Ignet

Gene Information

Gene symbol: MMP12

Gene name: matrix metallopeptidase 12 (macrophage elastase)

HGNC ID: 7158

Synonyms: HME

Related Genes

#	Gene Symbol	Number of hits
1	AMMECR1	1 hits
2	CCL2	1 hits
3	CCR2	1 hits
4	IL12A	1 hits
5	IL6	1 hits
6	MMP10	1 hits
7	MMP9	1 hits
8	NOS2A	1 hits
9	PTK2	1 hits

Related Sentences

#	PMID	Sentence
1	16816359	Role for macrophage metalloelastase in glomerular basement membrane damage associated with alport syndrome.
2	16816359	Alport syndrome is a glomerular basement membrane (GBM) disease caused by mutations in type IV collagen genes.
3	16816359	Here we show that macrophage metalloelastase (MMP-12) expression is >40-fold induced in glomeruli from Alport mice and is markedly induced in glomeruli of both humans and dogs with Alport syndrome.
4	16816359	We show that inhibition of CC chemokine receptor 2 (CCR2) receptor signaling with propagermanium blocks induction of MMP-12 mRNA and prevents GBM damage.
5	16816359	CCR2 receptor is expressed in glomerular podocytes of Alport mice, suggesting MCP-1 activation of CCR2 on podocytes may underlie induction of MMP-12.
6	16816359	These data indicate that the irregular GBM that characterizes Alport syndrome may be mediated, in part, by focal degradation of the GBM due to MMP dysregulation, in particular, MMP-12.
7	16816359	Thus, MMP-12/CCR2 inhibitors may provide a novel and effective therapeutic stra-tegy for Alport glomerular disease.
8	16816359	Role for macrophage metalloelastase in glomerular basement membrane damage associated with alport syndrome.
9	16816359	Alport syndrome is a glomerular basement membrane (GBM) disease caused by mutations in type IV collagen genes.
10	16816359	Here we show that macrophage metalloelastase (MMP-12) expression is >40-fold induced in glomeruli from Alport mice and is markedly induced in glomeruli of both humans and dogs with Alport syndrome.
11	16816359	We show that inhibition of CC chemokine receptor 2 (CCR2) receptor signaling with propagermanium blocks induction of MMP-12 mRNA and prevents GBM damage.
12	16816359	CCR2 receptor is expressed in glomerular podocytes of Alport mice, suggesting MCP-1 activation of CCR2 on podocytes may underlie induction of MMP-12.
13	16816359	These data indicate that the irregular GBM that characterizes Alport syndrome may be mediated, in part, by focal degradation of the GBM due to MMP dysregulation, in particular, MMP-12.
14	16816359	Thus, MMP-12/CCR2 inhibitors may provide a novel and effective therapeutic stra-tegy for Alport glomerular disease.
15	16816359	Role for macrophage metalloelastase in glomerular basement membrane damage associated with alport syndrome.
16	16816359	Alport syndrome is a glomerular basement membrane (GBM) disease caused by mutations in type IV collagen genes.
17	16816359	Here we show that macrophage metalloelastase (MMP-12) expression is >40-fold induced in glomeruli from Alport mice and is markedly induced in glomeruli of both humans and dogs with Alport syndrome.
18	16816359	We show that inhibition of CC chemokine receptor 2 (CCR2) receptor signaling with propagermanium blocks induction of MMP-12 mRNA and prevents GBM damage.
19	16816359	CCR2 receptor is expressed in glomerular podocytes of Alport mice, suggesting MCP-1 activation of CCR2 on podocytes may underlie induction of MMP-12.
20	16816359	These data indicate that the irregular GBM that characterizes Alport syndrome may be mediated, in part, by focal degradation of the GBM due to MMP dysregulation, in particular, MMP-12.
21	16816359	Thus, MMP-12/CCR2 inhibitors may provide a novel and effective therapeutic stra-tegy for Alport glomerular disease.
22	16816359	Role for macrophage metalloelastase in glomerular basement membrane damage associated with alport syndrome.
23	16816359	Alport syndrome is a glomerular basement membrane (GBM) disease caused by mutations in type IV collagen genes.
24	16816359	Here we show that macrophage metalloelastase (MMP-12) expression is >40-fold induced in glomeruli from Alport mice and is markedly induced in glomeruli of both humans and dogs with Alport syndrome.
25	16816359	We show that inhibition of CC chemokine receptor 2 (CCR2) receptor signaling with propagermanium blocks induction of MMP-12 mRNA and prevents GBM damage.
26	16816359	CCR2 receptor is expressed in glomerular podocytes of Alport mice, suggesting MCP-1 activation of CCR2 on podocytes may underlie induction of MMP-12.
27	16816359	These data indicate that the irregular GBM that characterizes Alport syndrome may be mediated, in part, by focal degradation of the GBM due to MMP dysregulation, in particular, MMP-12.
28	16816359	Thus, MMP-12/CCR2 inhibitors may provide a novel and effective therapeutic stra-tegy for Alport glomerular disease.
29	16816359	Role for macrophage metalloelastase in glomerular basement membrane damage associated with alport syndrome.
30	16816359	Alport syndrome is a glomerular basement membrane (GBM) disease caused by mutations in type IV collagen genes.
31	16816359	Here we show that macrophage metalloelastase (MMP-12) expression is >40-fold induced in glomeruli from Alport mice and is markedly induced in glomeruli of both humans and dogs with Alport syndrome.
32	16816359	We show that inhibition of CC chemokine receptor 2 (CCR2) receptor signaling with propagermanium blocks induction of MMP-12 mRNA and prevents GBM damage.
33	16816359	CCR2 receptor is expressed in glomerular podocytes of Alport mice, suggesting MCP-1 activation of CCR2 on podocytes may underlie induction of MMP-12.
34	16816359	These data indicate that the irregular GBM that characterizes Alport syndrome may be mediated, in part, by focal degradation of the GBM due to MMP dysregulation, in particular, MMP-12.
35	16816359	Thus, MMP-12/CCR2 inhibitors may provide a novel and effective therapeutic stra-tegy for Alport glomerular disease.
36	16816359	Role for macrophage metalloelastase in glomerular basement membrane damage associated with alport syndrome.
37	16816359	Alport syndrome is a glomerular basement membrane (GBM) disease caused by mutations in type IV collagen genes.
38	16816359	Here we show that macrophage metalloelastase (MMP-12) expression is >40-fold induced in glomeruli from Alport mice and is markedly induced in glomeruli of both humans and dogs with Alport syndrome.
39	16816359	We show that inhibition of CC chemokine receptor 2 (CCR2) receptor signaling with propagermanium blocks induction of MMP-12 mRNA and prevents GBM damage.
40	16816359	CCR2 receptor is expressed in glomerular podocytes of Alport mice, suggesting MCP-1 activation of CCR2 on podocytes may underlie induction of MMP-12.
41	16816359	These data indicate that the irregular GBM that characterizes Alport syndrome may be mediated, in part, by focal degradation of the GBM due to MMP dysregulation, in particular, MMP-12.
42	16816359	Thus, MMP-12/CCR2 inhibitors may provide a novel and effective therapeutic stra-tegy for Alport glomerular disease.
43	19346698	To clarify the mechanism of renal fibrosis, we investigated the expression and localization of macrophage metalloelastase (MMP-12), whose functions in kidney diseases are not fully understood, and its regulatory molecules, monocyte chemoattractive protein-1 (MCP-1) and CC chemokine receptor 2 (CCR2), in the kidneys of ICGN mice by RT-PCR, Western blotting and immunohistochemical staining, respectively.
44	19346698	Furthermore, MCP-1 and CCR2 were also increased in podocytes of the ICGN strain.
45	21519331	This study examined whether inhibition of the receptor for macrophage colony-stimulating factor (known as c-fms), which is selectively expressed by monocyte/macrophages, can eliminate the macrophage infiltrate in a rat model of crescentic anti-GBM glomerulonephritis.
46	21519331	In addition, fms-I treatment downregulated the glomerular expression of pro-inflammatory molecules (TNF-α, NOS2, MMP-12, CCL2 and IL-12) on days 1 and 5, suggesting a suppression of the macrophage M1-type response.
47	24700867	Suppression of kidney leukocyte accumulation in MyMRKO mice correlated with reductions in gene expression of proinflammatory molecules (TNF-α, inducible nitric oxide synthase, chemokine (C-C motif) ligand 2, matrix metalloproteinase-12), tubular damage, and renal fibrosis and was similar in EPL-treated mice.
48	24915008	Analysis of glomerular mRNA from both models demonstrates significant induction of MMP-9, MMP-10, MMP-12, MMPs linked to GBM destruction in Alport disease models, as well as the pro-inflammatory cytokine IL-6.
49	24915008	SiRNA knockdown of FAK in cultured podocytes significantly reduced expression of MMP-9, MMP-10 and IL-6, but not MMP-12.
50	24915008	Glomerular expression of MMP-9, MMP-10 and MMP-12 mRNAs was significantly reduced in TAE226 treated animals.
51	24915008	Analysis of glomerular mRNA from both models demonstrates significant induction of MMP-9, MMP-10, MMP-12, MMPs linked to GBM destruction in Alport disease models, as well as the pro-inflammatory cytokine IL-6.
52	24915008	SiRNA knockdown of FAK in cultured podocytes significantly reduced expression of MMP-9, MMP-10 and IL-6, but not MMP-12.
53	24915008	Glomerular expression of MMP-9, MMP-10 and MMP-12 mRNAs was significantly reduced in TAE226 treated animals.
54	24915008	Analysis of glomerular mRNA from both models demonstrates significant induction of MMP-9, MMP-10, MMP-12, MMPs linked to GBM destruction in Alport disease models, as well as the pro-inflammatory cytokine IL-6.
55	24915008	SiRNA knockdown of FAK in cultured podocytes significantly reduced expression of MMP-9, MMP-10 and IL-6, but not MMP-12.
56	24915008	Glomerular expression of MMP-9, MMP-10 and MMP-12 mRNAs was significantly reduced in TAE226 treated animals.