Spontaneous Formation of Megakaryocyte Progenitors (CFU-MK) in Primary Thrombocythaemia

Zc, Han; Brière, J; Jf, Abgrall; Sensebé, Luc; Nedellec, G.; Parent, Dominique; Guern, G.

doi:10.1159/000205837

Cited by 32 publications

(19 citation statements)

References 3 publications

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“…Bone marrow cells harvested from the femurs were cultured using the plasma-clot culture method (35). Colony forming unit of megakaryocyte (CFU-MK) was identified by AchE and hematoxylin staining as described above.…”

Section: Hyperoxic Lung Damage and Plateletmentioning

confidence: 99%

Effects of Oxygen-Induced Lung Damage on Megakaryocytopoiesis and Platelet Homeostasis in a Rat Model

Yang

et al. 2003

Pediatr Res

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The association between lung injury and thrombocytopenia was investigated by comparing the megakaryocyte and platelet counts, and platelet activation using P-selectin as a marker, between the prepulmonary (right atrial) and postpulmonary (left atrial) blood in adult and neonatal (preterm and term) rats with and without hyperoxic lung injury. In the healthy controls, the postpulmonary blood had lower megakaryocyte count (prepulmonary versus postpulmonary: Preterm: 8.7[0.6] platelets, p ϭ 0.003). Peripheral platelet and intrapulmonary megakaryocyte counts in the lung-damaged rats were significantly lower than those in their respective controls. Intrapulmonary thrombi or platelet aggregation were detected in the lung-damaged rats but not in the controls. These findings showed that hyperoxic lung damage reduced circulating platelets through (1) failure of the lungs to retain and fragment megakaryocytes to release platelets, and (2) platelet activation leading to platelet aggregation, thrombi formation and platelet consumption. The magnitude of platelet reduction was physiologically significant, as demonstrated by higher counts of megakaryocyte colony forming units in the bone marrow culture of the animals in the hyperoxia group when compared with the controls. Thrombocytopenia is a common complication in neonates and may affect up to 7.6% of all newborns (1, 2). The condition is particularly prevalent in sick infants. In a survey by Castle et al. 58% and 22% of infants receiving intensive care had platelet count Ͻ150ϫ10 9 /L and 100ϫ10 9 /L, respectively (3). Congenital or early onset (Ͻ72 h of birth) neonatal thrombocytopenia may be caused by immunologic causes including isoimmune or maternal autoimmune thrombocytopenia, failure of platelet production such as that in the thrombocytopeniaabsent-radii syndrome, congenital infection, and bone marrow suppression due to maternal hypertension, preeclampsia, and diabetes mellitus (1, 4). The etiology however remains unclear in a large proportion of cases (3, 5, 6). The late onset (Ͼ72 h of birth) type of thrombocytopenia is often attributed to sepsis (7), although an infective cause is often not identifiable in the affected infants. Previous workers have observed that this category of thrombocytopenia is particularly common in newborns with lung disease such as respiratory distress syndrome (5, 8 -11), and the degree of platelet reduction is directly related to the severity of the underlying lung disease, the concentration of inspired oxygen (9, 11), and the ventilation pressure (8, 11). In a study on rabbits, mechanical ventilation

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Section: Hyperoxic Lung Damage and Plateletmentioning

confidence: 99%

Effects of Oxygen-Induced Lung Damage on Megakaryocytopoiesis and Platelet Homeostasis in a Rat Model

Yang

et al. 2003

Pediatr Res

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“…Its affinity for heparin and other sulfated glycans suggests that it may function as a prothrombotic agent. Effects of PF4 on cellular functions, such as inhibition of megakaryocytopoiesis (18) and angiogenesis (19), as well as modulation of cellular immune responses (17), have been described, but as yet no cell surface receptor has been identified. The finding that PF4 modulates growth factor receptor interactions (20,21) suggests that at least some of its effects are indirect.…”

mentioning

confidence: 99%

Platelet factor 4 binds to interleukin 8 receptors and activates neutrophils when its N terminus is modified with Glu-Leu-Arg.

Clark‐Lewis

Dewald

Geiser

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

242

109

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“…An increase in platelet count, for instance, which is common in patients with chronic MPDs, also may occur as a reactive phenomenon in patients with acute or chronic infectious or inflammatory conditions. Spontaneous growth of erythroid burst-forming units 4 or megakaryocyte colony-forming units 5 supports the diagnosis of PV and ET. However, these changes are not found in all patients.…”

Section: Chronic Myeloproliferative Diseases (Mpds) Are Not Associatementioning

confidence: 75%

Clonality Analysis Using X-Chromosome Inactivation at the Human Androgen Receptor Gene (HUMARA): Evaluation of Large Cohorts of Patients With Chronic Myeloproliferative Diseases, Secondary Neutrophilia, and Reactive Thrombocytosis

Mitterbauer¹,

Winkler²,

Gisslinger³

et al. 1999

Am J Clin Pathol

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Spontaneous Formation of Megakaryocyte Progenitors (CFU-MK) in Primary Thrombocythaemia

Cited by 32 publications

References 3 publications

Effects of Oxygen-Induced Lung Damage on Megakaryocytopoiesis and Platelet Homeostasis in a Rat Model

Effects of Oxygen-Induced Lung Damage on Megakaryocytopoiesis and Platelet Homeostasis in a Rat Model

Platelet factor 4 binds to interleukin 8 receptors and activates neutrophils when its N terminus is modified with Glu-Leu-Arg.

Clonality Analysis Using X-Chromosome Inactivation at the Human Androgen Receptor Gene (HUMARA): Evaluation of Large Cohorts of Patients With Chronic Myeloproliferative Diseases, Secondary Neutrophilia, and Reactive Thrombocytosis

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