Premium
Phenotypic characteristics of pulmonary supernumerary arterial endothelium may be involved in the formation of plexiform lesions (1089.21)
Author(s) -
Oshima Kaori,
Matsumoto Yuri,
O'Neill Kealan,
McMurtry Ivan,
Stevens Troy,
Oka Masahiko
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1089.21
Subject(s) - phenotype , pathology , vascular remodelling in the embryo , endothelium , pulmonary artery , lung , griffonia simplicifolia , lesion , pulmonary hypertension , biology , chemistry , medicine , immunohistochemistry , endocrinology , biochemistry , gene
The plexiform lesion (PL), which comprises proliferative endothelial marker (EC)‐positive channel cells and chromatin‐rich core cells, is the histological hallmark of severe pulmonary arterial hypertension (PAH). PLs preferentially form in supernumerary arteries (SAs) in SU5416/hypoxia/normoxia‐exposed PAH rats, which supports clinical observations. However, the underlying pathological mechanisms of this observation are unknown. SAs are unique small pulmonary branches with specific anatomical and functional properties, such as the phenotype of the ECs, which may contribute to the formation of PLs. The EC phenotype in PLs seems to be shared with pulmonary microvascular ECs (PMVECs), which are highly proliferative. Therefore, we tested the hypothesis that the ECs in SAs share the same phenotype as PMVECs that predisposes to the development of PLs. A lectin protein from Griffonia simplicifolia (GS), which selectively interacts with PMVECs was perfused through the pulmonary vasculature of control and PAH rats. Lung slices were prepared and examined by confocal fluorescence microscopy. In normal rats, ECs in SAs interacted with GS. However, ECs in SAs and occlusive vascular lesions in PAH rats had no apparent interaction with GS. The PMVEC‐like phenotype of ECs in SAs may contribute to the development of PLs, and there may be a phenotypic transformation of these cells during the progression of PAH. Grant Funding Source : Supported by NIH HL66299 and HL60024 to T.S.