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Loss of Endothelium-Derived Wnt5a Is Associated With Reduced Pericyte Recruitment and Small Vessel Loss in Pulmonary Arterial Hypertension
Author(s) -
Ke Yuan,
Elya A. Shamskhou,
Mark Orcholski,
Abinaya Nathan,
Sushma Reddy,
Hiroaki Honda,
V. N. Deiva Mani,
Yitian Zeng,
Mehmet Ozgün Ozen,
Lingli Wang,
Utkan Demirci,
Wen Tian,
Mark R. Nicolls,
Vinicio A. de Jesús Pérez
Publication year - 2019
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.118.037642
Subject(s) - wnt signaling pathway , pericyte , medicine , pulmonary hypertension , endothelium , hypoxia (environmental) , microbiology and biotechnology , wnt5a , cd31 , pathology , endothelial stem cell , immunology , biology , chemistry , signal transduction , in vitro , immunohistochemistry , biochemistry , organic chemistry , oxygen
Pulmonary arterial hypertension (PAH) is a life-threatening disorder of the pulmonary circulation associated with loss and impaired regeneration of microvessels. Reduced pericyte coverage of pulmonary microvessels is a pathological feature of PAH and is caused partly by the inability of pericytes to respond to signaling cues from neighboring pulmonary microvascular endothelial cells (PMVECs). We have shown that activation of the Wnt/planar cell polarity pathway is required for pericyte recruitment, but whether production and release of specific Wnt ligands by PMVECs are responsible for Wnt/planar cell polarity activation in pericytes is unknown.

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