Autophagy in platelets

Meenakshi Banerjee; Yunjie Huang; Madhu M. Ouseph; Smita Joshi; Irina Pokrovskaya; Brian Storrie; Jinchao Zhang; Sidney W. Whiteheart; Qing Jun Wang

doi:10.1007/978-1-4939-8873-0_32

Autophagy in platelets

Meenakshi Banerjee
, Yunjie Huang
, Madhu M. Ouseph
, Smita Joshi
, Irina Pokrovskaya
, Brian Storrie
, Jinchao Zhang
, Sidney W. Whiteheart
, Qing Jun Wang

Research output: Chapter in Book/Report/Conference proceeding › Chapter › peer-review

15 Scopus citations

Abstract

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.

Original language	English
Title of host publication	Methods in Molecular Biology
Pages	511-528
Number of pages	18
DOIs	https://doi.org/10.1007/978-1-4939-8873-0_32
State	Published - 2019

Publication series

Name	Methods in Molecular Biology
Volume	1880
ISSN (Print)	1064-3745

Bibliographical note

Publisher Copyright:
© Springer Science+Business Media, LLC, part of Springer Nature 2019.

Funding

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.).

Funders	Funder number
National Institutes of Health (NIH)	HL138179, HL56652
National Heart, Lung, and Blood Institute (NHLBI)	R01HL119393
Ellison Medical Foundation
American the American Heart Association	11PRE7500051, 15PRE25550020, AHA16GRNT31310020, AHA16GRNT27620001
Nurses Organization of Veterans Affairs

Keywords

Autophagy
Electron microscopy
Hemostasis
Live imaging
Platelets

ASJC Scopus subject areas

Molecular Biology
Genetics

Access to Document

10.1007/978-1-4939-8873-0_32

Cite this

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abstract = "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.",

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AU - Huang, Yunjie

AU - Ouseph, Madhu M.

AU - Joshi, Smita

AU - Pokrovskaya, Irina

AU - Storrie, Brian

AU - Zhang, Jinchao

AU - Whiteheart, Sidney W.

AU - Wang, Qing Jun

PY - 2019

Y1 - 2019

N2 - 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.

AB - 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.

KW - Autophagy

KW - Electron microscopy

KW - Hemostasis

KW - Live imaging

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Autophagy in platelets

Abstract

Publication series

Bibliographical note

Funding

Keywords

ASJC Scopus subject areas

Access to Document

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