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activation of toll-like receptors TLR2, TLR3 or TLR5 increased the expression of MMP-1. MMP-1 and MMP-9 in human epidermal keratinocytes are induced by Pam3CSK4, Poly(I:C) and flagellin, which are ligands for TLR2, TLR3 and TLR5, respectively, overview. The induction of MMP-1 by the receptor ligands is inhibited by pretreatment with BAY11-7082, a NF-kappaB inhibitor, or SP600125, a JNK inhibitor. p38 MAPK activation negatively regulates MMP-1 induction by TLR2 or TLR5 activation, but not by TLR3 activation
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bortezomib specifically increases the steady-state mRNA levels of MMP-1 and enhances the binding of c-Jun to the promoter of MMP-1. Disruption of the proximal AP-1-binding site in the promoter of MMP-1 severely impairs MMP-1 transcription in response to bortezomib. By altering the binding of at least two transcription factors, c-Jun and SP1, proteasome inhibition results in increased production of MMP-1 and decreases synthesis of type I collagen in human dermal fibroblasts
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both the MMP-1 and TIMP-1 mRNA expression level are dramatically downregulated by baicalin
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curcumin at the concentration of 2.5-5 mg/ml specifically downregulates MMP-1 mRNA in BT-483 and MDA-MB-231 breast cancer cell lines. Cell growth and proliferation is inhibited in presence of curcumin, overview
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curcumin, a potent inhibitor for AP-1, or simvastatin inhibit the expression of MMP-1. Suppression of c-Jun expression by RNA interference significantly inhibits MMP-1 expression
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dexamethasone suppression of MMP-1 gene expression
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dexamethasone, and less potent also interleukin-1Ra and TNF, decrease levels of pro-MMP-1
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enhanced collagen degradation, in case of epithelial-to-mesenchymal transition stimulated by transforming growth factor-beta as well as epidermal growth factor receptor, is coupled to a significant increase in matrix metalloproteinase MMP-1 expression and is involved a proteolytic axis composed of plasmin, MMP-10, ec 3.4.24.22, and MMP-1
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expression of MMP-1 in cartilages and synovial tissues is suppressed by the treatment of curcumin and indomethacin. Production of MMP-1 is inhibited by curcumin in tumor necrosis factor-alpha-stimulated rheumatoid arthritis fibroblast-like synoviocytes and chondrocytes in a dose-dependent manner putatively through the inhibition of PKCdelta and the JNK/c-Jun signaling pathway, overview
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expression of MMP-1 is markedly increased by both onion extract and quercetin in vitro in human skin fibroblasts
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expression of MMP-1 is markedly increased by both onion extract and quercetin in vivo in hairless mice
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fucoidan treatment significantly inhibits the expression of MMP-1
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hypoxia and specifically HIF-1a increase CXCR4, its ligand SDF1, and MMP1 expressions in JJ cell line and chondrosarcoma invasion in vitro, which can be inhibited by siRNA directed at HIF-1a or CXCR4, the CXCR4 inhibitor AMD3100, as well as with ERK inhibitor U0126 and ERK siRNA. Hypoxia increases MMP1 mRNA expression 9fold which is further increased to 23fold by SDF1 stimulation
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ibuprofen upregulates expressions of matrix metalloproteinase-1, as well as MMP-8, MMP-9, and MMP-13, without affecting expressions of types I and III collagen in tendon cells
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increased MMP1 expression in JJ cell line can be inhibited by siRNA directed at HIF-1a or CXCR4, the CXCR4 inhibitor AMD3100, as well as with ERK inhibitor U0126 and ERK siRNA
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induction of MMP-1 by UV-A irradiation treatment of cultured human dermal fibroblasts
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inhibition of MMP-1 expression by extracts of Kaempferia pandurata, overview
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inhibititory effects of potent antioxidant astaxanthin on the MMP-1 induction by UV-A irradiation, overview
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interleukin-6, high glucose, and lipopolysaccharide act in concert and synergistically upregulate MMP-1 expression by U-937 mononuclear phagocytes via ERK1/2 and JNK pathways and c-Jun, mechanism, overview. c-Jun is a key subunit of AP-1 known to be essential for MMP-1 transcription
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lithium specifically induces a rapid and pronounced up-regulation of MMP-1 at the mRNA and protein levels, whereas the induction of two the other senescent cell markers plasminogen activator inhibitor-1 and interleukin-8 is either delayed or weak, respectively. Lithium affects MMP-1 expression mainly at the transcriptional level but neither the AP1/Ets regulatory sites nor the redox sensitive -1607/2G site in MMP-1 promoter are involved in lithium-dependent MMP-1 regulation
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matrix metalloproteinase-1 expression is induced by interleukin-1beta requiring acid sphingomyelinase, overview
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methotrexate (MTX) increases the expression of MMP-1 in primary human neonatal, adult, and hypertrophic scar fibroblasts by 1.5fold 72 h after treatment with 50-500 ng/ml MTX
MMP-1 expression and secretion is induced by infection with Mycobacterium tuberculosis by 57.8%, the specific inhibitor TIMP-1 expression is also induced by 243.7%. The MMP-1 induction is specifically inhibited by 4-aminosalicyclic acid via inhibiting a p38 MAPK-prostaglandin signaling cascade, overview
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MMP-1 expression is induced by UV-B irradiation, the induction is inhibited by extracts of Kaempferia pandurata, as are phosphorylation of MAP kinases ERK, JNK, and p38, overview
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MMP-1 is 4.1fold induced by infection with Mycobacterium tuberculosis. Conditioned medium from Mycobacterium tuberculosis-infected human monocytes stimulates greater MMP-1 gene expression in human microglial cells than direct infection, overview. The induction is suppressed by dexamethasone. TNF-alpha and interleukin-1beta are necessary but not sufficient for upregulating MMP-1 secretion. NF-kappaB and AP-1 c-Jun/FosB heterodimers regulate induction of MMP-1 secretion by conditioned medium from Mycobacterium tuberculosis and are upregulated in granulomas from patients with cerebral tuberculosis. CoMTb upregulates MMP-1 gene expression and secretion in microglia
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MMP-1 is downregulated 4fold during trophoblast differentiation, reduced MMP-1 expression in pre-eclampsia and fetal growth restriction
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MMP-1 is induced in gingival fibroblasts in response to inflammatory cytokines, such as TNF and interleukin-1. TNF treatment of human gingival fibroblasts significantly induces the expression of MMP-1 severalfold, while enamel matrix derivative alone has no effect
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MMP-1 is upregulated after stroke in brain in the infarcted tissue compared to healthy control areas, overview
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phorbol 12-myristate 13-acetate and interleukin-1beta significantly stimulate the production of MMP-1 by periodontal ligament cells at both the transcriptional and the translational level
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production of MMP-1 is inhibited by curcumin in collagen-induced arthritis hind paw sections in a dose-dependent manner putatively through the inhibition of PKCdelta and the JNK/c-Jun signaling pathway, overview
Rac1 inhibitor NSC23766 suppresses MMP1 in dermal fibroblasts, and half-lives of type I collagen protein are increased
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recombinantly overexpressed RhoB enhances migration and MMP1 expression of prostate cancer DU145 cells, overview
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SB203580 and PD98059 suppress MMP-1 secretion
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TNF-alpha and IL-1beta stimulate production of MMPs through the activation of mitogen-activated protein kinases, NF-kappaB and AP-1
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UV-B irradiation induces MMP-1 expression and secretion. Inhibitory effects of Costaria costata fucoidan on UVB-induced MMP-1 promoter, mRNA, and protein expression in vitro by 41.8% at 10 ng/ml, 57.7% at 100 ng/ml, and 70% at 0.001 mg/ml compared to UV-B irradiation alone, overview
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UVA and UVB irradiation of dermal fibroblasts in vitro or human skin in vivo induces MMP-1 expression. MMP-1 expression and secretion induced by UV-B irradiation is inhibited by trans-zeatin, a cytokinin from Zea mays, and by PD98059, an ERK inhibitor, by SP600125, a JNK inhibitor and by SB203580, a p38 MAPK inhibitor. trans-Zeatin also inhibits UVB-induced ERK, JNK, p38 MAPK and c-Jun phosphorylation
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production of MMP-1 is inhibited by curcumin in collagen-induced arthritis hind paw sections in a dose-dependent manner putatively through the inhibition of PKCdelta and the JNK/c-Jun signaling pathway, overview
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production of MMP-1 is inhibited by curcumin in collagen-induced arthritis hind paw sections in a dose-dependent manner putatively through the inhibition of PKCdelta and the JNK/c-Jun signaling pathway, overview
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