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1 tissue growth factor and tissue inhibitor of matrix metalloproteinase 1.
2 , which is resistant to degradation by human matrix metalloproteinase 1.
3 cell migration through the up-regulation of matrix metalloproteinase 1.
4 n-6, monocyte chemoattractant protein 1, and matrix metalloproteinase 1.
5 that obtained via direct immunodepletion of matrix metalloproteinase-1.
6 ), cyclooxygenase-2, and tissue inhibitor of matrix metalloproteinase-1.
7 lammation-responsive genes including SAA and matrix metalloproteinase-1.
8 nd interleukin-8 and the remodeling mediator matrix metalloproteinase-1.
9 f extracellular matrix-modifying enzymes and matrix metalloproteinase-1.
10 was further characterized by upregulation of matrix metalloproteinases 1, 10, and 13, cathepsin L2, c
12 raised reactive oxygen species production or matrix metalloproteinase-1, -2 and -9 activity nor decre
13 sion across an ECM layer was quantitated and matrix metalloproteinase-1, -2, -3, -9, and -11 gene and
14 chemoattractant protein-1, cyclooxygenase-2, matrix metalloproteinases-1, -2, and -3 (MMP-1, -2, and
17 ecan mRNA levels and increased the levels of matrix metalloproteinases 1, 3, and 13 mRNA, as well as
18 dorferi infection revealed colocalization of matrix metalloproteinase-1, a degradative enzyme that de
19 al encoding angiogenic regulators, including matrix metalloproteinase-1, an interstitial collagenase,
20 in basic calcium phosphate crystal-mediated matrix metalloproteinase 1 and 3 expression in human fib
21 with elevated levels of tissue inhibitor of matrix metalloproteinase 1 and elastin in the infarct (P
22 se, in both groups there was upregulation of matrix metalloproteinase 1 and laminin 5 in the tumors.
24 280-320 nm) causes these changes by inducing matrix metalloproteinase 1 and suppressing type I collag
26 helin-1 inhibited both protein expression of matrix metalloproteinase 1 and zymographic activity excl
28 ed a peptide with micromolar K(i) values for matrix metalloproteinase-1 and -9 that are selective inh
29 gle treatment, as shown by lower IL-6, IL-8, matrix metalloproteinase-1 and matrix metalloproteinase-
31 emonstrated the presence of higher levels of matrix metalloproteinase-1 and SAF-1 in the inflamed joi
33 xpression of extracellular matrix-remodeling matrix metalloproteinases 1 and 10 (MMP1 and MMP10), sug
34 kin 1 to reduce production of collagenolytic matrix metalloproteinases 1 and 13 in tenosynovial tissu
35 ation of antimetastatic tissue inhibitors of matrix metalloproteinases 1 and 2 and plasminogen activa
36 epiregulin, the cyclooxygenase COX2, and the matrix metalloproteinases 1 and 2, when expressed in hum
37 ion, relaxin decreases endometrial levels of matrix metalloproteinases 1 and 3 and increases levels o
38 cellular matrix remodeling, and they include matrix metalloproteinases 1 and 3, IL-8, human beta-defe
39 f a number of chondrocyte proteins including matrix metalloproteinases 1 and 3, tissue inhibitor of m
41 ange in C-reactive protein (CRP) degraded by matrix metalloproteinases 1 and 8 (CRPM) from baseline t
42 n of inducible nitric oxide synthase (iNOS), matrix metalloproteinases 1 and 8 (MMP-1 and -8), bone m
43 ects were also associated with a decrease of matrix metalloproteinases 1 and 8, inducible nitric oxid
44 ors alpha and beta, and tissue inhibitors of matrix metalloproteinases-1 and -2, increased by 4 weeks
49 inases 7, 9, 10, and 12, tissue inhibitor of matrix metalloproteinase 1, and secreted protein acidic
50 mural and luminal flow induced expression of matrix metalloproteinase 1, and this up-regulation was r
51 vated levels of the matrix degrading protein matrix metalloproteinase-1, and a promigratory phenotype
52 protein A8, IL-6, IL-8, and tissue inhibitor matrix metalloproteinase-1 are up-regulated by these NOS
53 nd its inhibitor TIMP-1 (tissue inhibitor of matrix metalloproteinase 1) are regulated in a manner th
54 cells depend on up-regulation of Drosophila matrix metalloproteinase-1 as assessed by promoter activ
56 tril/valsartan decreased tissue inhibitor of matrix metalloproteinase 1 by 8% (95% confidence interva
58 indicate that the mechanism of repression of matrix metalloproteinase-1 by p21SNFT may be exploited i
60 decreases the expression of the collagenase, matrix metalloproteinase 1, by IL-34-Mphi and M-CSF-Mphi
61 e of collagen I and III, tissue inhibitor of matrix metalloproteinase 1, carboxyl-terminal telopeptid
63 al telopeptide of collagen type I (CITP) and matrix metalloproteinase-1 (CITP:MMP-1) was determined i
64 e designed to include cell-adhesion ligands, matrix metalloproteinase-1 cleavage sites, and full-leng
66 e plasminogen activator, tissue inhibitor of matrix metalloproteinase-1, cyclooxygenase-2, and VEGF r
67 or collagens, laminins, decorin, E-cadherin, matrix metalloproteinase-1, endorepellin, and several vi
68 ed with increased neutrophil recruitment and matrix metalloproteinase-1 expression, both involved in
69 GBP1 was required for EGFR-mediated MMP1 (matrix metalloproteinase 1) expression and glioma cell i
70 SLFN5 negatively controls expression of the matrix metalloproteinase 1 gene (MMP-1), MMP-13, and sev
71 dose UV-A1 irradiation significantly induced matrix metalloproteinase 1 gene expression, which increa
73 mulatory effect of insulin on collagenase-1 (matrix metalloproteinase-1) gene transcription a series
75 growth factor receptor, estrogen signaling, matrix metalloproteinase-1, histone deacetylase, methylt
76 degeneration through the regulation of human matrix metalloproteinase-1 (hMMP-1, collagenase-1) gene
77 , IL-20, chemokine C-X-C motif ligand 8, and matrix metalloproteinase 1, IL-19 had no clear influence
78 ype 1 collagen genes and tissue inhibitor of matrix metalloproteinase 1 in both wild-type and egr-1(-
81 coprotein transporter protein gene and MMP1 (Matrix Metalloproteinase 1), indicative of the invasive
82 a occludens-1, laminin), tissue inhibitor of matrix metalloproteinase-1, inflammation (interleukin-1b
83 of type I collagen were exposed in vitro to matrix metalloproteinase-1 (interstitial collagenase), a
85 rix metalloproteinase-2, tissue inhibitor of matrix metalloproteinase 1, left atrial volume), myocard
86 le to regression mediated by factors such as matrix metalloproteinase-1, matrix metalloproteinase-10,
87 eutralizing reagents blocked hypoxia-induced matrix metalloproteinase-1, matrix metalloproteinase-9 e
88 in humans suggest that PTX3, P-selectin, and matrix metalloproteinase-1 may be novel biomarkers that
89 fibroblasts in response to stimulation were matrix metalloproteinase 1, MCP-1, IL-1beta, IL-6, IL-8,
92 a1 (TGFbeta1) resulted in down-regulation of matrix metalloproteinase 1 (MMP-1) and MMP-13 concomitan
93 or retinoid X receptor, on the expression of matrix metalloproteinase 1 (MMP-1) and MMP-13 induced by
95 infection and elevated expression of tissue matrix metalloproteinase 1 (MMP-1) are both associated w
101 inase Calpha (PKCalpha) and the induction of matrix metalloproteinase 1 (MMP-1) through extracellular
103 duction of mRNA for CXCL8/IL-8, CCL5/RANTES, matrix metalloproteinase 1 (MMP-1), and MMP-3 after TNFa
106 or ligand superfamily member 13B (TNFSF13B), matrix metalloproteinase 1 (MMP-1), MMP-2, and MMP-3.
107 cytokine combination synergistically induced matrix metalloproteinase 1 (MMP-1), MMP-3, and MMP-13 mR
108 ative levels of mRNA for aggrecan, tenascin, matrix metalloproteinase 1 (MMP-1), MMP-3, and tissue in
110 ermal fibroblasts revealed overexpression of matrix metalloproteinase 1 (MMP-1), the gene encoding th
112 ulcerations of any form is the expression of matrix metalloproteinase 1 (MMP-1; collagenase-1) by lea
113 association occurred only in carriers of the matrix metalloproteinase-1 (MMP-1) 2G (rs1799750) or the
114 ric collagen I by both the human collagenase matrix metalloproteinase-1 (MMP-1) and collagenase from
115 ased the expression of MMP1, which codes for matrix metalloproteinase-1 (MMP-1) and is responsible fo
118 rin by type I collagen induces expression of matrix metalloproteinase-1 (MMP-1) and that MMP-1 activi
119 of endoglin in modulating Ang II effects on matrix metalloproteinase-1 (MMP-1) and type I collagen e
122 ainst interleukin-8 (IL-8) and inhibition of matrix metalloproteinase-1 (MMP-1) expression before and
124 terleukin-8 (IL-8) and for the inhibition of matrix metalloproteinase-1 (MMP-1) expression, an inflam
125 uent downstream transcriptional increases in matrix metalloproteinase-1 (MMP-1) expression, which wer
126 e that Met controls the transcription of the matrix metalloproteinase-1 (MMP-1) gene in carcinoma cel
127 reeclampsia involves increased expression of matrix metalloproteinase-1 (MMP-1) in endothelial cells,
133 cted to determine the following: (1) whether matrix metalloproteinase-1 (MMP-1) is increased in syste
136 amined the hypothesis that H. pylori induces matrix metalloproteinase-1 (MMP-1) secretion, with poten
137 hat smoke exposure leads to the induction of matrix metalloproteinase-1 (MMP-1) through the activatio
138 tokine release and the induction of mRNA for matrix metalloproteinase-1 (MMP-1) were also studied usi
140 ll forms of cutaneous wounds, collagenase-1 (matrix metalloproteinase-1 (MMP-1)) is invariably expres
141 roblasts, and the production of collagenase (matrix metalloproteinase-1 (MMP-1)), the major enzyme in
142 The expression of cyclooxygenase-2 (COX-2), matrix metalloproteinase-1 (MMP-1), and the production o
143 howing that it transcriptionally upregulates matrix metalloproteinase-1 (MMP-1), and using rescue app
144 or collagens, laminins, decorin, E-cadherin, matrix metalloproteinase-1 (MMP-1), endorepellin, and se
147 A levels of six senescence-associated genes, matrix metalloproteinase-1 (MMP-1), was decreased, while
148 ype I procollagen and concurrently increases matrix metalloproteinase-1 (MMP-1), which initiates fibr
149 e production of the interstitial collagenase matrix metalloproteinase-1 (MMP-1), which is expressed s
150 ary tube regression in these cocultures in a matrix metalloproteinase-1 (MMP-1)-, MMP-10-, and ADAM-1
155 ns retinoic acid (atRA) on the expression of matrix metalloproteinase-1 (MMP-1, interstitial collagen
156 ture and human skin organ culture, levels of matrix metalloproteinase-1 (MMP-1; interstitial collagen
157 .000), IL-8/CXCL8 (P=0.006), IL-6 (P=0.002), matrix metalloproteinase-1 (MMP-1; P=0.002), and MMP-3 (
158 press increased levels of collagen-degrading matrix metalloproteinases-1 (MMP-1) in aged (>80 years o
159 Gene expression and protein production of matrix metalloproteinases-1 (MMP-1), -2, -3, -13, and -1
160 loid protein A [SAA]), inflammatory markers (matrix metalloproteinase 1 [MMP-1] and heme oxygenase 1
162 a induced significant levels of collagenase (matrix metalloproteinase 1 [MMP-1]) within 4 hours, and
165 e upregulated genes (lactotransferrin [LTF], matrix metalloproteinase-1 [MMP-1], MMP-3, interferon in
166 e accumulation and interstitial collagenase (matrix metalloproteinase-1, MMP-1) expression in the les
167 and degradation by interstitial collagenase (matrix metalloproteinase-1, MMP-1) may determine whether
168 of SphK1 in the regulation of expression of matrix metalloproteinase 1 (MMP1) in dermal fibroblasts,
169 sed by preincubating HCECs with capsazepine, matrix metalloproteinase 1 (MMP1) inhibitor TIMP-1, broa
171 hermore, inhibition of Akt upregulated basal matrix metalloproteinase 1 (MMP1) production and reverse
173 essential for controlling the expression of matrix metalloproteinase 1 (Mmp1), a major regulator of
176 r matrix (ECM) organization-related enzymes (matrix metalloproteinase-1 (MMP1) and metalloproteinase
177 nase (JNK)/AP-1 signaling, and expression of matrix metalloproteinase-1 (Mmp1) are activated downstre
178 ), augmenter of liver regeneration (alr) and Matrix metalloproteinase-1 (Mmp1) expressed specifically
181 actor-alpha (TNF), interleukin-1beta (IL1B), matrix metalloproteinase-1 (MMP1), MMP-2, MMP-9, tissue
182 ase with thrombospondin motifs (ADAMTS1) and matrix metalloproteinase-1 (MMP1), orchestrate a paracri
183 ry dermal fibroblast cultures confirmed that matrix metalloproteinase 1 mRNA, MMP1, increased with ag
184 ry dermal fibroblast cultures confirmed that matrix metalloproteinase 1 mRNA, MMP1, increased with ag
185 lpha caused a rapid synergistic induction of matrix metalloproteinase 1 mRNA, which was sustained ove
189 tion by binding to activated membrane type 1-matrix metalloproteinase 1 (MT1-MMP) on the plasma membr
192 ion darkened skin slightly and did not alter matrix metalloproteinase 1 or type I procollagen gene ex
197 ession and suppress transcription of a human matrix metalloproteinase 1 promoter reporter construct i
200 eceptor mRNA expression also correlated with matrix metalloproteinase-1 promoter region, tissue inhib
202 y-terminal telopeptide of collagen type-I to matrix metalloproteinase-1 ratio) and with excessive myo
203 ry products (ie, matrix metalloproteinase 12/matrix metalloproteinase 1/S100A9) were upregulated in b
204 collagen deposition and tissue inhibitor of matrix metalloproteinase-1 secretion induced by hepatic
206 els of PTX3 and its mediators P-selectin and matrix metalloproteinase-1 than normotensive subjects (n
207 f type III collagen, and tissue inhibitor of matrix metalloproteinase 1 that was subsequently evaluat
208 F-kappaB, promote induction of membrane-type matrix metalloproteinase-1 that then activates pro-MMP-2
209 ammation-responsive genes, including SAA and matrix metalloproteinase-1, that are implicated in the p
210 tion, the maintenance of tissue inhibitor of matrix metalloproteinase-1, the consequent preservation
211 d selective induction of tissue inhibitor of matrix metalloproteinase-1; this extracellular matrix re
212 -1 (MMP1), MMP-2, MMP-9, tissue inhibitor of matrix metalloproteinase 1 (TIMP-1), TIMP-2, and hypoxan
213 or are increased whereas tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) expression in the ir
215 SNX, and the effects of tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) neutralization on th
216 or-alpha (TNF-alpha) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) while up-regulating
218 hage markers arginase-1, tissue inhibitor of matrix metalloproteinase-1 (TIMP-1), and macrophage gala
219 mRNAs as well as that of tissue inhibitor of matrix metalloproteinases 1 (TIMP-1) compared to subleth
221 nic role of the cytokine tissue inhibitor of matrix metalloproteinases 1 (TIMP1) in primary pancreati
222 (Col1a2) promoter, but in contrast to reduce matrix metalloproteinase 1 transcript expression and sup
223 ndothelial growth factor, interleukin-1beta, matrix metalloproteinase-1, versican, and fibronectin.
224 cid synthase 2 was highly expressed, whereas matrix metalloproteinase 1 was elevated in the dermal pa
226 proteinases-1 and -9 and tissue inhibitor of matrix metalloproteinase-1 were strongly upregulated by
227 irradiation also induced tissue inhibitor of matrix metalloproteinases-1, which regulates the enzyme.
228 uding serum amyloid A, gamma-fibrinogen, and matrix metalloproteinase 1, whose abnormal expression is
229 increased expression of tissue inhibitor of matrix metalloproteinase-1 with decreased activity of ma