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PMID:11226291

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Citation

Meneton, P, Bloch-Faure, M, Hagege, AA, Ruetten, H, Huang, W, Bergaya, S, Ceiler, D, Gehring, D, Martins, I, Salmon, G, Boulanger, CM, Nussberger, J, Crozatier, B, Gasc, JM, Heudes, D, Bruneval, P, Doetschman, T, Ménard, J and Alhenc-Gelas, F (2001) Cardiovascular abnormalities with normal blood pressure in tissue kallikrein-deficient mice. Proc. Natl. Acad. Sci. U.S.A. 98:2634-9

Abstract

Tissue kallikrein is a serine protease thought to be involved in the generation of bioactive peptide kinins in many organs like the kidneys, colon, salivary glands, pancreas, and blood vessels. Low renal synthesis and urinary excretion of tissue kallikrein have been repeatedly linked to hypertension in animals and humans, but the exact role of the protease in cardiovascular function has not been established largely because of the lack of specific inhibitors. This study demonstrates that mice lacking tissue kallikrein are unable to generate significant levels of kinins in most tissues and develop cardiovascular abnormalities early in adulthood despite normal blood pressure. The heart exhibits septum and posterior wall thinning and a tendency to dilatation resulting in reduced left ventricular mass. Cardiac function estimated in vivo and in vitro is decreased both under basal conditions and in response to beta-adrenergic stimulation. Furthermore, flow-induced vasodilatation is impaired in isolated perfused carotid arteries, which express, like the heart, low levels of the protease. These data show that tissue kallikrein is the main kinin-generating enzyme in vivo and that a functional kallikrein-kinin system is necessary for normal cardiac and arterial function in the mouse. They suggest that the kallikrein-kinin system could be involved in the development or progression of cardiovascular diseases.

Links

PubMed PMC30190 Online version:10.1073/pnas.051619598

Keywords

Animals; Base Sequence; Blood Pressure; Cardiovascular Abnormalities/genetics; Carotid Arteries/physiology; DNA Primers; Echocardiography; Genotype; Kallikreins/genetics; Kallikreins/physiology; Mice; Regional Blood Flow; Ventricular Function, Left

Significance

Annotations

Gene product Qualifier GO Term Evidence Code with/from Aspect Extension Notes Status

MOUSE:K1KB1

acts_upstream_of_or_within

GO:0002255: tissue kallikrein-kinin cascade

ECO:0000315: mutant phenotype evidence used in manual assertion

MGI:MGI:3513115

P

Seeded From UniProt

complete

MOUSE:K1KB1

acts_upstream_of_or_within

GO:0003220: left ventricular cardiac muscle tissue morphogenesis

ECO:0000315: mutant phenotype evidence used in manual assertion

MGI:MGI:3513115

P

  • results_in_morphogenesis_of:(EMAPA:17337)

Seeded From UniProt

complete

MOUSE:K1KB1

acts_upstream_of_or_within

GO:0003073: regulation of systemic arterial blood pressure

ECO:0000315: mutant phenotype evidence used in manual assertion

MGI:MGI:3513115

P

Seeded From UniProt

complete

MOUSE:K1KB1

acts_upstream_of_or_within

GO:0002936: bradykinin biosynthetic process

ECO:0000315: mutant phenotype evidence used in manual assertion

MGI:MGI:3513115

P

Seeded From UniProt

complete

MOUSE:K1KB1

acts_upstream_of_or_within

GO:0060048: cardiac muscle contraction

ECO:0000315: mutant phenotype evidence used in manual assertion

MGI:MGI:3513115

P

Seeded From UniProt

complete

MOUSE:K1KB1

acts_upstream_of_or_within

GO:0042311: vasodilation

ECO:0000315: mutant phenotype evidence used in manual assertion

MGI:MGI:3513115

P

Seeded From UniProt

complete


See also

References

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