Figure 6.

Hypothesis on the interaction between hyperoxia, platelet biogenesis, and lung injury. Hyperoxia may reduce the number of megakaryocytes in the lung and increase platelet consumption by activating platelets, leading to decreased platelet count directly. Hyperoxia may also impair the developing lung by inhibiting alveolarization and vascularization, leading to BPD. The reduction of the vascular bed in BPD, together with impaired lung function might result in reduced shedding of megakaryocytes and pro-platelets trapped in pulmonary capillaries. Meanwhile, reduced PLT may hamper lung development by interacting with LEC and PCEC via ligands and receptors. ROS, reactive oxygen species; LEC, lymphatic endothelial cells; PCEC, pulmonary capillary endothelial cells; Clec-2, C-type lectin-like receptor-2; SDF-1, stromal-cell-derived factor-1; CXCR4 and CXCR7, receptors of SDF-1 on PCEC.