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Literature summary for 3.4.24.24 extracted from

  • Kopaliani, I.; Martin, M.; Zatschler, B.; Mueller, B.; Deussen, A.
    Whey peptide isoleucine-tryptophan inhibits expression and activity of matrix metalloproteinase-2 in rat aorta (2016), Peptides, 82, 52-59 .
    View publication on PubMed
Search for more literature for 3.4.24.24

Protein Variants

Protein Variants Comment Organism
down peptide isoleucine-tryptophan (Ile-Trp) inhibits expression and activity of matrix metalloproteinase-2 in rat aorta Rattus norvegicus

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
Gelatin + H2O Rattus norvegicus
-
 ?
-
 ?

Organism

Organism UniProt Comment Textmining
Rattus norvegicus P33436
-
-

Source Tissue

Source Tissue Comment Organism Textmining
aorta
-
 Rattus norvegicus
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endothelial cell
-
 Rattus norvegicus
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smooth muscle cell
-
 Rattus norvegicus
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
Gelatin + H2O
-
 Rattus norvegicus ?
-
 ?

Synonyms

Synonyms Comment Organism
matrix metalloproteinase-2
-
 Rattus norvegicus
MMP2
-
 Rattus norvegicus

Expression

Organism Comment Expression
Rattus norvegicus peptide Ile-Trp isoleucine-tryptophan inhibits expression and activity of matrix metalloproteinase-2 in rat aorta, mechanism of action, overview. The inhibitor significantly inhibits ANGI, but not ANGII mediated increase in expression of MMP2, while losartan also blocks effects of ANGII. Signaling pathways regulating MMP2 expression in endothelial cells and smooth muscle cells are similarly inhibited after treatment with Ile-Trp or captopril. Ile-Trp not only inhibits the MMP2 expression, but also its activation assessed with gelatin zymography down
Rattus norvegicus in vitro, both angiotensin II (ANGII) and ANGI stimulation significantly increase expression of MMP2 up

General Information

General Information Comment Organism
metabolism aortic stiffness is an independent risk factor for development of cardiovascular diseases. Activation of renin-angiotensin-aldosterone system (RAAS) including angiotensin converting enzyme (ACE) activity leads to overproduction of angiotensin II (ANGII) from its precursor angiotensin I (ANGI). ANGII leads to overexpression and activation of matrix metalloproteinase-2 (MMP2), which is critically associated with pathophysiology of aortic stiffness Rattus norvegicus