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Scholars Day: April 11, 2012

MCH Signaling is Attenuated by Beta-arrestin Overexpression But Enhanced by Caveolin-1 RNAi in BHK 570 cells.

Melanin-concentrating hormone (MCH) is a peptide that regulates appetite and energy expenditure in mammals. In adipocytes, MCH triggers production of leptin, an appetite suppressing hormone. The MCH receptor, MCHR1, desensitizes to MCH following stimulation and receptor internalization may be involved. Using a leptin promoter driven luciferase reporter, we investigated how beta-arrestin 1 and 2 effect MCH signaling. Beta-arrestin 1 and 2 are involved in clathrin mediated endocytosis. In BHK 570 cells expressing MCHR1, we observed a 1.2 fold increase in reporter activity following a six hour MCH treatment. Beta-arrestin-1 and 2 overexpression in these cells resulted in 1.1 and 1.0 fold increases respectively following MCH treatment. We also investigated effects of knocking down Caveolin-1 with RNAi in BHK cells. Caveolin-1 is involved in an independent endocytosis pathway. We observed a 1.4 fold increase in reporter activity following treatment. These results support the idea that receptor internalization contributes to MCH desensitization.


Please note that presentation times are approximate. If you are interested in attending sessions with multiple presentations, please be in the room at the start of the session.
Presenter: Robert Carroll (Undergraduate Student)
Topic: Biology
Location: 217 Hartwell
Time: 9:40 am Session I