MMP9
LOCUS ID4318
GENE_SYMBOLMMP9
GENE NAMEmatrix metallopeptidase 9 (gelatise B 92kDa gelatise 92kDa type IV collagese)
SYNONYMNSGELB, CLG4B, MMP-9, MANDP2
CHROMOSOME20
HOMOLOGENE ID3659
microRNAsNANA
GENE SUMMARY
Proteins of the matrix metalloproteise (MMP) family are involved in the breakdown of extracellular matrix in normal physiological processes such as embryonic development reproduction and tissue remodeling as well as in disease processes such as arthritis and metastasis. Most MMP's are secreted as ictive proproteins which are activated when cleaved by extracellular proteises. The enzyme encoded by this gene degrades type IV and V collagens. Studies in rhesus monkeys suggest that the enzyme is involved in IL-8-induced mobilization of hematopoietic progenitor cells from bone marrow and murine studies suggest a role in tumor-associated tissue remodeling. [provided by RefSeq Jul 2008]

OBSERVATIONS

Complication Evidence PMID
Nephropathy1. The CCL2, IL8, CCR5 and MMP9 polymorphisms were found to be associated with the risk of diabetic nephropathy. Frequency of CCL2 II, IL8 -251AA, CCR5 59029AA and MMP9 279Gln/Gln genotypes were significantly higher in DN than in DM group (p<0.05) and associated with an increased risk of nephropathy in both North and South Indian cohorts.19357773
Cardiovascular1. Although no serum or bone marrow inflammation was seen, HFS increased visceral fat, serum leptin and insulin at week 19 and induced further alterations in lipid profile, serum adiponectin, and TGFbeta1, TIMP1, MMP2, and MMP9, suggesting a prediabetic phenotype and cardiovascular dysfunction at week 27 more pronounced in M than G.26175082
Retinopathy1. Gelatise B may play an important role in extracellular matrix degradation associated with neovascularization in proliferative diabetic retinopathy 2. Donors with diabetic retinopathy had increased MMP9 activity in their retinal microvessels, the site of histopathology associated with diabetic retinopathy, and this was accompanied by activated H-Ras signaling pathway (Raf-1/ERK). Collectively, these suggest that RaRaf-1/MEK/ERK cascade has an important role in the activation of retinal MMP9 ing in the apoptosis of its capillary cells9.65E+14
Atherosclerosis1. In human carotid atherosclerotic plaques, TIMP3 was significantly reduced in subjects with type 2 diabetes, leading to ADAM17 and MMP9 overactivity. Reduced expression of TIMP3 was associated in vivo with SirT1 levels19581416