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1 flammation (C-reactive protein, soluble ST2, tissue inhibitor of metalloproteinase 1).
2 d in increased expression of MMP3, MMP8, and tissue inhibitor of metalloproteinase 1.
3 the expression of the antiangiogenic factor tissue inhibitor of metalloproteinase 1.
4 ic responses in HSCs, including secretion of tissue inhibitor of metalloproteinase-1.
5 l mRNA levels of aggrecan, collagen IIa, and tissue inhibitor of metalloproteinase-1.
6 with a concomitant decrease in expression of tissue inhibitor of metalloproteinase-1.
7 f 4) and truncation is completely blocked by tissue inhibitor of metalloproteinase-1.
8 MA was completely blocked by the addition of tissue inhibitor of metalloproteinases 1.
9 IL-6 and IL-6sR enhanced the expression of tissue inhibitor of metalloproteinases 1.
10 the expression of its natural inhibitor, the tissue inhibitor of metalloproteinases-1.
11 st up-regulated genes (e.g., caspase-3, p21, tissue inhibitor of metalloproteinases 1, 2, and 3, and
12 levels of mRNA encoding alpha1-antitrypsin, tissue inhibitor of metalloproteinase-1, -2, and -4, and
13 enic factors (eg, ANG [angiogenin], TIMP1/2 [tissue inhibitor of metalloproteinases 1/2], and RANTES
14 8 (IL-8), human beta-defensin 1 (hBD-1), and tissue inhibitor of metalloproteinase 1 and 2 (TIMP-1 an
15 tivator inhibitor-1 and aprotinin but not by tissue inhibitor of metalloproteinase-1 and -2, suggesti
16 ases, including MMP-13 but downregulation of tissue inhibitor of metalloproteinase-1 and -2, thus mag
17 -type plasminogen activator while increasing tissue inhibitor of metalloproteinase-1 and plasminogen
18 teinase-2 and -9 but was linked to decreased tissue inhibitor of metalloproteinase-1 and plasminogen
21 3 (IL-23), IL-1 receptor I (IL-1RI), IL-17R, tissue inhibitors of metalloproteinase 1 and 2 (TIMP-1 a
24 increased in TAA tissue homogenates, whereas tissue inhibitors of metalloproteinases 1 and 4 decrease
25 MP) inhibitors and their in vivo regulators, tissue inhibitors of metalloproteinases-1 and -2, abroga
26 owth factor receptor beta, desmin, vimentin, tissue inhibitor of metalloproteinase-1) and fibrosis (r
27 , including transforming growth factor beta, tissue inhibitor of metalloproteinase 1, and connective
29 and Lix/CXCL-5), matrix metalloproteinase-9, tissue inhibitor of metalloproteinase-1, and apoptosis r
30 s syndrome); and matrix metalloproteinase-3, tissue inhibitor of metalloproteinase-1, and CXCL13 in A
31 he other, with neutrophil elastase degrading tissue inhibitor of metalloproteinase-1, and macrophage
33 with gene expression for alpha2(I) collagen, tissue inhibitor of metalloproteinase-1, and transformin
34 n expression of MMP-1, collagen type 1alpha, tissue inhibitor of metalloproteinase-1, and vascular re
35 ulmonary and activation-regulated chemokine, tissue inhibitor of metalloproteinases 1, and soluble CD
36 scores with the lowest levels of IFN-alpha, tissue inhibitor of metalloproteinases 1, and vascular e
37 including matrix metalloproteinases 1 and 3, tissue inhibitor of metalloproteinases-1, and glycoprote
38 to analyze serum levels of hyaluronic acid, tissue inhibitor of metalloproteinases-1, and propeptide
39 e, reference hydroxamic acid MMP inhibitors, tissue inhibitor of metalloproteinases-1, and tissue inh
40 kin 6 [IL-6]; stromal cell-derived factor 1; tissue inhibitor of metalloproteinases 1; and vascular c
41 initis pigmentosa GTPase regulator ( RPGR ), tissue inhibitor of metalloproteinases 1, androgen recep
43 ter the levels of tissue PA, total MMP-2, or tissue inhibitor of metalloproteinase-1, but did increas
45 linkage, we demonstrate that the recombinant tissue inhibitor of metalloproteinase-1 could block the
46 MP-1 was up-regulated, whereas expression of tissue inhibitor of metalloproteinase 1 decreased before
47 ns of prostaglandin-endoperoxide synthase 2, tissue inhibitor of metalloproteinase 1, Dpp4, nitric ox
48 factor-beta1, alpha-smooth muscle actin, and tissue inhibitor of metalloproteinase 1 expression and a
49 ries of Dicer(d/d) mice partially normalized tissue inhibitor of metalloproteinase 1 expression and C
50 s after biliary decompression, both MMP3 and tissue inhibitor of metalloproteinase 1 expression decli
51 th a balance between metalloproteinase-8 and tissue inhibitor of metalloproteinase-1 expressions.
53 nogen activator inhibitor (PAI)-1, vimentin, tissue inhibitor of metalloproteinase-1, fibronectin, gr
54 ate cells (HSCs) were activated and produced tissue inhibitor of metalloproteinase 1 in a sphingosine
55 s tightly associated with down-regulation of tissue inhibitor of metalloproteinase-1 in a dose-depend
56 ase-8 expression and decreased expression of tissue inhibitor of metalloproteinase-1 in pulmonary acu
58 prometastatic matrix metalloproteinase 8 and tissue inhibitor of metalloproteinases 1 in metastatic n
59 DAMTS-5 increased approximately 40-fold, and tissue inhibitor of metalloproteinases 1 increased appro
62 increased messenger RNA levels of collagen, tissue inhibitor of metalloproteinase 1, matrix metallop
63 the eye, and the imbalance between MMP-1 and tissue inhibitor of metalloproteinase 1 may play a role
64 broblasts, reduced hepatic procollagen I and tissue inhibitor of metalloproteinase 1 messenger RNA ex
66 or the inhibitory N-terminal domain of human tissue inhibitor of metalloproteinases 1 (N-TIMP-1) has
67 itory N-terminal domain of recombinant human tissue inhibitor of metalloproteinases-1 (N-TIMP-1) has
68 protein-10 (IP-10), interleukin (IL)-6, and tissue inhibitor of metalloproteinases-1 on days 8-9 aft
69 y prevented by a treatment of the cells with tissue inhibitor of metalloproteinase-1 or deprivation o
72 transforming growth factor beta1 (P=0.0004), tissue inhibitor of metalloproteinase 1 (P=0.0009), gran
73 03), MMP-2 (p = 0.06), MMP-3 (p = 0.02), and tissue inhibitor of metalloproteinase-1 (p = 0.04) in el
74 reases levels of their endogenous inhibitor, tissue inhibitor of metalloproteinase 1, resulting in ma
75 g induction of matrix metalloproteinases and tissue inhibitor of metalloproteinases-1 suggests that b
76 oteinase 9 (MMP-9) and increased circulating tissue inhibitor of metalloproteinase 1 (TIMP-1) and TIM
77 91(phox(-/-) ) than in WT mice after CCl(4.) Tissue inhibitor of metalloproteinase 1 (TIMP-1) and TIM
79 including COX-2 itself, lipocalin 2 (LCN2), tissue inhibitor of metalloproteinase 1 (TIMP-1), interl
80 expression of fibrogenic genes IL-1beta and tissue inhibitor of metalloproteinase 1 (TIMP-1), with t
83 llagen was completely blocked by recombinant tissue inhibitor of metalloproteinase-1 (TIMP-1) and by
84 is substantially resistant to inhibition by tissue inhibitor of metalloproteinase-1 (TIMP-1) and TIM
86 a novel enhancer element (i.e. HTE-1) of the tissue inhibitor of metalloproteinase-1 (TIMP-1) gene to
88 x-LDL would regulate expression of MMP-9 and tissue inhibitor of metalloproteinase-1 (TIMP-1) in mono
91 lagen I type I, fibronectin, COL1alpha1, and tissue inhibitor of metalloproteinase-1 (TIMP-1) were in
92 and angiogenic inhibitors including maspin, tissue inhibitor of metalloproteinase-1 (TIMP-1), alpha1
93 treated with IL-1beta express high levels of tissue inhibitor of metalloproteinase-1 (TIMP-1), an imp
94 rix metalloproteinase-2 and 9 (MMP-2 and 9), tissue inhibitor of metalloproteinase-1 (TIMP-1), macrop
95 who underwent routine measurements of plasma tissue inhibitor of metalloproteinase-1 (TIMP-1), metall
96 sults, in part, from increased expression of tissue inhibitor of metalloproteinase-1 (TIMP-1), which
103 inity inhibition of stromelysin 1 (MMP-3) by tissue inhibitor of metalloproteinases 1 (TIMP-1) helps
105 expression of hepatic alpha1(I) collagen and tissue inhibitor of metalloproteinases 1 (TIMP-1) messen
107 trix metalloproteinase 1 (MMP-1), MMP-3, and tissue inhibitor of metalloproteinases 1 (TIMP-1) were d
108 ase (matrix metalloproteinase 1 [MMP-1]) and tissue inhibitor of metalloproteinases 1 (TIMP-1) were m
109 catabolism and production of stromelysin and tissue inhibitor of metalloproteinases 1 (TIMP-1) were m
110 lloproteinase 1 [MMP-1], MMP-13, and MMP-3), tissue inhibitor of metalloproteinases 1 (TIMP-1), and c
111 hen used to transduce these cells with human tissue inhibitor of metalloproteinases 1 (TIMP-1), and t
112 smosine, matrix metalloproteinase 2 (MMP-2), tissue inhibitor of metalloproteinases 1 (TIMP-1), and T
113 d wine and ethanol upregulated expression of tissue inhibitor of metalloproteinases 1 (TIMP-1), downr
114 ecreased collagenase, but not stromelysin or tissue inhibitor of metalloproteinases 1 (TIMP-1), messe
115 AM-TS5, respectively), MMP-1, MMP-3, MMP-13, tissue inhibitor of metalloproteinases 1 (TIMP-1), TIMP-
116 invasion assay in the presence or absence of tissue inhibitor of metalloproteinases 1 (TIMP-1), TIMP-
117 r metalloproteinase 2 (MMP-2), MMP-3, MMP-9, tissue inhibitor of metalloproteinases 1 (TIMP-1), TIMP-
118 explants induced synthesis and secretion of tissue inhibitor of metalloproteinases 1 (TIMP-1), which
123 s to determine whether genetic deficiency of tissue inhibitor of metalloproteinases-1 (TIMP-1) could
124 nd induction of mRNA for the AP-1 responsive tissue inhibitor of metalloproteinases-1 (TIMP-1) gene.
125 is via its transcriptional regulation of the tissue inhibitor of metalloproteinases-1 (TIMP-1) gene.
126 role in extracellular matrix remodeling, the tissue inhibitor of metalloproteinases-1 (TIMP-1) has be
132 blasts results in a synergistic induction of tissue inhibitor of metalloproteinases-1 (TIMP-1) protei
134 nd were quenched by co-expression of a human tissue inhibitor of metalloproteinases-1 (TIMP-1) transg
135 n effective method for refolding recombinant tissue inhibitor of metalloproteinases-1 (TIMP-1), a 21-
137 MMP-9), and the inhibitors of these enzymes (tissue inhibitor of metalloproteinases 1 [TIMP-1] and TI
139 ssion of MMP-1 and its endogenous inhibitor (tissue inhibitor of metalloproteinases-1, TIMP-1) by imm
140 a region flanked by the dystrophin (DMD) and tissue inhibitor of metalloproteinase 1 (TIMP1) genes, a
141 oducts (collagen type 1 alpha 1 (CoL1A1) and tissue inhibitor of metalloproteinase 1 (TIMP1)) were al
143 smooth muscle actin (alphaSMA), collagen I, tissue inhibitor of metalloproteinase-1 (TIMP1) and tran
145 faip6), matrix metalloproteinase 19 (Mmp19), tissue inhibitor of metalloproteinases 1 (Timp1), and po
147 al injury including Cystatin C, Osteopontin, Tissue Inhibitor of Metalloproteinases-1 (TIMP1), beta2-
149 terleukin-1 beta converting enzyme (ICE) and tissue inhibitor of metalloproteinases-1 was upregulated
150 , whereas vascular expression of collagen or tissue inhibitor of metalloproteinase-1 were down-regula
151 mor necrosis factor receptor 2 or IL-10, and tissue inhibitor of metalloproteinases 1) were identifie
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