Publication:
Role of naofen, a novel wd repeat-containing protein, in reducing nitric oxide-induced relaxation

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Issued Date

2008

Resource Type

Article

File Type

application/pdf

ISSN

3051870

DOI

10.1111/j.1440-1681.2008.05008.x

Other identifier(s)

2-s2.0-55349108566

Rights Holder(s)

มหาวิทยาลัยศรีนครินทรวิโรฒ

Bibliographic Citation

Clinical and Experimental Pharmacology and Physiology. Vol 35, No.12 (2008), p.1447-1453

Suggested Citation

Feng G.-G., Yamada M., Wongsawatkul O., Li C., Huang L., An J., Komatsu T., Fujiwara Y., Naohisa I. Role of naofen, a novel wd repeat-containing protein, in reducing nitric oxide-induced relaxation. Clinical and Experimental Pharmacology and Physiology. Vol 35, No.12 (2008), p.1447-1453. doi:10.1111/j.1440-1681.2008.05008.x Retrieved from: https://hdl.handle.net/20.500.14740/3805

Title

Role of naofen, a novel wd repeat-containing protein, in reducing nitric oxide-induced relaxation

Author(s)

Feng G.-G.
 Yamada M.
 Wongsawatkul O.
 Li C.
 Huang L.
 An J.
 Komatsu T.
 Fujiwara Y.
 Naohisa I.

Abstract

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.

Subject(s)

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

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URI

https://hdl.handle.net/20.500.14740/3805

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Scopus: Year 1983-2021

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