Research ArticleBlood Disorders

Noninvasive low-level laser therapy for thrombocytopenia

Science Translational Medicine  27 Jul 2016:
Vol. 8, Issue 349, pp. 349ra101
DOI: 10.1126/scitranslmed.aaf4964

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Let there be light

Rather than platelet transfusion, noninvasive laser light therapy aimed at the whole body could stimulate platelet regeneration in vivo. A low number of platelets is characteristic of thrombocytopenia—a disease that can manifest from several different insults or from genetics, resulting in uncontrollable bleeding and death. Zhang et al. exposed mice to low-level laser light and found that it induced the generation of platelets from blood-producing cells, called megakaryocytes, in the bone marrow, in three different models of thrombocytopenia. The authors linked these beneficial effects to mitochondria and suggest that this mechanism would be conserved if the technology could be adapted for whole-body illumination of patients (something hinted at being already in the works).

Abstract

Thrombocytopenia is a common hematologic disorder that is managed primarily by platelet transfusions. We report here that noninvasive whole-body illumination with a special near-infrared laser cures acute thrombocytopenia triggered by γ-irradiation within 2 weeks in mice, as opposed to a 5-week recovery time required in controls. The low-level laser (LLL) also greatly accelerated platelet regeneration in the presence of anti-CD41 antibody that binds and depletes platelets, and prevented a severe drop in platelet count caused by a common chemotherapeutic drug. Mechanistically, LLL stimulated mitochondrial biogenesis specifically in megakaryocytes owing to polyploidy of the cells. LLL also protected megakaryocytes from mitochondrial injury and apoptosis under stress. The multifaceted effects of LLL on mitochondria bolstered megakaryocyte maturation; facilitated elongation, branching, and formation of proplatelets; and doubled the number of platelets generated from individual megakaryocytes in mice. LLL-mediated platelet biogenesis depended on megakaryopoiesis and was inversely correlated with platelet counts, which kept platelet biogenesis in check and effectively averted thrombosis even after repeated uses, in sharp contrast to all current agents that stimulate the differentiation of megakaryocyte progenitors from hematopoietic stem cells independently of platelet counts. This safe, drug-free, donor-independent modality represents a paradigm shift in the prophylaxis and treatment of thrombocytopenia.

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