educators
Copyright
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Location
Room 212
Abstract for the conference program
In addition to its reproductive role, progesterone (P4) also has anti-inflammatory effects. While the precise mechanisms have never been clearly elucidated in RAW 246.7 cells, it seems logical to assume that this response is a consequence of the activation of the progesterone receptor (P4-R). However, it has been shown that in a rat model this anti-inflammatory effect is independent of the progesterone receptor. In this project, the aim was to characterize this response by assaying nitric oxide production from lipopolysaccharide-challenged RAW cells. To determine the involvement of the P4-R, cells were incubated in the presence and absence of RU-486 – a potent P4-R antagonist. Our results indicate that the anti-inflammatory response of progesterone was through activation of the P4-R as cells incubated in the antagonist show a reversal of this inhibitory effect of P4 as was seen in cells incubated in the absence of this ligand.
Proposal Track
Research Project
Proposal Track
T1: Teaching and Learning in the STEM Field
Start Date
3-3-2017 9:30 AM
End Date
3-3-2017 10:00 AM
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.
Recommended Citation
Brandon, Christopher I. Jr. and George, Bagie, "The Progesterone Receptor - To Be or Not to Be: The Anti-inflammatory Effects of Progesterone in RAW 264.7 Cells" (2017). Interdisciplinary STEM Teaching & Learning Conference (2012-2019) (Archived). 5.
https://digitalcommons.georgiasouthern.edu/stem/2017/2017/5
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The Progesterone Receptor - To Be or Not to Be: The Anti-inflammatory Effects of Progesterone in RAW 264.7 Cells
Room 212
In addition to its reproductive role, progesterone (P4) also has anti-inflammatory effects. While the precise mechanisms have never been clearly elucidated in RAW 246.7 cells, it seems logical to assume that this response is a consequence of the activation of the progesterone receptor (P4-R). However, it has been shown that in a rat model this anti-inflammatory effect is independent of the progesterone receptor. In this project, the aim was to characterize this response by assaying nitric oxide production from lipopolysaccharide-challenged RAW cells. To determine the involvement of the P4-R, cells were incubated in the presence and absence of RU-486 – a potent P4-R antagonist. Our results indicate that the anti-inflammatory response of progesterone was through activation of the P4-R as cells incubated in the antagonist show a reversal of this inhibitory effect of P4 as was seen in cells incubated in the absence of this ligand.
