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UKnowledge > Office of the Vice President for Research > Office of Undergraduate Research > Kaleidoscope > Vol. 7 (2008)

 

Abstract

Platelets undergo morphological changes upon activation, such as shape change and aggregation. These changes are known to be the result of actin remodeling, whereas the role of microtubule remodeling has been controversial. The objective of this study was to re-examine the role of actin and microtubule dynamics in platelet function. We used aggregometry to measure the effect of cytoskeletal inhibitors on platelet shape change, aggregation, and dense core release. Microtubule assembly was found to have no role in platelet function, because treatment with vinblastine or nocodazole had no effect on shape change, aggregation, or secretion. Microtubule disassembly was necessary for some aspects of platelet function, because treatment with paclitaxel inhibited aggregation and secretion, but not shape change. Actin assembly was confirmed to be an essential event in platelet activation. We then assessed the role of microtubule disassembly and actin assembly in ADP-ribosylation factor 6 (Arf6) activation, because Arf6 is a key signaling component in platelet activation. Using GST-GGA3, we monitored Arf6-GTP levels over time in paclitaxel and latrunculin A-treated platelets. Paclitaxel and latrunculin A treatment blocked Arf6 activation in thrombin and convulxin-stimulated platelets, respectively. These results suggest that microtubule disassembly and actin assembly are important for Arf6 activation in platelets.

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