Hyperproliferative apoptosis-resistant endothelial cells in idiopathic pulmonary arterial hypertension.

@article{Masri2007HyperproliferativeAE,
  title={Hyperproliferative apoptosis-resistant endothelial cells in idiopathic pulmonary arterial hypertension.},
  author={Fares A. Masri and Weiling Xu and Suzy A. Comhair and Kewal Asosingh and Michelle Koo and Amit Vasanji and Judith A. Drazba and Bela Anand-Apte and Serpil C Erzurum},
  journal={American journal of physiology. Lung cellular and molecular physiology},
  year={2007},
  volume={293 3},
  pages={
          L548-54
        }
}
  • F. MasriWeiling Xu S. Erzurum
  • Published 1 September 2007
  • Biology, Medicine
  • American journal of physiology. Lung cellular and molecular physiology
Idiopathic pulmonary arterial hypertension (IPAH) is characterized by plexiform vascular lesions, which are hypothesized to arise from deregulated growth of pulmonary artery endothelial cells (PAEC). Here, functional and molecular differences among PAEC derived from IPAH and control human lungs were evaluated. Compared with control cells, IPAH PAEC had greater cell numbers in response to growth factors in culture due to increased proliferation as determined by bromodeoxyuridine incorporation… 
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Autocrine fibroblast growth factor-2 signaling contributes to altered endothelial phenotype in pulmonary hypertension.

The findings suggest that excessive autocrine release of endothelial-derived FGF2 in IPAH contributes to the acquisition and maintenance of an abnormal EC phenotype, enhancing proliferation through constitutive activation of ERK1/2 and decreasing apoptosis by increasing BCL2 and BCL-xL.

Evidence for cell fusion is absent in vascular lesions associated with pulmonary arterial hypertension.

  • S. MajkaM. Skokan J. West
  • Biology, Medicine
    American journal of physiology. Lung cellular and molecular physiology
  • 2008
Analysis of CD45/CD133 localization, cell fusion, and proliferation during late-stage PAH in human lung tissue from control subjects and subjects with idiopathic (IPAH) and familial (FPAH) PAH suggest that abnormal lesion formation in PAH occurs in the absence of cell fusion.

Suppression of endothelial CD39/ENTPD1 is associated with pulmonary vascular remodeling in pulmonary arterial hypertension.

Sustained attenuation of CD39 activity through ATP accumulation is tightly linked to vascular dysfunction and remodeling in PAH and could represent a novel target for therapy.

Vascular pathobiology of pulmonary hypertension

Endothelial Apoptosis in Pulmonary Hypertension Is Controlled by a microRNA/Programmed Cell Death 4/Caspase-3 Axis

Findings support the existence of a microRNA-21–responsive PDCD4/caspase-3 pathway in the pulmonary tissues that when active serves to promote endothelial apoptosis in vitro and PH in vivo.

Evidence of dysfunction of endothelial progenitors in pulmonary arterial hypertension.

Evidence is provided of the involvement of progenitor cells in the vascular remodeling associated with PAH, and Dysfunction of circulating progenitors in PAH may contribute to this process.

Endothelial cell energy metabolism, proliferation, and apoptosis in pulmonary hypertension.

The phenotypic changes of the endothelium in PAH are reviewed and the biochemical mechanisms accounting for the proliferative, glycolytic, and strongly proangiogenic phenotype of these dysfunctional cells are reviewed, which consequently foster the panvascular progressive pulmonary remodeling inPAH.

Circulating angiogenic precursors in idiopathic pulmonary arterial hypertension.

Vascular remodeling in idiopathic pulmonary arterial hypertension (IPAH) involves hyperproliferative and apoptosis-resistant pulmonary artery endothelial cells. In this study, we evaluated the…

Dehydroepiandrosterone inhibits the Src/STAT3 constitutive activation in pulmonary arterial hypertension.

DHEA reverses pulmonary hypertension in part by inhibiting the Src/STAT3 axis inhibition and improves experimental PAH (monocrotaline rats) by decreasing mean PA pressure and right ventricle hypertrophy.
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