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Title: Protection of atherogenesis in thromboxane A2 receptor-deficient mice is not associated with thromboxane A2 receptor in bone marrow-derived cells

Abstract

In the previous study, we generated mice lacking thromboxane A2 receptor (TP) and apolipoprotein E, apoE{sup -/-}TP{sup -/-} mice, and reported that the double knockout mice developed markedly smaller atherosclerotic lesions than those in apoE{sup -/-} mice. To investigate the mechanism responsible for reduced atherosclerosis in apoE{sup -/-}TP{sup -/-} mice, we examined the role of TP in bone marrow (BM)-derived cells in the development of the atherosclerotic lesions. When we compared the function of macrophages in apoE{sup -/-} and in apoE{sup -/-}TP{sup -/-} mouse in vitro, there was no difference in the expression levels of cytokines and chemokines after stimulation with lipopolysaccharide. We then transplanted the BM from either apoE{sup -/-} or apoE{sup -/-}TP{sup -/-} mice to either apoE{sup -/-} or apoE{sup -/-}TP{sup -/-} mice after sublethal irradiation. After 12 weeks with high fat diet, we analyzed the atherosclerotic lesion of aortic sinus. When the BM from apoE{sup -/-} or apoE{sup -/-}TP{sup -/-} mice was transplanted to apoE{sup -/-} mice, the lesion size was almost the same as that of apoE{sup -/-} mice without BM transplantation. In contrast, when the BM from apoE{sup -/-} or apoE{sup -/-}TP{sup -/-} mice was transplanted to apoE{sup -/-}TP{sup -/-} mice, the lesion size wasmore » markedly reduced. These results indicate that the protection of atherogenesis in TP{sup -/-} mice is not associated with TP in BM-derived cells.« less

Authors:
 [1];  [2];  [1];  [1];  [3];  [3];  [4];  [1]
  1. Department of Clinical Innovative Medicine, Kyoto University Graduate School of Medicine, 54 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507 (Japan)
  2. Department of Geriatric Medicine, Kyoto University Graduate School of Medicine, 54 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507 (Japan). E-mail: harai@kuhp.kyoto-u.ac.jp
  3. Department of Cell Biology, Kyoto University Graduate School of Medicine, 54 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507 (Japan)
  4. Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine, 54 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507 (Japan)
Publication Date:
OSTI Identifier:
20857937
Resource Type:
Journal Article
Resource Relation:
Journal Name: Biochemical and Biophysical Research Communications; Journal Volume: 351; Journal Issue: 4; Other Information: DOI: 10.1016/j.bbrc.2006.10.121; PII: S0006-291X(06)02364-3; Copyright (c) 2006 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA)
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ARTERIOSCLEROSIS; BONE MARROW; FATS; IN VITRO; KNOCK-OUT REACTIONS; LYMPHOKINES; MACROPHAGES; MICE; RECEPTORS; SINUSES; SUBLETHAL IRRADIATION

Citation Formats

Zhuge Xin, Arai, Hidenori, Xu, Yang, Murayama, Toshinori, Kobayashi, Takuya, Narumiya, Shuh, Kita, Toru, and Yokode, Masayuki. Protection of atherogenesis in thromboxane A2 receptor-deficient mice is not associated with thromboxane A2 receptor in bone marrow-derived cells. United States: N. p., 2006. Web. doi:10.1016/j.bbrc.2006.10.121.
Zhuge Xin, Arai, Hidenori, Xu, Yang, Murayama, Toshinori, Kobayashi, Takuya, Narumiya, Shuh, Kita, Toru, & Yokode, Masayuki. Protection of atherogenesis in thromboxane A2 receptor-deficient mice is not associated with thromboxane A2 receptor in bone marrow-derived cells. United States. doi:10.1016/j.bbrc.2006.10.121.
Zhuge Xin, Arai, Hidenori, Xu, Yang, Murayama, Toshinori, Kobayashi, Takuya, Narumiya, Shuh, Kita, Toru, and Yokode, Masayuki. Fri . "Protection of atherogenesis in thromboxane A2 receptor-deficient mice is not associated with thromboxane A2 receptor in bone marrow-derived cells". United States. doi:10.1016/j.bbrc.2006.10.121.
@article{osti_20857937,
title = {Protection of atherogenesis in thromboxane A2 receptor-deficient mice is not associated with thromboxane A2 receptor in bone marrow-derived cells},
author = {Zhuge Xin and Arai, Hidenori and Xu, Yang and Murayama, Toshinori and Kobayashi, Takuya and Narumiya, Shuh and Kita, Toru and Yokode, Masayuki},
abstractNote = {In the previous study, we generated mice lacking thromboxane A2 receptor (TP) and apolipoprotein E, apoE{sup -/-}TP{sup -/-} mice, and reported that the double knockout mice developed markedly smaller atherosclerotic lesions than those in apoE{sup -/-} mice. To investigate the mechanism responsible for reduced atherosclerosis in apoE{sup -/-}TP{sup -/-} mice, we examined the role of TP in bone marrow (BM)-derived cells in the development of the atherosclerotic lesions. When we compared the function of macrophages in apoE{sup -/-} and in apoE{sup -/-}TP{sup -/-} mouse in vitro, there was no difference in the expression levels of cytokines and chemokines after stimulation with lipopolysaccharide. We then transplanted the BM from either apoE{sup -/-} or apoE{sup -/-}TP{sup -/-} mice to either apoE{sup -/-} or apoE{sup -/-}TP{sup -/-} mice after sublethal irradiation. After 12 weeks with high fat diet, we analyzed the atherosclerotic lesion of aortic sinus. When the BM from apoE{sup -/-} or apoE{sup -/-}TP{sup -/-} mice was transplanted to apoE{sup -/-} mice, the lesion size was almost the same as that of apoE{sup -/-} mice without BM transplantation. In contrast, when the BM from apoE{sup -/-} or apoE{sup -/-}TP{sup -/-} mice was transplanted to apoE{sup -/-}TP{sup -/-} mice, the lesion size was markedly reduced. These results indicate that the protection of atherogenesis in TP{sup -/-} mice is not associated with TP in BM-derived cells.},
doi = {10.1016/j.bbrc.2006.10.121},
journal = {Biochemical and Biophysical Research Communications},
number = 4,
volume = 351,
place = {United States},
year = {Fri Dec 29 00:00:00 EST 2006},
month = {Fri Dec 29 00:00:00 EST 2006}
}