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1 ts and blood vessels, invade the mineralized cartilage matrix.
2 AP-positive cells resorbing the hypertrophic cartilage matrix.
3 nce of the structural integrity of articular cartilage matrix.
4 y role in maintaining the integrity of human cartilage matrix.
5 melysin inhibitor that blocks the erosion of cartilage matrix.
6 to cleavage and removal of collagen from the cartilage matrix.
7  is characterized by progressive loss of the cartilage matrix.
8 disrupted circadian rhythms and degraded the cartilage matrix.
9 ndrocyte differentiation and production of a cartilage matrix.
10  reduction in cell size and in the amount of cartilage matrix.
11 grafts contained a mixed hyaline and fibrous cartilage matrix.
12 shearing, and transport of TGF-beta into the cartilage matrix.
13 rocyte biology, leading to catabolism of the cartilage matrix.
14 g they may be formed during calcification of cartilage matrix.
15 cyte terminal maturation and turnover of the cartilage matrix.
16 nterfere with the structural assembly of the cartilage matrix.
17 e is complete and homogenous pigmentation of cartilage matrix.
18 rther enhanced by removing aggrecan from the cartilage matrix.
19 nd respond to environment in the surrounding cartilage matrix.
20 y is associated with damage to the articular cartilage matrix.
21 mol/L, indicating proteoglycan loss from the cartilage matrix.
22                       Compression-associated cartilage matrix alterations such as glycosaminoglycan a
23                                              Cartilage matrix analysis showed that the short alpha1(I
24 between the molecular charges present in the cartilage matrix and an ionic contrast agent, resulting
25 the deep zone of all OA specimens, where the cartilage matrix and chondrocyte morphology appeared nor
26  accompanied by loss of Alcian blue-staining cartilage matrix and downregulation of cartilage-specifi
27 enic cells which exhibit loss of Alcian blue cartilage matrix and downregulation of cartilage-specifi
28 RI) T1 and T2 mapping to detect and quantify cartilage matrix and meniscal degeneration between norma
29 es are distinct in producing lower levels of cartilage matrix and not being replaced by bone, yet how
30 in total proteoglycan content accumulated in cartilage matrix, and in the ability of chondrocytes to
31 ascular endothelium invades the hypertrophic cartilage matrix, and osteoblasts differentiate and begi
32  and overall concentration of the CPA in the cartilage matrix, and the shrinkage and stress-strain in
33 These Irx factors suppress the production of cartilage matrix at the joint in part by preventing the
34 itable factors influence serum levels of the cartilage matrix biomarker COMP.
35                       Nitric oxide may alter cartilage matrix by interfering with chondrocyte mitocho
36 gic scoring), and integrity of the articular cartilage matrix (by retention of toluidine blue stain)
37 gent relationships of 3 NTPPPH isozymes with cartilage matrix calcification and sought to identify th
38                       Meniscal and articular cartilage matrix calcification are prevalent in osteoart
39 ccurrence of type I collagen in concert with cartilage matrix calcification suggests that the protein
40 ates osteoarthritis and pathologic articular cartilage matrix calcification.
41 mplicate inflammation in the pathogenesis of cartilage matrix calcification.
42 otential pathogenic factor for knee meniscal cartilage matrix calcification.
43        Chondrocytes that elaborate a typical cartilage matrix can be seen in the affected arteries.
44 ken to investigate whether activin A affects cartilage matrix catabolism and how its production is re
45                           Both the increased cartilage matrix catabolism and the inhibition of matrix
46 here it promotes chondrocyte hypertrophy and cartilage matrix catabolism.
47 ast 21 d, inducing the expression of hyaline cartilage matrix components and anabolic signaling pathw
48 mapping has been shown to be associated with cartilage matrix composition (hydration, collagen conten
49 usive transport through the dense, avascular cartilage matrix comprised of negatively charged glycosa
50                        In jawed vertebrates, cartilage matrix consists predominantly of type II colla
51 ive MMP-13-mediated proteolysis of these key cartilage matrix constituents.
52                                     Hspg2-/- cartilage matrix contained reduced and disorganized coll
53                                        Mouse cartilage matrix deficiency (cmd) is an autosomal recess
54 artilage-specific molecules and results in a cartilage matrix deficient in required structural compon
55 uble IL-1 receptor had significantly reduced cartilage matrix degradation and white blood cell infilt
56  EGFR signaling is an important regulator of cartilage matrix degradation during SOC formation and ep
57 GAL to protect MMP-9 activity is relevant to cartilage matrix degradation in OA and may represent an
58  close to the marrow space and decreased the cartilage matrix degradation in the SOC.
59                                        Human cartilage matrix degradation was determined by dimethylm
60 f vIL-10 significantly reduced leukocytosis, cartilage matrix degradation, and levels of endogenous r
61 inflammation, suppress joint destruction and cartilage matrix degradation, with negligible in vivo to
62 in the regulation of downstream mediators of cartilage matrix degradation.
63 n a specific elevation of the release of the cartilage matrix-degrading enzyme MMP-3 (stromelysin 1).
64 xosaminidase, represent a distinct subset of cartilage matrix-degrading enzymes that are activated by
65 hat joint swelling, synovial thickening, and cartilage matrix depletion induced by the injection of a
66  their role in regulating chondrogenesis and cartilage matrix deposition by encapsulated MSCs.
67 h higher quality and quantity, with enhanced cartilage matrix deposition, concomitant with lower leve
68 ein to a chondrogenic culture system reduced cartilage matrix deposition.
69 ant signaling component of cytokine-mediated cartilage matrix destruction in articular chondrocytes,
70 ion suggest that it could play a role in the cartilage matrix destruction seen in OA.
71             These mice exhibited a defective cartilage matrix devoid of type II collagen protein (Col
72 , and the shrinkage and stress-strain in the cartilage matrix during CPA loading are neglected.
73 by further compromising the integrity of the cartilage matrix during degenerative joint diseases such
74 gest that excessive release of bFGF from the cartilage matrix during injury, with loading, or in arth
75 d new synthetic synovial fluid additives and cartilage matrix enhancers.
76 ysis of the joint tissues identifies ectopic cartilage matrix expressing genes for cartilage and fibr
77 ticipate in the invasion of the hypertrophic cartilage matrix, followed by endothelial cells derived
78       However, elastic stresses may restrict cartilage matrix formation and alter the chondrocyte phe
79 ing increase in the volume of interconnected cartilage matrix formed by chondrocytes.
80 supports cartilage homeostasis by protecting cartilage matrix from inflammation-induced degradation.
81                                          The cartilage matrix from these patients stained poorly with
82 n factors that control the expression of the cartilage matrix gene, cd-rap.
83 d in collagen sponges are induced to express cartilage matrix genes after 7 days' culture with demine
84  stimulated the expression of Sox9-regulated cartilage matrix genes and induced histone acetylation a
85 oliferation and migration and underexpressed cartilage matrix genes.
86  hypertrophic chondrocytes, and suggest that cartilage matrix has a role in chondrocyte differentiati
87 s of the metalloproteinases that degrade the cartilage matrix have been hampered by a lack of specifi
88 retinoid signaling pathways is known to tilt cartilage matrix homeostasis toward catabolism.
89 ent increased cartilage thickness, supported cartilage matrix homeostasis, and supported cell-based t
90 on play important roles in the regulation of cartilage matrix homeostasis.
91 Ss under loading circumstances formed better cartilage matrix in an ex vivo osteochondral defect than
92 associated with excessive degradation of the cartilage matrix in degenerative joint diseases such as
93                           Destruction of the cartilage matrix in joints is an important feature of ar
94 at contributes to the ongoing degradation of cartilage matrix in osteoarthritis.
95  activity in chondrocytes is associated with cartilage matrix inorganic pyrophosphate (PPi) supersatu
96                                      Loss of cartilage matrix is accompanied by an increase in matrix
97 s and chemokines suggests that damage to the cartilage matrix is capable of inducing a proinflammator
98 resulted in reduced mechanical properties of cartilage matrix later in chondrogenesis.
99 ulation of excess inorganic pyrophosphate in cartilage matrix leads to calcium pyrophosphate dihydrat
100                          Degradation of this cartilage matrix leads to the development of osteoarthri
101 rtilage explants with HA(oligos) resulted in cartilage matrix loss with increased secreted caseinolyt
102 tilage oligomeric matrix protein (COMP) is a cartilage matrix macromolecule.
103 mooth muscle marker calponin 1, decreases in cartilage matrix markers, and alterations in cell signal
104 r (bFGF) during loading and/or injury of the cartilage matrix may contribute to the onset or progress
105 ates chondrocytes in vitro to synthesize new cartilage matrix, measured by enhanced uptake of 35S-sul
106       Following injurious compression of the cartilage, matrix metalloproteinase 3 (MMP-3) and MMP-13
107 a2+ influx, intralumenal crystal growth, and cartilage matrix mineralization.
108 hus promoting the initiation of hypertrophic cartilage matrix mineralization.
109 tomes is conserved through the activation of cartilage matrix molecules and suggest that a collagenou
110 erentiated into chondrocytes and synthesized cartilage matrix more robustly than control cells.
111 o) and T2 enable detection of changes in the cartilage matrix of ACL-reconstructed knees as early as
112      Our data suggest that the defect in the cartilage matrix of mice that are heterozygous for a typ
113 s detected in the growth plate and articular cartilage matrix of transgenic mice.
114                    Characterization of these cartilage matrix peptides may help in the development of
115  an immature state, with the lower levels of cartilage matrix produced by these immature cells contri
116 fish Irx7 and mouse IRX1 are able to repress cartilage matrix production in a murine chondrogenic cel
117 action that directly links ROCK to increased cartilage matrix production via activation of SOX9 in re
118                                 Hyaline-like cartilage matrix production was observed in both VEGF-tr
119 a CRISPR-dCas9-VP64 - significantly enhanced cartilage matrix production.
120 )i-NPs) were able to penetrate deep into the cartilage matrix, prolong retention in the joint space,
121              One matched the NH2 terminus of cartilage matrix protein (CMP) as reported for tracheal
122                                              Cartilage matrix protein (CMP) is a major component of d
123                                              Cartilage matrix protein (CMP) is the prototype of the n
124 dues 1 to 227), which contains homology with cartilage matrix protein (CMP).
125 ce linking chondrocyte lipid peroxidation to cartilage matrix protein (collagen) oxidation and degrad
126 th type II collagen becoming the predominant cartilage matrix protein after the divergence of jawless
127 wo genes assigned to 1p34-p35 were excluded: cartilage matrix protein and avian myelocytosis viral on
128 study the role of chondrocyte-derived ROS in cartilage matrix protein degradation.
129       One potential antigen is matrilin-1, a cartilage matrix protein found uniquely in the tracheal,
130                Type II collagen is the major cartilage matrix protein in the jawed vertebrate skeleto
131 cellular immune response directed toward the cartilage matrix protein matrilin-1.
132  of the expression of prehypertrophic marker cartilage matrix protein.
133 de corresponding to the C-terminal domain of cartilage matrix protein.
134 equence shows similar domain organization to cartilage matrix protein/matrilin-1, but information on
135  The levels of messenger RNA (mRNA) encoding cartilage matrix proteins and interleukin-1beta (IL-1bet
136 ades interstitial collagens as well as other cartilage matrix proteins and TGF beta1, may signify a s
137  by which NGAL may contribute to the loss of cartilage matrix proteins in OA.
138 dergo myogenesis can be converted to express cartilage matrix proteins in vitro when cultured in chon
139 otides and calcium, include cross-linking of cartilage matrix proteins, binding of fibronectin, and h
140 at the expression of Cd-rap, like many other cartilage matrix proteins, is repressed by interleukin 1
141 duction of collagen II, and eventually other cartilage matrix proteins, leading to major skeletal ano
142 -6 and were assessed for breakdown of tibial cartilage matrix proteoglycan (aggrecan) and type II col
143 entrations, almost complete normalization of cartilage matrix proteoglycan turnover was achieved.
144                    MMP-9-mediated release of cartilage matrix proteoglycans was significantly higher
145         OPG treatment also prevented loss of cartilage matrix proteoglycans, an indirect consequence
146 There were continuous increases in mRNAs for cartilage matrix (proteoglycans and COL2, -9, -10, and -
147 ighly sulfated glycosaminoglycans within the cartilage matrix provide structural rigidity to the tiss
148                                              Cartilage matrix-related proteins were assessed by enzym
149  data provide evidence that ANGPTL4 promotes cartilage matrix remodeling by inhibiting expression of
150 enhanced expression of key genes involved in cartilage-matrix remodeling and turnover.
151 ne the role of cell-associated hyaluronan in cartilage matrix retention, human articular chondrocytes
152 meric matrix protein (COMP) is essential for cartilage matrix stability, as mutations in Col9a1, Col9
153 aminoglycan-type XI collagen interactions to cartilage matrix stabilization is discussed.
154 s primarily via diffusion or convection, and cartilage matrix structure and composition may affect di
155 fically, Smad3 maintains the balance between cartilage matrix synthesis and degradation by inducing t
156 lar cartilage degeneration due to imbalanced cartilage matrix synthesis and degradation.
157  results with regards to its precise role in cartilage matrix synthesis and degradation.
158  much is understood about how SOX9 regulates cartilage matrix synthesis and hence joint function, how
159 phatidylinositol 3-kinase-Akt and MEK-ERK in cartilage matrix synthesis and suggest that elevated lev
160 over the mechanism by which hypoxia enhances cartilage matrix synthesis by human articular chondrocyt
161 show that LNA043 promotes chondrogenesis and cartilage matrix synthesis in vitro and regenerates hyal
162 in-like growth factor I (IGF-I) to stimulate cartilage matrix synthesis is reduced in aged and osteoa
163 e a novel mechanism whereby hypoxia promotes cartilage matrix synthesis specifically through HIF-2alp
164  synovitis, while maintaining high levels of cartilage matrix synthesis.
165 duced DIAS cells produced greater amounts of cartilage matrix than constructs from the rest of the de
166  aggrecan is an important major component of cartilage matrix that gives articular cartilage the abil
167 are impaired, and the net result is degraded cartilage matrix that is devoid of blood vessels.
168 method for stimulating the repair of damaged cartilage matrix, there is evidence that with aging and/
169 y which synovial cells induce degradation of cartilage matrix through SDF-1 signaling in RA and OA.
170 rom mineralized type II/type X collagen-rich cartilage matrix to type I collagen-rich bone matrix.
171  maintaining normal homeostasis in articular cartilage matrix turnover.
172  colony-stimulating factor, and can regulate cartilage matrix turnover.
173 d for their ability to degrade reconstituted cartilage matrix using a well-characterized cartilage in
174  chondrocyte, the cell type that synthesizes cartilage matrix, was central to the evolution of the ve
175 r cartilage and loss of proteoglycans in the cartilage matrix, was diminished with treatment.
176 oteoglycan aggrecan, a main component of the cartilage matrix, were associated with idiopathic short
177 osteopontin, and by expansion of mineralized cartilage matrix, which is characteristic of terminal hy
178 us-induced arthritis, acting to preserve the cartilage matrix, which is damaged during alphavirus inf

 
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