Outgrowth Formation in MT1-CHO Cells is Dependent Upon Gi Protein Activation, Elevated and Sustained MAP Kinase Activation and Intact Microtubules

Corry Bondi

Defense Date

8-25-2006

Graduation Date

Fall 1-1-2006

Availability

Campus Only

Submission Type

thesis

Degree Name

MS

Department

Pharmacology-Toxicology

School

School of Pharmacy

Committee Chair

Paula Witt-Enderby

Committee Member

Vicki L. Davis

Committee Member

Wilson S. Meng

Committee Member

Melissa Melan

Keywords

MAP kinase, melatonin, microtubules, MT1-CHO cells, outgrowths

Abstract

Melatonin has been shown to induce filamentous outgrowths in MT1-CHO cells. Therefore, we wanted to determine if chronic melatonin treatment (1µM) for five hours induces a sustained activation of MEK/ERK (1/2) and to assess the pathway's cellular location. Additionally, morphological effects were investigated by measurements of cellular area, circumference, length, and width. Treatments to block the internalization process via clathrin-coated pits, depolymerize microtubules, and uncouple Gi protein from the MT1 receptor were used to assess their impact on these processes. Immunocytochemical analyses of melatonin treated cells showed significantly increased activation of MEK/ERK 1/2 as well as their location in the cytoplasm and nucleus. Melatonin treatment resulted in an increase in circumference and length, a decrease in width, and no change in total area. Melatonin induced outgrowth formation is dependent on Gi protein activation, elevated and sustained MEK/ERK (1/2) activation, intact microtubules, and internalization of MT1 melatonin receptors.

Format

PDF

Language

English

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