| First Author | Ishida J | Year | 1998 |
| Journal | Biochem Biophys Res Commun | Volume | 252 |
| Issue | 3 | Pages | 610-6 |
| PubMed ID | 9837754 | Mgi Jnum | J:51346 |
| Mgi Id | MGI:1315123 | Doi | 10.1006/bbrc.1998.9707 |
| Citation | Ishida J, et al. (1998) Rescue of angiotensinogen-knockout mice. Biochem Biophys Res Commun 252(3):610-6 |
| abstractText | Angiotensinogen, the precursor of angiotensins I and II, is a critical component of the renin-angiotensin system that plays an important role in regulating blood pressure and electrolyte homeostasis. Genetically altered mice lacking angiotensinogen (Agt-KO) showed an expected phenotype, such as marked hypotension, but unexpected ones including abnormal kidney morphology, reduced survival rates of newborns, and impaired blood-brain barrier function after cold injury. To examine whether disruption of the angiotensinogen gene is responsible for the observed phenotypes, we generated a line of mice heterozygous for the mouse angiotensinogen gene under the control of a mouse metallothionein- I promoter (MT-Agt) and crossmated transgenic mice with Agt-KO mice. The resulting mice (MT-Agt(+/-)/Agt(-/-):MT-Agt/KO) produced the plasma level of angiotensin I comparable to that of wild-type mice, and the mutant phenotypes were rescued. These results indicated that the resultant phenotypes due to the genetic deficiency of mouse angiotensinogen can be corrected by restoring angiotensinogen and angiotensin I in the circulation. Copyright 1998 Academic Press. |
