In Vitro Inhibition of the Activation of Pro-matrix Metalloproteinase 1 (Pro-MMP-1) and Pro-matrix Metalloproteinase 9 (Pro-MMP-9) by Rice and Soybean Bowman−Birk Inhibitors

2004 ◽  
Vol 52 (15) ◽  
pp. 4730-4736 ◽  
Author(s):  
Hiba A. Bawadi ◽  
Tania Maria Antunes ◽  
Fred Shih ◽  
Jack N. Losso
Keyword(s):  
Matrix Metalloproteinase ◽  
Matrix Metalloproteinase 9 ◽  
Matrix Metalloproteinase 1 ◽  
In Vitro Inhibition ◽  
Metalloproteinase 9

Interferon β-1b decreases the migration of T lymphocytes in vitro: Effects on matrix metalloproteinase-9

1996 ◽  
Vol 40 (6) ◽  
pp. 853-863 ◽  
Author(s):  
Olaf Stüve ◽  
Nora P. Dooley ◽  
Joon H. Uhm ◽  
Jack P. Antel ◽  
Gordon S. Francis ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Matrix Metalloproteinase ◽  
Matrix Metalloproteinase 9 ◽  
Interferon Β ◽  
In Vitro Effects ◽  
Metalloproteinase 9

Matrix Metalloproteinase-9 and Tissue Inhibitors of Matrix Metalloproteinase-1 in Plasma of Patients Co-Infected with HCV and HIV

2002 ◽  
Vol 3 (4) ◽  
pp. 310-315 ◽  
Author(s):  
Mastroianni Claudio M. ◽  
Liuzzi Grazia M. ◽  
d’Ettorre, Gabriella ◽  
Lichtner Miriam ◽  
Forcina Gabriele ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Matrix Metalloproteinase 9 ◽  
Tissue Inhibitors ◽  
Matrix Metalloproteinase 1 ◽  
Metalloproteinase 9

scholarly journals Hydrogen sulfide deficiency and diabetic renal remodeling: role of matrix metalloproteinase-9

2013 ◽  
Vol 304 (12) ◽  
pp. E1365-E1378 ◽  
Author(s):  
Sourav Kundu ◽  
Sathnur B. Pushpakumar ◽  
Aaron Tyagi ◽  
Denise Coley ◽  
Utpal Sen
Keyword(s):  
Hydrogen Sulfide ◽  
Matrix Metalloproteinase ◽  
Therapeutic Potential ◽  
Matrix Metalloproteinase 9 ◽  
Double Knockout ◽  
Diabetic Kidney ◽  
Connexin 40 ◽  
Akita Mice ◽  
Metalloproteinase 9

Matrix metalloproteinase-9 (MMP-9) causes adverse remodeling, whereas hydrogen sulfide (H2S) rescues organs in vascular diseases. The involvement of MMP-9 and H2S in diabetic renovascular remodeling is, however, not well characterized. We determined whether MMP-9 regulates H2S generation and whether H2S modulates connexin through N-methyl-d-aspartate receptor (NMDA-R)-mediated pathway in the diabetic kidney. Wild-type (WT, C57BL/6J), diabetic (Akita, C57BL/6J- Ins2 Akita), MMP-9−/− (M9KO), double knockout (DKO) of Akita/MMP-9−/− mice and in vitro cell culture were used in our study. Hyperglycemic Akita mice exhibited increased level of MMP-9 and decreased production of H2S. H2S-synthesizing enzymes cystathionine-β-synthase and cystathionine-γ-lyase were also diminished. In addition, increased expressions of NMDA-R1 and connexin-40 and -43 were observed in diabetic kidney. As expected, MMP-9 mRNA was not detected in M9KO kidneys. However, very thin protein expression and activity were detected. No other changes were noticed in M9KO kidney. In DKO mice, all the above molecules showed a trend toward baseline despite hyperglycemia. In vitro, glomerular endothelial cells treated with high glucose showed induction of MMP-9, attenuated H2S production, NMDA-R1 induction, and dysregulated conexin-40 and -43 expressions. Silencing MMP-9 by siRNA or inhibition of NMDA-R1 by MK801 or H2S treatment preserved connexin-40 and -43. We conclude that in diabetic renovascular remodeling MMP-9 plays a major role and that H2S has therapeutic potential to prevent adverse diabetic renal remodeling.

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