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Literature summary for 3.4.24.24 extracted from

  • Nishihama, K.; Yasuma, T.; Yano, Y.; D Alessandro-Gabazza, C.N.; Toda, M.; Hinneh, J.A.; Baffour Tonto, P.; Takeshita, A.; Totoki, T.; Mifuji-Moroka, R.; Kobayashi, T.; Iwasa, M.; Takei, Y.; Morser, J.; Cann, I.; Gabazza, E.C.
    Anti-apoptotic activity of human matrix metalloproteinase-2 attenuates diabetes mellitus (2018), Metab. Clin. Exp., 82, 88-99 .
    View publication on PubMed
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Protein Variants

Protein Variants Comment Organism
additional information generation of transgenic C57BL/6 mice overexpressing human MMP2, phenotype, overview Homo sapiens

Localization

Localization Comment Organism GeneOntology No. Textmining
extracellular
-
 Homo sapiens
-
-

Metals/Ions

Metals/Ions Comment Organism Structure
Ca2+ required Homo sapiens
Zn2+ metalloproteinase Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens P08253
-
-

Source Tissue

Source Tissue Comment Organism Textmining
additional information circulating hMMP2is significantly increased in diabetic patients compared to controls and significantly correlated with the serum C-peptide levels Homo sapiens
-
pancreatic islet beta-cell Homo sapiens
-

Synonyms

Synonyms Comment Organism
matrix metalloproteinase-2
-
 Homo sapiens
MMP-2
-
 Homo sapiens

General Information

General Information Comment Organism
malfunction induction of diabetes in transgenic mice overexpressing human MMP2 show ignificant improvements in glycemia, glucose tolerance and insulin secretion compared to diabetic wild-type mice. Increased hMMP2 levels in mice correlate with significant reduction in islet beta-cell apoptosis compared to wild-type counterparts, and an inhibitor of hMMP2 reverses this mitigating activity against diabetes Homo sapiens
physiological function chronic progression of diabetes is associated with decreased pancreatic islet mass due to apoptosis of beta-cells. Patients with diabetes have increased circulating matrix metalloproteinase-2 (MMP2). MMP2 might inhibit cell apoptosis, including islet beta-cells. The increased activation of Akt and BAD induced by hMMP2 in beta-cells compared to controls, links this signaling pathway to the anti-apoptotic activity of hMMP2, a property that is reversible by both an hMMP2 inhibitor and antibody against integrin-beta3. hMMP2 may attenuate the severity of diabetes by protecting islet beta-cells from apoptosis through an integrin-mediated activation of the Akt/BAD pathway. Preliminary treatment of cells, e.g. HepG2 cells, HUVE cells, and NHM cells, with active hMMP2 for 30-min significantly inhibits apoptosis (induced by starvation), hMMP2 inhibits apoptosis of beta-cell lines, which is modulated by intergrins Homo sapiens