Please use this identifier to cite or link to this item: https://ir.swu.ac.th/jspui/handle/123456789/14817
ชื่อเรื่อง: Role of naofen, a novel wd repeat-containing protein, in reducing nitric oxide-induced relaxation
ผู้แต่ง: Feng G.-G.
Yamada M.
Wongsawatkul O.
Li C.
Huang L.
An J.
Komatsu T.
Fujiwara Y.
Naohisa I.
Keywords: acetylcholine
cell protein
cyclohydrolase I
deoxycorticosterone acetate
hydrolase
naofen
nitric oxide
potassium
renin
sodium
unclassified drug
verotoxin 2
animal cell
animal experiment
animal model
animal tissue
article
blood pressure
blood vessel reactivity
controlled study
electrolyte blood level
endothelium cell
gene expression
heart rate
hypertension
immunohistochemistry
male
nonhuman
nucleotide sequence
plasma renin activity
rat
thoracic aorta
Wistar Kyoto rat
Acetylcholine
Animals
Aorta, Thoracic
Cell Line
Male
Mice
Nitric Oxide
Proteins
Rats
Rats, Inbred WKY
Vasodilation
วันที่เผยแพร่: 2008
บทคัดย่อ: 1. Naofen, a novel WD40 repeat domain-containing protein, has recently been found in the intracellular compartment. The aim of the present study was to determine whether naofen affects thoracic aortic vascular reactivity in normotensive and hypertensive rats and whether naofen is present in the thoracic aorta. In addition, we examined whether naofen modulates acetylcholine (ACh)-stimulated nitric oxide (NO) release from the endothelium. 2. Immunohistochemistry showed greater naofen expression in endothelial cells in the DOCA-salt group compared with controls. There was increased naofen mRNA expression in deoxycorticosterone acetate (DOCA)-salt hypertensive rats compared with normotensive rats. 3. Acetylcholine-induced relaxation of rat aortic strips was decreased in DOCA-salt hypertensive rats compared with normotensive rats. Naofen-N- but not naofen-C-terminal protein caused a significant decrease in ACh-induced relaxation of aortic strips from normotensive rats. 4. Using a nitrite assay in a murine aortic endothelial cell line demonstrated that naofen-N-terminal protein, but not naofen-C-terminal protein, significantly reduced ACh-induced NO production, suggesting that naofen interferes with NO production. 5. Administration of naofen-N-terminal protein, but not naofen-C-terminal protein, significantly inhibited cyclohydrolase (GCH) I mRNA expression in a murine aortic endothelial cell line, suggesting that naofen-N-terminal protein interferes with NO synthesis by inhibiting GCH I mRNA expression. 6. The results of the present study suggest that naofen is present in vascular endothelial cells and has an inhibitory effect on ACh-induced relaxation under normotensive conditions. The findings reinforce the functional significance of naofen-N-terminal protein on rat vascular reactivity. © 2008 The Authors.
URI: https://ir.swu.ac.th/jspui/handle/123456789/14817
https://www.scopus.com/inward/record.uri?eid=2-s2.0-55349108566&doi=10.1111%2fj.1440-1681.2008.05008.x&partnerID=40&md5=d8e7ef56513d2b759ddfac44eef0de12
ISSN: 3051870
Appears in Collections:Scopus 1983-2021

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