Journal
JOURNAL OF THROMBOSIS AND HAEMOSTASIS
Volume 19, Issue 8, Pages 2029-2043Publisher
ELSEVIER SCIENCE INC
DOI: 10.1111/jth.15252
Keywords
megakaryocytes; photobiomodulation therapy; platelets; thrombocytopenia; thrombopoietin
Categories
Funding
- Science and Technology Program of Guangzhou [2019050001]
- National Natural Science Foundation of China [61361160414, 62005085, 31470072]
- science and technology project of Guangzhou [201805010002]
- Science and Technology Planning Project of Guangdong Province (Guangdong-Hong Kong Joint Innovation Project), China [2014B050504009]
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Photobiomodulation therapy (PBMT) prevents chemotherapy-induced thrombocytopenia by increasing platelet production and upregulating hepatic TPO expression. PBMT activates Src protein through reactive oxygen species, leading to the promotion of megakaryocytopoiesis and thrombopoiesis. This research suggests that PBMT is a promising therapeutic strategy for the treatment of CIT.
Background Chemotherapy-induced thrombocytopenia (CIT) can increase the risk of bleeding, which may delay or prevent the administration of anticancer treatment schedules. Photobiomodulation therapy (PBMT), a non-invasive physical treatment, has been proposed to improve thrombocytopenia; however, its underlying regulatory mechanism is not fully understood. Objective To further investigate the mechanism of thrombopoietin (TPO) in megakaryocytopoiesis and thrombopoiesis. Methods Multiple approaches such as western blotting, cell transfection, flow cytometry, and animal studies were utilized to explore the effect and mechanism of PBMT on thrombopoiesis. Results PBMT prevented a severe drop in platelet count by increasing platelet production, and then ameliorated CIT. Mechanistically, PBMT significantly upregulated hepatic TPO expression in a thrombocytopenic mouse model, which promoted megakaryocytopoiesis and thrombopoiesis. The levels of TPO mRNA and protein increased by PBMT via the Src/ERK/STAT3 signaling pathway in hepatic cells. Furthermore, the generation of the reactive oxygen species was responsible for PBMT-induced activation of Src and its downstream target effects. Conclusions Our research suggests that PBMT is a promising therapeutic strategy for the treatment of CIT.
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