Autophagy in Platelets
Anucleate platelets are produced by fragmentation of megakaryocytes. Platelets circulate in the bloodstream for a finite period: upon vessel injury, they are activated to participate in hemostasis; upon senescence, unused platelets are cleared. Platelet hypofunction leads to bleeding. Conversely, pathogenic platelet activation leads to occlusive events that precipitate strokes and heart attacks. Recently, we and others have shown that autophagy occurs in platelets and is important for platelet production and normal functions including hemostasis and thrombosis. Due to the unique properties of platelets, such as their lack of nuclei and their propensity for activation, methods for studying platelet autophagy must be specifically tailored. Here, we describe useful methods for examining autophagy in both human and mouse platelets.
Key wordsPlatelets Autophagy Hemostasis Live imaging Electron microscopy
The authors thank the laboratory personnel and collaborators who conducted the research on platelet autophagy over the years. The authors thank Dr. Zhenyu Li for helpful discussion. The authors also thank Dr. Harry Chanzu and Laura Tichachek for their careful perusal of this manuscript. This work was supported by a New Scholar in Aging award from the Ellison Medical Foundation (to Q.J.W.), Grant-in-Aid awards from the American Heart Association (AHA16GRNT31310020 to Q.J.W. and AHA16GRNT27620001 to S.W.W.), Predoctoral Fellowships from the American Heart Association (AHA 15PRE25550020 to S.J. and AHA 11PRE7500051 to Y.H.), National Institutes of Health (HL56652 and HL138179 to S.W.W., HL119393 to B.S.), and a Veterans Affairs Merit Award (to S.W.W.).