[Pulmonary arterial hypertension, bone marrow, endothelial cell precursors and serotonin]

Biol Aujourdhui. 2016;210(2):79-88. doi: 10.1051/jbio/2016012. Epub 2016 Sep 30.
[Article in French]

Abstract

Serotonin and bone-marrow-derived stem cells participate together in triggering pulmonary hypertension. Our work has shown that the absence of 5-HT2B receptors generates permanent changes in the composition of the blood and bone-marrow in the myeloid lineages, particularly in endothelial cell progenitors. The initial functions of 5-HT2B receptors in pulmonary arterial hypertension (PAH) are restricted to bone-marrow cells. They contribute to the differentiation/proliferation/mobilization of endothelial progenitor cells from the bone-marrow. Those bone-marrow-derived cells have a critical role in the development of pulmonary hypertension and pulmonary vascular remodeling. These data indicate that bone-marrow derived endothelial progenitors play a key role in the pathogenesis of PAH and suggest that interactions involving serotonin and bone morphogenic protein type 2 receptor (BMPR2) could take place at the level of the bone-marrow.

MeSH terms

  • Animals
  • Bone Marrow / physiology*
  • Bone Marrow Cells / physiology
  • Bone Morphogenetic Protein Receptors, Type II / physiology
  • Endothelial Cells / physiology*
  • Humans
  • Hypertension, Pulmonary / etiology*
  • Mice
  • Serotonin / physiology*
  • Stem Cells / physiology*

Substances

  • Serotonin
  • BMPR2 protein, human
  • Bone Morphogenetic Protein Receptors, Type II