RGD Reference Report - Human chymase expression in a mice induces mild hypertension with left ventricular hypertrophy. - Rat Genome Database

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Human chymase expression in a mice induces mild hypertension with left ventricular hypertrophy.

Authors: Koga, T  Urata, H  Inoue, Y  Hoshino, T  Okamoto, T  Matsunaga, A  Suzuki, M  Miyazaki, J  Ideishi, M  Arakawa, K  Saku, K 
Citation: Koga T, etal., Hypertens Res. 2003 Sep;26(9):759-68.
RGD ID: 5128600
Pubmed: PMID:14620933   (View Abstract at PubMed)

A number of in vitro studies have suggested potential pathophysiological roles of human (h-) chymase. However, the lack of an appropriate animal model has left the in vivo roles of chymase unclear. To approach this problem, a transgenic mouse (TGM) model carrying the h-chymase gene was established. The h-chymase cDNA transgene was constructed with the chicken beta actin promoter and cytomegalovirus immediate early gene enhancer, and injected into mouse oocytes. Homozygous mice with a high copy number of the h-chymase gene suffered from intrauterine death. In three heterozygous TGM lines, h-chymase transgene expression was detected in entire organs, including the heart, vessels, skin, liver, lung, and brain. The h-chymase immunoreactivity was localized in the extracellular matrices of each organ, especially on the basement membranes of vessels. Aortic and hepatic chymase-dependent angiotensin II formations were significantly higher than those in the wild-type littermates. Three independent TGM lines showed the same phenotypic changes: elevation of blood pressure, left ventricular hypertrophy, emaciation with reduction in the lipid tissue, leukocytosis, and oligotrichia. The angiotensin II subtype 1 (AT1) receptor antagonist valsartan suppressed the elevated blood pressure completely and left ventricular hypertrophy incompletely, but did not affect the other phenotypes. These data suggested that in vivo expression of h-chymase caused mild hypertension (AT1 receptor-dependent) with left ventricular hypertrophy (partially AT1 receptor-dependent), and also chronic inflammatory changes (AT1 receptor-independent).



RGD Manual Disease Annotations    Click to see Annotation Detail View
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
CMA1HumanLeft Ventricular Hypertrophy  IMP human gene in mouse modelRGD 
Cma1RatLeft Ventricular Hypertrophy  ISOCMA1 (Homo sapiens)human gene in mouse modelRGD 
Cma1MouseLeft Ventricular Hypertrophy  ISOCMA1 (Homo sapiens)human gene in mouse modelRGD 

Objects Annotated

Genes (Rattus norvegicus)
Cma1  (chymase 1)

Genes (Mus musculus)
Cma1  (chymase 1, mast cell)

Genes (Homo sapiens)
CMA1  (chymase 1)


Additional Information