Faculty Advisor

Thomas Peeler

Start Date

25-4-2017 12:00 PM

End Date

25-4-2017 1:00 PM

Description

The growing obesity epidemic has led to an increased interest in the study of adipogenesis, which can be modeled in mouse 3T3-L1 fibroblast cells. Extracellular matrix remodeling is a critical process during adipogenesis that is facilitated by matrix metalloproteinases (MMPs). To better understand the function of MMPs, the MMP inhibitor Ilomostat was used on 3T3-L1 preadipocytes along with rosiglitazone, a drug that upregulates the transcription factor peroxisome-proliferator-activated receptor γ (PPARγ). We predicted that if MMP inhibition prevents activation of the transcription factor CCAAT/enhancer-binding protein β (C/EBPβ), the effect of Ilomostat should overcome the upregulation of downstream PPARγ by rosiglitazone. Results suggest that MMP inhibition prevents adipogenic conversion despite the addition of the PPARγ agonist, and that PPARγ expression was slightly decreased in cells treated with both rosiglitazone and Ilomostat. These results will help clarify the downstream effects of MMPs during adipogenesis and provide more insight into specific targets for obesity treatment.

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Apr 25th, 12:00 PM Apr 25th, 1:00 PM

The Effect of Matrix Metalloproteinase Inhibition on Intracellular Signaling in Adipogenic Differentiation of 3T3-L1 Cells

The growing obesity epidemic has led to an increased interest in the study of adipogenesis, which can be modeled in mouse 3T3-L1 fibroblast cells. Extracellular matrix remodeling is a critical process during adipogenesis that is facilitated by matrix metalloproteinases (MMPs). To better understand the function of MMPs, the MMP inhibitor Ilomostat was used on 3T3-L1 preadipocytes along with rosiglitazone, a drug that upregulates the transcription factor peroxisome-proliferator-activated receptor γ (PPARγ). We predicted that if MMP inhibition prevents activation of the transcription factor CCAAT/enhancer-binding protein β (C/EBPβ), the effect of Ilomostat should overcome the upregulation of downstream PPARγ by rosiglitazone. Results suggest that MMP inhibition prevents adipogenic conversion despite the addition of the PPARγ agonist, and that PPARγ expression was slightly decreased in cells treated with both rosiglitazone and Ilomostat. These results will help clarify the downstream effects of MMPs during adipogenesis and provide more insight into specific targets for obesity treatment.

 

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