@article{oai:hirosaki.repo.nii.ac.jp:00003657,
 author = {Ashitate, Toshihiro and Osanai, Tomohiro and Tanaka, Makoto and Magota, Koji and Echizen, Takashi and Tomita, Hirofumi and Okumura, Ken},
 issue = {1/2/3/4},
 journal = {弘前医学},
 month = {Mar},
 note = {application/pdf, We showed that endogenous prostacyclin inhibitor coupling factor 6 （CF6） is released from vascular
endothelial cells and its release is stimulated by tumor necrosis factor-α, which is related to congestive heart failure
（CHF）. We also showed that CF6 increases the gene expression related to CHF. To investigate the role of CF6 in
the genesis of CHF, we generated CF6-overexpressing transgenic（ TG） mice, and characterized the phenotype. DNA
fragment consisting of human elongation factor 1α promoter, and human calcitonin/CF6 fused gene was injected into
the embryo of C57BL/6J mouse, and homozygous TG mice were generated. In TG mice, CF6 gene was overexpressed
by two fold in overall tissues compared with wild type（ WT） mice. Under normal salt diet, blood pressure, heart rate,
and the expression of energy metabolism-related genes were similar between TG and WT mice. When the mice were
fed with 8% -salt diet for 35 weeks, the mortality of TG mice was higher than that of WT mice（ survival rate; 50% in
TG versus 92% in WT, p<0.05 by log-rank test）. This preliminary report indicates that further examination, especially
analysis of the cardiac function, is needed to clarify the cause of high mortality of TG mice under high salt intake., 弘前医学. 60(1/2/3/4), 2009, p.18-26},
 pages = {18--26},
 title = {Generation and Characterization of Coupling Factor 6-Overexpressing Transgenic Mice},
 volume = {60},
 year = {2009}
}