|Strain name||hRN 8-12|
|Former Common name||No Data|
|H-2 Haplotype||No Data|
|Genotype||a/a B/B C/C|
|Strain development||Developed by Dr. Akiyoshi Fukamizu, University of Tsukuba in 1991. C57BL/6 background.|
|Strain description||Human renin gene transgenic mice with integration of 10 copies of a 15 kbp human DNA fragment containing the renin gene (hRN 8-12 mice). The renin-angiotensin system (RAS) is one of the determinant factors in regulating blood pressure and sodium absorption. RAS has been shown to accelerate various diseases such as renal failure, atherosclerosis, cardiac hypertrophy, and pulmonary hypertension. The reaction between renin, produced in the kidney, and its substrate angiotensinogen, produced in the liver, is the initial and rate-limiting step in the enzymatic cascade that generates angiotensin I. Angiotensin-converting enzyme in the lung converts angiotensin I to the potent vasoconstrictor angiotensin II (Ang II). The depositor reported that overactivation of the RAS induces hypertension in the F1 generation obtained from breeding between a female carrying the human renin gene (hRN+/+) and a male possessing the human angiotensinogen gene (hAG+/+). Moreover, female hAG+/+ mice when bred with male hRN+/+ mice are hypertensive specifically in late pregnancy, suggesting possible implications for preeclampsia or pregnancy-induced hypertension, a life-threatening disorder for human mothers and fetuses. hRN+/+ and hANG+/+ mice provide the opportunity to understand the role of the RAS in hypertension and other common diseases. hRN8-12 mice (RBRC01122), hAG 2-5 mice (RBRC01123), hRN8-12 x hAG2-5)F1 mice (RBRC02432).|
|Colony maintenance||Carrier x Carrier (Homozygote x Homozygote) Homozygous mice are viable and fertile.|
|Symbol name||renin 1 structural (human)|
|Common name||Ren, Ren-1, Ren-A, Ren1d, Rn-1, Rnr|
|Symbol description||No Data|
|References||Biochem Biophys Res Commun. 1989 Dec 15;165(2):826-32.
Tissue-specific expression of the human renin gene in transgenic mice.
|Research applications||Cell Biology Research,
|Specific Term and Conditions||The following terms and conditions will be requested by the DEPOSITOR.
The RECIPIENT of BIOLOGICAL RESOURCE shall obtain a prior written consent on use of it from the DEPOSITOR.
In publishing the research results obtained by use of the BIOLOGICAL RESOURCE, a citation of the following literature(s) designated by the DEPOSITOR is requested.
Biochemical and Biophysical Research Communications, 165, 826-832 (1989).
|1||Mouse of the Month May 2012
Systolic blood pressure
|2||Lab HP (Japanese)|
|3||Genotyping protocol <PCR>|
|Depositor||Fukamizu, Akiyoshi (University of Tsukuba)|
|Strain Status /
|Exaggeration of focal cerebral ischemia in transgenic mice carrying human Renin and human angiotensinogen genes.||Stroke.40(2): 597-603 (2009).(19023100)|
|Inaba S, Iwai M, Tomono Y, Senba I, Furuno M, Kanno H, Okayama H, Mogi M, Higaki J, Horiuchi M.|
|Continuous activation of renin-angiotensin system impairs cognitive function in renin/angiotensinogen transgenic mice.||Hypertension.53(2): 356-62 (2009).(19047580)|
|Inaba S, Iwai M, Furuno M, Tomono Y, Kanno H, Senba I, Okayama H, Mogi M, Higaki J, Horiuchi M.|
|Exercise training can attenuate preeclampsia-like features in an animal model.||J Hypertens.28(12): 2446-53 (2010).(20811291)|
|Falcao S, Bisotto S, Michel C, Lacasse AA, Vaillancourt C, Gutkowska J, Lavoie JL.|
|Impaired post-infarction cardiac remodeling in chronic kidney disease is due to excessive renin release.||Lab Invest. (2012).(22986786)|
|Ogawa M, Suzuki JI, Takayama K, Senbonmatsu T, Hirata Y, Nagai R, Isobe M.|