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Upregulation of Prokineticin 2 and Prokineticin Receptor 1 in low shear stress‐induced vascular remodeling in mice
Author(s) -
Jiang Zhilong,
Huang Qi,
Jiang Yue,
Liao Qingchuan,
Zhang Youzhi
Publication year - 2020
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.2020.34.s1.00028
Subject(s) - neointima , adventitia , vascular smooth muscle , vascular remodelling in the embryo , shear stress , medicine , microbiology and biotechnology , anatomy , biology , materials science , composite material , restenosis , smooth muscle , stent
Low shear stress induced vascular remodeling emerging atherosclerosis. Prokineticin 2 (PK2) via prokineticin receptor 1(PKR1), is an angiogenic factor. However, little is known about the effect of the low shear stress on PK2/PKR1 signaling in vascular remodeling. The present study aimed that the PK2/PKR1 signaling was involved in low shear stress‐induced vascular remodeling in vivo. Higher protein expression of PK2 and PKR1 was examined in the aortic arch exerting low shear stress in physiological conditions. Further, in pathological conditions, murine model of partial carotid ligation exerted low shear stress, which induced neointima formation with media and adventitia growth, emerging vascular remodeling. It was worth noting that positive staining of PK2 distributed more in neointima area in ligated mice. Lastly, ligated carotid arteries also exerted higher protein expression of PK2 and PKR1. Thus, PK2/PKR1 signaling was involved in the low shear stress‐ induced vascular remodeling in physiological curvature of aortic arch and pathological ligation, which attempted to analyze a potential role of PK2/PKR1 signaling in vascular remodeling associated with atherosclerosis. Support or Funding Information The National Natural Science Foundation of China (NO. 81603110).