Literature DB >> 31157255

Enhancing autophagy protects platelets in immune thrombocytopenia patients.

Chun-Yan Wang1,2, Sai Ma2, Shao-Jie Bi3, Le Su4, Shu-Ya Huang4, Jun-Ying Miao4, Chun-Hong Ma5, Cheng-Jiang Gao5, Ming Hou6,7, Jun Peng2,8.   

Abstract

BACKGROUND: Immune thrombocytopenia (ITP) is an autoimmune bleeding disorder and involves increased apoptosis of platelets. Autophagy is an essential process for platelets to maintain their life and physiological functions. However, the role of autophagy in ITP platelets was previously unclear.
METHODS: In the present study, the expression of autophagy-related protein and autophagy flux were detected in platelets from ITP patients and healthy controls by immunofluorescence staining and immunoblotting, and the influence of autophagy on the viability and apoptosis of ITP platelets was further explored.
RESULTS: We found that platelet autophagy was diminished in ITP patients. Platelet autophagy in ITP was regulated by the PI3K/AKT/mTOR pathway, with mTOR (mammalian target of rapamycin) as a negative regulator and class III PtdIns3K playing a crucial role in the process. Importantly, the small-molecule compound ABO (6-amino-2,3-dihydro-3-hydroxymethyl-1,4-benzoxazine) enhanced autophagy in ITP platelets. Enhancing platelet autophagy alleviated platelet destruction by inhibiting apoptosis and improving platelet viability.
CONCLUSIONS: These results suggest a role for autophagy regulation in the pathogenesis of ITP, and offer a novel treatment for these patients.

Entities:  

Keywords:  6-amino-2,3-dihydro-3-hydroxymethyl-1,4-benzoxazine (ABO); Immune thrombocytopenia (ITP); autophagy

Year:  2019        PMID: 31157255      PMCID: PMC6511561          DOI: 10.21037/atm.2019.03.04

Source DB:  PubMed          Journal:  Ann Transl Med        ISSN: 2305-5839


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