ライフサイエンスコーパス: chondrocytic

1 m that pericytes can differentiate along the chondrocytic and adipocytic lineages in vivo, these cell

2 lcium phosphate material is deposited in the chondrocytic and fibrocytic matrices.

3 e syndrome, CPA6 is expressed in a number of chondrocytic and nervous tissues during embryogenesis.

4 chymal precursor cells for selecting between chondrocytic and osteoblastic fates as well as a mechani

5 ted ATX and B10/PDNP3 expression in central (chondrocytic) and, to a lesser degree, peripheral (fibro

6 ls capable of differentiating to osteocytic, chondrocytic, and adipocytic lineages when stimulated un

7 lated with cells of irregular shape and less-chondrocytic appearance, contained abundant intracellula

8 ively reproduced the experimentally observed chondrocytic arrangements in growth plate of each of the

9 d evaluated its activity in osteoblastic and chondrocytic cell culture models.

10 n chondrocytes from OA cartilage and a human chondrocytic cell line C28/I2 but was up-regulated by th

11 lase (PLSCR1), during maturation of a murine chondrocytic cell line, N1511.

12 rid system and a cDNA library derived from a chondrocytic cell line.

13 differentiating cells in the lymphocytic and chondrocytic cell lineages.

14 cytes by generating stably transfected mouse chondrocytic cell lines.

15 is we studied the effects of Wnt on cultured chondrocytic cells and differentiating limb-bud mesenchy

16 Using primary chondrocytes and T/C-28a2 chondrocytic cells as model systems, we report that prol

17 monstrate that induction of MMP-1 by IL-1 in chondrocytic cells depends on unique combinations of sig

18 indicate a possible synovial origin for the chondrocytic cells found in rheumatoid pannus.

19 ecan in both notochord cells and surrounding chondrocytic cells of presumptive inner annuli and verte

20 ift assay using nuclear extracts from TMC-23 chondrocytic cells revealed that the NF-kappaB subunits

21 Exposure of T/C-28a2 chondrocytic cells to fluid shear results in co-regulati

22 irs of sites eliminated enhancer activity in chondrocytic cells, as did the mutation of any one of th

23 ressed SOX9 activated these enhancers in non-chondrocytic cells, as it also activates the Col2a1 enha

24 ever, in normal or immortalized (e.g. ATDC5) chondrocytic cells, Runx2 expression is suppressed durin

25 ansfection of TG2 site-directed mutants into chondrocytic cells, we observed that wild type TG2, and

26 Using chondrocytic cells, we previously determined that IL-1 i

27 ction by proinflammatory cytokine-stimulated chondrocytic cells.

28 n the medial part of menisci, which contains chondrocytic cells.

29 cers and can activate these enhancers in non-chondrocytic cells.

30 ondrocytes, and immortalized human articular chondrocytic CH-8 cells were transfected with CXCR1/CXCR

31 accharides induced a dose-dependent state of chondrocytic chondrolysis, including near-total loss of

32 m to mesoderm, before differentiating into a chondrocytic culture comprising cell aggregates.

33 However, the cells were capable of chondrocytic differentiation and formed cartilage tissue

34 n growth plate chondrocytes stimulates their chondrocytic differentiation and maturation toward hyper

35 We demonstrate that this defect in chondrocytic differentiation can be attributed to lack o

36 ker expression and aberrant osteoblastic and chondrocytic differentiation in a TEAD-dependent fashion

37 eration and saturation density but repressed chondrocytic differentiation.

38 steoblastic differentiation while repressing chondrocytic differentiation.

39 cyte proliferation and maturation, increased chondrocytic expression of Rankl, matrix metalloproteina

40 e understanding the coordinate regulation of chondrocytic genes.

41 FR) are thought to be negative regulators of chondrocytic growth, as exemplified by achondroplasia an

42 embryo fibroblasts could be induced into the chondrocytic lineage ex vivo, but these cells failed to

43 , commitment of cells to the osteoblastic or chondrocytic lineage may involve inhibition of alternati

44 rentiation within either the osteoblastic or chondrocytic lineage.

45 as melanocytic, adipocytic, osteocytic, and chondrocytic lineages, which recapitulates the plasticit

46 formed nodules and expressed high levels of chondrocytic marker proteins when cultured on Pln.

47 xpression and protein production in terms of chondrocytic markers when compared with unpurified dermi

48 as evidenced by lack of expression of other chondrocytic markers, such as aggrecan and collagen type

49 , suggesting that, in the majority of cases, chondrocytic miRNAs do not directly regulate target RNA

50 Chondrocytic MMP-3, but not MMP-7, was required for disc

51 idenced by the formation of large numbers of chondrocytic nodules on aggrecan-coated surfaces.

52 fferentiate exclusively into the adipocytic, chondrocytic, or osteocytic lineages.

53 provide new insights into the regulation of chondrocytic, osteoblastic, and osteoclastic differentia

54 BMP-4-expressing MDSCs acquired a chondrocytic phenotype in vitro more effectively than di

55 e ability of transplanted cells to acquire a chondrocytic phenotype.

56 operties of cartilage or the regulation of a chondrocytic phenotype.

57 mad and MAPK pathways in expression of early chondrocytic phenotypes and identify important changes i

58 of relative positioning of the proliferative chondrocytic population based on ciliary orientation.

59 ee-dimensional orientation patterns that the chondrocytic primary cilium forms in articular cartilage

60 search investigates the role of the immotile chondrocytic primary cilium in the growth plate.

61 on of Col2a1 and possibly other genes of the chondrocytic program.

62 Furthermore, inhibitory effects of FGF2 on chondrocytic proliferation were partially reduced in p21

63 regulatory response to genotoxic stress in a chondrocytic survival pathway is potentially also releva

64 The functional effects of miR-146a on human chondrocytic, synovial, and microglia cells were studied

65 ivities, achieved via direct transfection of chondrocytic TC28 and meniscal cells, both induced matri

66 ce of the Notch ligand Jag1, vSMCs acquire a chondrocytic transcriptional repertoire that can lead to

67 n deposition in the arterial wall upon osteo/chondrocytic transformation of vascular smooth muscle ce

68 knee OA articular cartilage and the central (chondrocytic) zone of OA menisci.

69 The chondrocytic zones of the growth plates also appeared no