Dissection of autophagy in human platelets

• Published in: Autophagy Vol. 10; no. 4; pp. 642 - 651
• Main Authors: Feng, Wenfeng, Chang, Chunmei, Luo, Dongjiao, Su, Hua, Yu, Shanshan, Hua, Wen, Chen, Zhihua, Hu, Hu, Liu, Wei
• Format: Journal Article
• Language: English
• Published: United States Taylor & Francis 01.04.2014; Landes Bioscience
• Subjects: Animals; Apoptosis Regulatory Proteins - metabolism; autophagosome; autophagy; Autophagy - physiology; Basic Research Paper; Beclin 1; Bleeding Time; Blood Platelets - cytology; Blood Platelets - metabolism; Heterozygote; Humans; Mice; Phosphatidylinositol 3-Kinases - metabolism; platelet; Signal Transduction - physiology; thrombus; TOR Serine-Threonine Kinases - antagonists & inhibitors; TOR Serine-Threonine Kinases - metabolism; Transcriptional Activation - physiology; platelet; autophagy; thrombus; autophagosome; Beclin 1
• ISSN: 1554-8627; 1554-8635
• DOI: 10.4161/auto.27832

Continuous turnover of intracellular components by autophagy is necessary to preserve cellular homeostasis in all tissues. Despite recent advances in identifying autophagy-related genes and understanding the functions of autophagy in developmental and pathological conditions, so far, the role of autophagy in platelet, a specific anucleate cell type, is poorly understood. In this study, we showed that human platelets express the autophagy-related proteins ATG5, ATG7, and LC3. The same as in nucleated mammalian cells, autophagy was stimulated by cell starvation or the MTOR inhibitor rapamycin in a phosphatidylinositol 3-kinase (PtdIns3K)-dependent manner. Disruption of autophagic flux led to impairment of platelet aggregation and adhesion. Furthermore, Becn1 heterozygous knockout mice displayed a prolonged bleeding time and reduced platelet aggregation. These results suggest a potential role of autophagy in the regulation of platelet function, and imply that gene transcription may not be an essential prerequisite for adaptive autophagy.