Platelet activation in experimental murine neonatal pulmonary hypertension

Our study utilized a murine bleomycin model of pulmonary hypertension (PH) to study the hypothesis that platelets from mice with PH circulate in an activated state and that circulating and lung platelet ‐derived factors, as well as the number of platelets in the lungs of neonatal mice with PH, is significantly increased. Through an extensive characterization of the functional status of platelets from bleomycin‐treated mice, we demonstrate that mice with bleomycin‐induced PH exhibit qualitativ e but not quantitative platelet changes. Circulating platelets from mice with PH exhibit hyperactivity as measured directly by adhesion and aggregation under flow and the presence of activation markers and indirectly by quantification of platelet‐specific proteins in plasma. Interestingly, we have also found that the absolute number of platelets within the lungs of mice with PH is significantly higher all together suggesting that platelets could directly be promoting PH. AbstractSerotonin (5 ‐HT) contributes to the pathogenesis of experimental neonatal pulmonary hypertension (PH) associated with bronchopulmonary dysplasia (BPD). Platelets are the primary source of circulating 5‐HT and is released upon platelet activation. Platelet transfusions are associated with neonatal mortality and increased rates of BPD. As BPD is often complicated by PH, we tested the hypothesis that circulating platelets are activated and also increased in the lungs of neonatal mice with bleomycin‐in...
Source: Physiological Reports - Category: Physiology Authors: Tags: ORIGINAL RESEARCH Source Type: research

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