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Pericyte coverage of abnormal blood vessels in myelofibrotic bone marrows

Eva Zetterberg1, Alessandro M Vannucchi, Anna Rita Migliaccio

  • 1Division of Hematology and Center for Inflammation and Hematology Research, Department of Medicine, The Karolinska Institutet at Karolinska University Hospital, Huddinge, Stockholm, Sweden.

Haematologica
|May 10, 2007
PubMed
Abstract

Insights

Myelofibrosis involves abnormal blood vessel growth (angiogenesis) in bone marrow, characterized by increased vessel density and extensive pericyte coating in both humans and mice. This suggests a common mechanism linked to abnormal megakaryocytopoiesis.

Area of Science:

  • Hematology
  • Oncology
  • Vascular Biology

Background:

  • Myelofibrosis is characterized by abnormal bone marrow angiogenesis, but the underlying mechanisms remain unclear.
  • Pericyte abnormalities are known in solid tumors, prompting investigation into their role in myelofibrosis.

Purpose of the Study:

  • To investigate differences in bone marrow vessel morphology and pericyte coverage between myelofibrosis patients and controls.
  • To analyze these parameters in mouse models of myelofibrosis.

Main Methods:

  • Assessed microvascular density (MVD), vessel morphology, and pericyte coverage in bone marrow samples from 19 myelofibrosis patients and 9 controls.
  • Examined these parameters in two mouse models of myelofibrosis involving genetic alterations in megakaryocyte differentiation.

Main Results:

  • Myelofibrotic bone marrow showed significantly higher MVD (3.8-fold) and larger vessel perimeters (5.9-fold) compared to controls.
  • Vessels in myelofibrosis patients were more extensively pericyte-coated (92%) versus controls (51%).
  • Increased MVD and aberrant, pericyte-coated vessels were observed in both human and murine myelofibrosis models.

Conclusions:

  • Angiogenesis is significantly altered in myelofibrosis, mirroring findings in human and mouse models.
  • Intense pericyte coating of vessels is a hallmark of myelofibrosis.
  • Abnormal megakaryocytopoiesis is a likely contributor to the observed angiogenic abnormalities.

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