ライフサイエンスコーパス: cartilage matrix

1 is characterized by progressive loss of the cartilage matrix.

2 ts and blood vessels, invade the mineralized cartilage matrix.

3 AP-positive cells resorbing the hypertrophic cartilage matrix.

4 nce of the structural integrity of articular cartilage matrix.

5 y role in maintaining the integrity of human cartilage matrix.

6 melysin inhibitor that blocks the erosion of cartilage matrix.

7 to cleavage and removal of collagen from the cartilage matrix.

8 reduction in cell size and in the amount of cartilage matrix.

9 grafts contained a mixed hyaline and fibrous cartilage matrix.

10 shearing, and transport of TGF-beta into the cartilage matrix.

11 rocyte biology, leading to catabolism of the cartilage matrix.

12 cyte terminal maturation and turnover of the cartilage matrix.

13 nterfere with the structural assembly of the cartilage matrix.

14 e is complete and homogenous pigmentation of cartilage matrix.

15 rther enhanced by removing aggrecan from the cartilage matrix.

16 nd respond to environment in the surrounding cartilage matrix.

17 y is associated with damage to the articular cartilage matrix.

18 mol/L, indicating proteoglycan loss from the cartilage matrix.

19 Compression-associated cartilage matrix alterations such as glycosaminoglycan a

20 Cartilage matrix analysis showed that the short alpha1(I

21 between the molecular charges present in the cartilage matrix and an ionic contrast agent, resulting

22 the deep zone of all OA specimens, where the cartilage matrix and chondrocyte morphology appeared nor

23 accompanied by loss of Alcian blue-staining cartilage matrix and downregulation of cartilage-specifi

24 enic cells which exhibit loss of Alcian blue cartilage matrix and downregulation of cartilage-specifi

25 es are distinct in producing lower levels of cartilage matrix and not being replaced by bone, yet how

26 in total proteoglycan content accumulated in cartilage matrix, and in the ability of chondrocytes to

27 ascular endothelium invades the hypertrophic cartilage matrix, and osteoblasts differentiate and begi

28 and overall concentration of the CPA in the cartilage matrix, and the shrinkage and stress-strain in

29 These Irx factors suppress the production of cartilage matrix at the joint in part by preventing the

30 itable factors influence serum levels of the cartilage matrix biomarker COMP.

31 Nitric oxide may alter cartilage matrix by interfering with chondrocyte mitocho

32 gic scoring), and integrity of the articular cartilage matrix (by retention of toluidine blue stain)

33 gent relationships of 3 NTPPPH isozymes with cartilage matrix calcification and sought to identify th

34 Meniscal and articular cartilage matrix calcification are prevalent in osteoart

35 ccurrence of type I collagen in concert with cartilage matrix calcification suggests that the protein

36 mplicate inflammation in the pathogenesis of cartilage matrix calcification.

37 otential pathogenic factor for knee meniscal cartilage matrix calcification.

38 ates osteoarthritis and pathologic articular cartilage matrix calcification.

39 Chondrocytes that elaborate a typical cartilage matrix can be seen in the affected arteries.

40 ken to investigate whether activin A affects cartilage matrix catabolism and how its production is re

41 Both the increased cartilage matrix catabolism and the inhibition of matrix

42 here it promotes chondrocyte hypertrophy and cartilage matrix catabolism.

43 mapping has been shown to be associated with cartilage matrix composition (hydration, collagen conten

44 In jawed vertebrates, cartilage matrix consists predominantly of type II colla

45 ive MMP-13-mediated proteolysis of these key cartilage matrix constituents.

46 Hspg2-/- cartilage matrix contained reduced and disorganized coll

47 Mouse cartilage matrix deficiency (cmd) is an autosomal recess

48 artilage-specific molecules and results in a cartilage matrix deficient in required structural compon

49 uble IL-1 receptor had significantly reduced cartilage matrix degradation and white blood cell infilt

50 EGFR signaling is an important regulator of cartilage matrix degradation during SOC formation and ep

51 GAL to protect MMP-9 activity is relevant to cartilage matrix degradation in OA and may represent an

52 close to the marrow space and decreased the cartilage matrix degradation in the SOC.

53 Human cartilage matrix degradation was determined by dimethylm

54 f vIL-10 significantly reduced leukocytosis, cartilage matrix degradation, and levels of endogenous r

55 in the regulation of downstream mediators of cartilage matrix degradation.

56 n a specific elevation of the release of the cartilage matrix-degrading enzyme MMP-3 (stromelysin 1).

57 xosaminidase, represent a distinct subset of cartilage matrix-degrading enzymes that are activated by

58 hat joint swelling, synovial thickening, and cartilage matrix depletion induced by the injection of a

59 their role in regulating chondrogenesis and cartilage matrix deposition by encapsulated MSCs.

60 ein to a chondrogenic culture system reduced cartilage matrix deposition.

61 ant signaling component of cytokine-mediated cartilage matrix destruction in articular chondrocytes,

62 ion suggest that it could play a role in the cartilage matrix destruction seen in OA.

63 These mice exhibited a defective cartilage matrix devoid of type II collagen protein (Col

64 , and the shrinkage and stress-strain in the cartilage matrix during CPA loading are neglected.

65 by further compromising the integrity of the cartilage matrix during degenerative joint diseases such

66 gest that excessive release of bFGF from the cartilage matrix during injury, with loading, or in arth

67 ticipate in the invasion of the hypertrophic cartilage matrix, followed by endothelial cells derived

68 However, elastic stresses may restrict cartilage matrix formation and alter the chondrocyte phe

69 ing increase in the volume of interconnected cartilage matrix formed by chondrocytes.

70 supports cartilage homeostasis by protecting cartilage matrix from inflammation-induced degradation.

71 The cartilage matrix from these patients stained poorly with

72 n factors that control the expression of the cartilage matrix gene, cd-rap.

73 d in collagen sponges are induced to express cartilage matrix genes after 7 days' culture with demine

74 stimulated the expression of Sox9-regulated cartilage matrix genes and induced histone acetylation a

75 oliferation and migration and underexpressed cartilage matrix genes.

76 hypertrophic chondrocytes, and suggest that cartilage matrix has a role in chondrocyte differentiati

77 s of the metalloproteinases that degrade the cartilage matrix have been hampered by a lack of specifi

78 retinoid signaling pathways is known to tilt cartilage matrix homeostasis toward catabolism.

79 on play important roles in the regulation of cartilage matrix homeostasis.

80 associated with excessive degradation of the cartilage matrix in degenerative joint diseases such as

81 activity in chondrocytes is associated with cartilage matrix inorganic pyrophosphate (PPi) supersatu

82 Loss of cartilage matrix is accompanied by an increase in matrix

83 s and chemokines suggests that damage to the cartilage matrix is capable of inducing a proinflammator

84 ulation of excess inorganic pyrophosphate in cartilage matrix leads to calcium pyrophosphate dihydrat

85 Degradation of this cartilage matrix leads to the development of osteoarthri

86 rtilage explants with HA(oligos) resulted in cartilage matrix loss with increased secreted caseinolyt

87 tilage oligomeric matrix protein (COMP) is a cartilage matrix macromolecule.

88 mooth muscle marker calponin 1, decreases in cartilage matrix markers, and alterations in cell signal

89 r (bFGF) during loading and/or injury of the cartilage matrix may contribute to the onset or progress

90 ates chondrocytes in vitro to synthesize new cartilage matrix, measured by enhanced uptake of 35S-sul

91 Following injurious compression of the cartilage, matrix metalloproteinase 3 (MMP-3) and MMP-13

92 a2+ influx, intralumenal crystal growth, and cartilage matrix mineralization.

93 hus promoting the initiation of hypertrophic cartilage matrix mineralization.

94 tomes is conserved through the activation of cartilage matrix molecules and suggest that a collagenou

95 erentiated into chondrocytes and synthesized cartilage matrix more robustly than control cells.

96 o) and T2 enable detection of changes in the cartilage matrix of ACL-reconstructed knees as early as

97 Our data suggest that the defect in the cartilage matrix of mice that are heterozygous for a typ

98 s detected in the growth plate and articular cartilage matrix of transgenic mice.

99 Characterization of these cartilage matrix peptides may help in the development of

100 an immature state, with the lower levels of cartilage matrix produced by these immature cells contri

101 fish Irx7 and mouse IRX1 are able to repress cartilage matrix production in a murine chondrogenic cel

102 action that directly links ROCK to increased cartilage matrix production via activation of SOX9 in re

103 Hyaline-like cartilage matrix production was observed in both VEGF-tr

104 One matched the NH2 terminus of cartilage matrix protein (CMP) as reported for tracheal

105 Cartilage matrix protein (CMP) is a major component of d

106 Cartilage matrix protein (CMP) is the prototype of the n

107 dues 1 to 227), which contains homology with cartilage matrix protein (CMP).

108 ce linking chondrocyte lipid peroxidation to cartilage matrix protein (collagen) oxidation and degrad

109 th type II collagen becoming the predominant cartilage matrix protein after the divergence of jawless

110 wo genes assigned to 1p34-p35 were excluded: cartilage matrix protein and avian myelocytosis viral on

111 study the role of chondrocyte-derived ROS in cartilage matrix protein degradation.

112 One potential antigen is matrilin-1, a cartilage matrix protein found uniquely in the tracheal,

113 Type II collagen is the major cartilage matrix protein in the jawed vertebrate skeleto

114 cellular immune response directed toward the cartilage matrix protein matrilin-1.

115 of the expression of prehypertrophic marker cartilage matrix protein.

116 de corresponding to the C-terminal domain of cartilage matrix protein.

117 equence shows similar domain organization to cartilage matrix protein/matrilin-1, but information on

118 The levels of messenger RNA (mRNA) encoding cartilage matrix proteins and interleukin-1beta (IL-1bet

119 ades interstitial collagens as well as other cartilage matrix proteins and TGF beta1, may signify a s

120 by which NGAL may contribute to the loss of cartilage matrix proteins in OA.

121 dergo myogenesis can be converted to express cartilage matrix proteins in vitro when cultured in chon

122 otides and calcium, include cross-linking of cartilage matrix proteins, binding of fibronectin, and h

123 at the expression of Cd-rap, like many other cartilage matrix proteins, is repressed by interleukin 1

124 duction of collagen II, and eventually other cartilage matrix proteins, leading to major skeletal ano

125 -6 and were assessed for breakdown of tibial cartilage matrix proteoglycan (aggrecan) and type II col

126 entrations, almost complete normalization of cartilage matrix proteoglycan turnover was achieved.

127 MMP-9-mediated release of cartilage matrix proteoglycans was significantly higher

128 OPG treatment also prevented loss of cartilage matrix proteoglycans, an indirect consequence

129 There were continuous increases in mRNAs for cartilage matrix (proteoglycans and COL2, -9, -10, and -

130 ighly sulfated glycosaminoglycans within the cartilage matrix provide structural rigidity to the tiss

131 data provide evidence that ANGPTL4 promotes cartilage matrix remodeling by inhibiting expression of

132 enhanced expression of key genes involved in cartilage-matrix remodeling and turnover.

133 ne the role of cell-associated hyaluronan in cartilage matrix retention, human articular chondrocytes

134 meric matrix protein (COMP) is essential for cartilage matrix stability, as mutations in Col9a1, Col9

135 aminoglycan-type XI collagen interactions to cartilage matrix stabilization is discussed.

136 s primarily via diffusion or convection, and cartilage matrix structure and composition may affect di

137 fically, Smad3 maintains the balance between cartilage matrix synthesis and degradation by inducing t

138 lar cartilage degeneration due to imbalanced cartilage matrix synthesis and degradation.

139 results with regards to its precise role in cartilage matrix synthesis and degradation.

140 much is understood about how SOX9 regulates cartilage matrix synthesis and hence joint function, how

141 phatidylinositol 3-kinase-Akt and MEK-ERK in cartilage matrix synthesis and suggest that elevated lev

142 over the mechanism by which hypoxia enhances cartilage matrix synthesis by human articular chondrocyt

143 in-like growth factor I (IGF-I) to stimulate cartilage matrix synthesis is reduced in aged and osteoa

144 e a novel mechanism whereby hypoxia promotes cartilage matrix synthesis specifically through HIF-2alp

145 synovitis, while maintaining high levels of cartilage matrix synthesis.

146 duced DIAS cells produced greater amounts of cartilage matrix than constructs from the rest of the de

147 aggrecan is an important major component of cartilage matrix that gives articular cartilage the abil

148 are impaired, and the net result is degraded cartilage matrix that is devoid of blood vessels.

149 method for stimulating the repair of damaged cartilage matrix, there is evidence that with aging and/

150 y which synovial cells induce degradation of cartilage matrix through SDF-1 signaling in RA and OA.

151 rom mineralized type II/type X collagen-rich cartilage matrix to type I collagen-rich bone matrix.

152 colony-stimulating factor, and can regulate cartilage matrix turnover.

153 maintaining normal homeostasis in articular cartilage matrix turnover.

154 d for their ability to degrade reconstituted cartilage matrix using a well-characterized cartilage in

155 chondrocyte, the cell type that synthesizes cartilage matrix, was central to the evolution of the ve

156 r cartilage and loss of proteoglycans in the cartilage matrix, was diminished with treatment.

157 oteoglycan aggrecan, a main component of the cartilage matrix, were associated with idiopathic short

158 osteopontin, and by expansion of mineralized cartilage matrix, which is characteristic of terminal hy

159 us-induced arthritis, acting to preserve the cartilage matrix, which is damaged during alphavirus inf