Ignet

Gene Information

Gene symbol: MMP9

Gene name: matrix metallopeptidase 9 (gelatinase B, 92kDa gelatinase, 92kDa type IV collagenase)

HGNC ID: 7176

Related Genes

#	Gene Symbol	Number of hits
1	AIM2	1 hits
2	CASP1	1 hits
3	CDKN2A	1 hits
4	CXCL6	1 hits
5	CYP2E1	1 hits
6	HMGB1	1 hits
7	IFNA1	1 hits
8	IFNG	1 hits
9	IL1A	1 hits
10	IL1B	1 hits
11	IL6	1 hits
12	ITGA2	1 hits
13	LCN2	1 hits
14	MKI67	1 hits
15	MMP1	1 hits
16	NFKB1	1 hits
17	NLRP3	1 hits
18	NOD1	1 hits
19	NOD2	1 hits
20	STAT1	1 hits
21	STMN2	1 hits
22	TNF	1 hits
23	VEGFA	1 hits

Related Sentences

#	PMID	Sentence
1	27806943	Incubation of the chorioamniotic membranes with HMGB1 1) induced the release of mature IL-1beta and IL-6; 2) upregulated the mRNA expression of the pro-inflammatory mediators NFKB1, IL6, TNF, IL1A, IFNG, and HMGB1 receptors RAGE and TLR2; 3) upregulated the mRNA expression of the inflammasome components NLRP3 and AIM2 as well as NOD proteins (NOD1 and NOD2); 4) increased the protein concentrations of NLRP3 and NOD2; 5) increased the concentration of caspase-1 and the quantity of its active form (p20); and 6) upregulated the mRNA expression and active form of MMP-9.
2	25924700	To test the hypothesis that MMP expression in luteal cells is regulated by luteolytic factors, we investigated the effects of prostaglandin F2α (PGF), interferon γ (IFNG) and tumor necrosis factor α (TNF) on the mRNA expression of MMPs and TIMPs in cultured luteal cells.
3	25924700	Luteal cells obtained from the CL at the mid-luteal stage (days 8-12 after ovulation) were cultured with PGF (0.01, 0.1, 1 μM), IFNG (0.05, 0.5, 5 nM) and TNF (0.05, 0.5, 0.5 nM) alone or in combination for 24 h.
4	25924700	PGF and IFNG significantly increased the expression of MMP-1 mRNA.
5	25924700	In addition, 1 μM PGF in combination with 5 nM IFNG stimulated MMP-1 and MMP-9 mRNA expression significantly more than either treatment alone.
6	25924700	In contrast, IFNG significantly decreased the level of MMP-14 mRNA.
7	25924700	The mRNA expression of TIMP-1, which preferentially inhibits MMP-1, was suppressed by 5 nM INFG.
8	25924700	One μM PGF and 5 nM IFNG suppressed TIMP-2 mRNA expression.
9	25924700	These results suggest a new role of MMPs: luteal MMPs stimulated by PGF and IFNG break down the extracellular matrix surrounding luteal cells, which accelerates detachment from the CL during luteolysis, providing an essential prerequisite for outflow of luteal cells from the CL to lymphatic vessels.
10	24808182	Myelin oligodendrocyte glycoprotein-specific T cells in culture exhibited an increased expression of Il17a, Ifng, Rorc, and Tbet after treatment with recombinant LCN2 protein.
11	24808182	Moreover, LCN2-treated glial cells expressed higher levels of proinflammatory cytokines, chemokines, and MMP-9.
12	21646723	Absence of IFN-γ accelerates thrombus resolution through enhanced MMP-9 and VEGF expression in mice.
13	21646723	Absence of IFN-γ accelerates thrombus resolution through enhanced MMP-9 and VEGF expression in mice.
14	21646723	Activation of the IFN-γ/Stat1 signal pathway suppressed PMA-induced Mmp9 and Vegf gene expression in peritoneal macrophages.
15	21646723	Activation of the IFN-γ/Stat1 signal pathway suppressed PMA-induced Mmp9 and Vegf gene expression in peritoneal macrophages.
16	15661146	The most noteworthy changes in gene expression mainly affected the transcriptional network regulated by interferons (IFNs), including both IFN-alpha/beta-inducible genes (STAT1, STAT2, ISGF3G/IRF9, IFI27, G1P3, G1P2, OAS2, MX1) and IFN-gamma-inducible genes (CXCL9, CXCL10, CXCL11).
17	15661146	Interesting, upregulation of IFN-alpha/beta-inducible genes (but not IFN-gamma-inducible genes) was independent of histological scores (grade and stage of fibrosis) and HCV characteristics (hepatic HCV mRNA levels and the HCV genotype), and was specific to HCV (as compared to hepatitis B virus (HBV)).
18	15661146	Other genes dysregulated in F1-CH-C, albeit less markedly than IFN-alpha/beta- and IFN-gamma-inducible genes, were mainly involved in the activation of lymphocytes infiltrating the liver (IFNG, TNF, CXCL6, IL6, CCL8, CXCR3, CXCR4, CCR2), cell proliferation (p16/CDKN2A, MKI67, p14/ARF), extracellular matrix remodeling (MMP9, ITGA2), lymphangiogenesis (XLKD1/LYVE), oxidative stress (CYP2E1), and cytoskeleton microtubule organization (STMN2/SCG10).