TY - JOUR
T1 - Knockout of the l-pgds gene aggravates obesity and atherosclerosis in mice
AU - Tanaka, Reiko
AU - Miwa, Yoshikazu
AU - Mou, Kin
AU - Tomikawa, Morimasa
AU - Eguchi, Naomi
AU - Urade, Yoshihiro
AU - Takahashi-Yanaga, Fumi
AU - Morimoto, Sachio
AU - Wake, Norio
AU - Sasaguri, Toshiyuki
N1 - Funding Information:
We are grateful to Yuko Kubota for technical assistance. This study was supported by grants from the Ministry of Education, Culture, Sports, Science and Technology (Wakate B, No. 18790178) and Uehara Foundation.
PY - 2009/1/23
Y1 - 2009/1/23
N2 - This study was designed to determine whether lipocalin type-prostaglandin D synthase (l-pgds) deficiency contributes to atherogenesis using gene knockout (KO) mice. A high-fat diet was given to 8-week-old C57BL/6 (wild type; WT), l-pgds KO (LKO), apolipoprotein E (apo E) KO (AKO) and l-pgds/apo E double KO (DKO) mice. The l-pgds deficient mice showed significantly increased body weight, which was accompanied by increased size of subcutaneous and visceral fat tissues. Fat deposition in the aortic wall induced by the high-fat diet was significantly increased in LKO mice compared with WT mice, although there was no significant difference between AKO and DKO mice. In LKO mice, atherosclerotic plaque in the aortic root was also increased and, furthermore, macrophage cellularity and the expression of pro-inflammatory cytokines such as interleukin-1β and monocyte chemoattractant protein-1 were significant increased. In conclusion, l-pgds deficiency induces obesity and facilitates atherosclerosis, probably through the regulation of inflammatory responses.
AB - This study was designed to determine whether lipocalin type-prostaglandin D synthase (l-pgds) deficiency contributes to atherogenesis using gene knockout (KO) mice. A high-fat diet was given to 8-week-old C57BL/6 (wild type; WT), l-pgds KO (LKO), apolipoprotein E (apo E) KO (AKO) and l-pgds/apo E double KO (DKO) mice. The l-pgds deficient mice showed significantly increased body weight, which was accompanied by increased size of subcutaneous and visceral fat tissues. Fat deposition in the aortic wall induced by the high-fat diet was significantly increased in LKO mice compared with WT mice, although there was no significant difference between AKO and DKO mice. In LKO mice, atherosclerotic plaque in the aortic root was also increased and, furthermore, macrophage cellularity and the expression of pro-inflammatory cytokines such as interleukin-1β and monocyte chemoattractant protein-1 were significant increased. In conclusion, l-pgds deficiency induces obesity and facilitates atherosclerosis, probably through the regulation of inflammatory responses.
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U2 - 10.1016/j.bbrc.2008.11.152
DO - 10.1016/j.bbrc.2008.11.152
M3 - Article
C2 - 19070593
AN - SCOPUS:57849159302
SN - 0006-291X
VL - 378
SP - 851
EP - 856
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 4
ER -
