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1  the effects of F4 in IL-1beta-stimulated OA chondrocytes.
2 ynamics in the pericellular matrix of living chondrocytes.
3 ne expression is repressed by SIRT1 in human chondrocytes.
4 t) in effecting MMP13 transcription in human chondrocytes.
5  cytotoxicity against normal human articular chondrocytes.
6 , mechanoelectrical transduction pathways in chondrocytes.
7 creep, for three-dimensional (3D) culture of chondrocytes.
8  on RUNX2-driven MMP13 gene expression in OA chondrocytes.
9 ne its role in regulating gene expression in chondrocytes.
10 1-mediated MMP13 gene expression in human OA chondrocytes.
11 levels and RUNX2 gene expression in human OA chondrocytes.
12 OX9 rescued the differentiation of MSCs into chondrocytes.
13  of miRNAs in normal and osteoarthritis (OA) chondrocytes.
14 divide more slowly than underlying articular chondrocytes.
15 tional and post transcriptional levels in OA chondrocytes.
16 nding of the mechanisms of action of ELF3 in chondrocytes.
17 induction of multiple signalling pathways in chondrocytes.
18 ring catabolic and inflammatory responses in chondrocytes.
19 mal stem cells, osteoblasts, osteocytes, and chondrocytes.
20  and other catabolic marker expression in OA chondrocytes.
21 sequestered in SGs in IL-1beta-stimulated OA chondrocytes.
22 x metalloproteinases in both mouse and human chondrocytes.
23  the hyperglucidic-mediated dysregulation of chondrocytes.
24 ting that SAHA inhibits IL-6 signaling in OA chondrocytes.
25 nt of methods to direct vectors to articular chondrocytes.
26 fferentiate into osteocytes, adipocytes, and chondrocytes.
27 of interconnected cartilage matrix formed by chondrocytes.
28 toire of miRNAs and isomiRs in primary human chondrocytes.
29 by deep sequencing analysis of primary human chondrocytes.
30 rtilage de novo, entirely substituting fetal chondrocytes.
31 s to a blockage of the autophagy flux in LSD chondrocytes.
32 s are derived via direct transformation from chondrocytes.
33 e growth by regulating glucose metabolism in chondrocytes.
34 artly by regulating the abundance of SOX9 in chondrocytes.
35 , MMP-13 and ADAMTS-4 in IL-1beta-treated OA chondrocytes.
36   MiR-146b expression was up-regulated in OA chondrocytes.
37 no up-regulation of markers for hypertrophic chondrocytes, a TUNEL assay showed a marked increase in
38 RF-R1 and CRF-R2, in primary human articular chondrocytes (AC) and demonstrate its role as an autocri
39 nditional deletion of the Phd2 gene (cKO) in chondrocytes accelerated the transition of progenitors t
40                 Therefore, we summarize that chondrocytes actively mitigate local joint inflammation,
41 ntiate down multiple cell lineages including chondrocytes, adipocytes, osteoblasts, and multiple neur
42  we show that both pathways are activated in chondrocytes after treatment with TGF-beta and that TGF-
43 h of bones occurs at the growth plates where chondrocytes align into columns that allow directional g
44 on of endogenous glucocorticoid signaling in chondrocytes also modulates the course and severity of a
45           In this study, we found defects in chondrocyte and osteoblast differentiation in Spop-null
46              Indian Hedgehog (Ihh) regulates chondrocyte and osteoblast differentiation through the G
47                         Panx3 regulates both chondrocyte and osteoblast differentiation via the activ
48 ed open chromatin regions recapitulate known chondrocyte and skeletal biology, are enriched at height
49 hat have the characteristics of osteoblasts, chondrocytes and adipocytes.
50 cells exhibit progenitor activity for stable chondrocytes and are able to self-organize three-dimensi
51 strated the key contribution of growth plate chondrocytes and articular chondrocytes, not only for lo
52 aphy, showed that superficial cells generate chondrocytes and contribute to the growth and reshaping
53  as a result of aging or injury contain dead chondrocytes and damaged cartilage.
54 nsition into prehypertrophic and hypetrophic chondrocytes and finally into osteoblasts expressing Col
55 catabolic gene expression in human articular chondrocytes and is sufficient to attenuate MMP activiti
56 rked cell-to-cell heterogeneity amongst both chondrocytes and mesenchymal stem cells undergoing chond
57           To elucidate the interplay between chondrocytes and nanocapsules and their therapeutic effe
58 dent phenotypic overlap between hypertrophic chondrocytes and osteoblasts at the chondro-osseous bord
59 , postnatal Gli1(+) cells contribute to both chondrocytes and osteoblasts during bone fracture healin
60 rom the proliferation and differentiation of chondrocytes and osteoprogenitor cells.
61 1/2 phosphorylation in cultured hypertrophic chondrocytes and perform essential, but partially redund
62 e osteogenic differentiation of hypertrophic chondrocytes and provided insight into the pathogenesis
63 ts metabolite, fall after treatment of mouse chondrocytes and rat tibia explants with IL-1beta, an in
64 ssion and signaling of Fgfr3 in growth plate chondrocytes and suppression of chondrocyte proliferatio
65 levels of phosphorylated VEGFR2 in articular chondrocytes and synovial cells and reduce levels of pho
66 GF is associated with catabolic processes in chondrocytes and synovial cells.
67 that obesity enhances the cross-talk between chondrocytes and synovial fibroblasts via raised levels
68 lture, mutant disc cells differentiated into chondrocytes and synthesized cartilage matrix more robus
69 ence for dysregulation within the glycome of chondrocytes and the network of a family of adhesion/gro
70 was observed between RUNX2 mRNA levels in OA chondrocytes and the percentage methylation of the CpG s
71 d for postnatal differentiation of articular chondrocytes and the timely ossification of bones in joi
72 they physically interact in the cytoplasm of chondrocytes, and loss of FlnA enhances FlnB expression
73 issues through its secretion by osteoblasts, chondrocytes, and mesenchymal cells.
74 lls, also including osteocytes, hypertrophic chondrocytes, and odontoblasts.
75 eas ablation of C-Raf decreases hypertrophic chondrocyte apoptosis and impairs vascularization of the
76 atrix loss without proteoglycan replacement, chondrocyte apoptosis at day 5, synovitis present at day
77  required for phosphate-induced hypertrophic chondrocyte apoptosis, mice lacking all three Raf isofor
78                                              Chondrocyte apoptosis, synovitis, and ectopic calcificat
79 /1) phosphorylation, leading to hypertrophic chondrocyte apoptosis.
80 2 immunoreactivity and impaired hypertrophic chondrocyte apoptosis.
81 mia causes rickets by impairing hypertrophic chondrocyte apoptosis.
82 e lower jaw of adult zebrafish, we show that chondrocytes are crucial for generating thick bone durin
83                                    Senescent chondrocytes are found in cartilage tissue isolated from
84 ning how hypoxia affects lipid metabolism in chondrocytes are lacking.
85 t mechanical load and the resulting force on chondrocytes are necessary during active growth for prop
86                                              Chondrocytes are responsible for the formation of the sk
87 rogenitors to hypertrophic (differentiating) chondrocytes as revealed by reduced SZ thickness, and in
88 ated with the ectopic chondrogenic cells and chondrocytes, as indicated by phosphorylated Smad 1/5/8
89  the proximal MMP13 AP-1 motif in stimulated chondrocytes at time points that no longer supported bin
90       Endogenous glucocorticoid signaling in chondrocytes attenuates joint inflammation and damage.
91  production, indicating an important role in chondrocyte biology.
92 otifs of transcription factors with roles in chondrocyte biology.
93 lts define a regulatory mechanism that links chondrocyte BMAL1 to the maintenance and repair of carti
94 ting S-phase entry and cell proliferation of chondrocytes both in vitro and in vivo, at least in part
95 H promoted expression of markers of immature chondrocytes but inhibited chondrocyte hypertrophy while
96 ) mRNA is observed in IL-1beta-stimulated OA chondrocytes but the synthesis of protein found signific
97 specifically suppresses protein synthesis in chondrocytes, but not in any other cells of mesenchymal
98 ese changes were prevented in cultured human chondrocytes by adenoviral expression of catalase target
99  specifically deleted in Aggrecan-expressing chondrocytes by administering tamoxifen at 8-weeks of ag
100             We found that lysis of articular chondrocytes by PBMC or polyclonal NK cells was potentia
101 x3 regulates the terminal differentiation of chondrocytes by promoting vascular endothelial growth fa
102 l types encountered in vivo, including human chondrocytes (C28/I2), human hepatic epithelial cells (L
103 eta-catenin signaling, a pathway involved in chondrocyte catabolism and OA.
104          Here we show that Eed deficiency in chondrocytes causes severe kyphosis and a growth defect
105 ssive destruction of articular cartilage and chondrocyte cell death.
106 B-cell) and mesenchymal (osteoblast lineage, chondrocyte) cell types.
107                                              Chondrocytes challenged with IL-1beta, a cytokine involv
108 redominant isoform expressed in hypertrophic chondrocytes, chondrocyte-specific c-Raf knockout mice (
109    During jawbone regeneration, we find that chondrocytes co-express genes associated with osteoblast
110 f the knee was increased in mice with intact chondrocytes compared with animals whose chondrocytes ha
111                                              Chondrocytes constitutively expressed LLT1, a ligand of
112 findings suggest that inhibition of Runx2 in chondrocytes could at least partially rescue DMM-induced
113                           LLT1 expression by chondrocytes could be upregulated by IL-1alpha and TNF.
114 equivalents formed from hydrogels containing chondrocytes could provide a solution for replacing dama
115                    In this work we show that chondrocytes cultured in hypoxia and normoxia can be dif
116 ace chondrocytes in mice and determined that chondrocyte death did not lead to cartilage damage.
117 hondrocytes had been killed, suggesting that chondrocyte death does not drive cartilage damage in res
118           In this study, we examined whether chondrocyte death undermines cartilage integrity in agin
119 activity, and CRISPR/Cas9 targeting of human chondrocytes demonstrates that the region regulates CHSY
120 served the absence of lineage progression of chondrocyte-derived bone cells to form osteoblasts and o
121 ion from synovial fibroblasts was induced by chondrocyte-derived IL-6.
122 e formation in much of the mandibular ramus (chondrocyte-derived) with intramembranous bone formation
123 s bone formation of the mandibular body (non-chondrocyte-derived).
124 ption factor that plays an essential role in chondrocyte development by directing the expression of c
125 interplay between Sox9 and AP-1 in mammalian chondrocyte development.
126                                Primary human chondrocytes did not show any adverse effects upon nanoc
127 esses, whereas suppression of ECM1 enhances, chondrocyte differentiation and hypertrophy in vitro and
128                           Rapamycin promotes chondrocyte differentiation and restores these defects i
129 indings that PHD2 is a negative regulator of chondrocyte differentiation and that hypoxia signaling i
130 ein and subsequently disrupting hypertrophic chondrocyte differentiation.
131 CDS-associated abnormalities in hypertrophic chondrocyte differentiation.
132 ecific inhibitor of PHD2, promoted articular chondrocyte differentiation.
133 iferation, its inactivation is essential for chondrocyte differentiation.
134  study, we established a role for lncRNAs in chondrocyte differentiation.
135 f this method for detecting abnormalities in chondrocyte distribution in mice lacking lubricin (Prg4)
136                     A- and B-Raf ablation in chondrocytes does not alter skeletal development, wherea
137 GF acts as a survival factor in growth plate chondrocytes during development but only up until a few
138 eny of superficial cells fully replace fetal chondrocytes during early postnatal life.
139 ich is in marked contrast to the behavior of chondrocytes during facial skeletal development.
140 in the intracellular inflammation cascade of chondrocytes during the progress of osteoarthritis.
141 ined with cartilage, comprised of individual chondrocytes embedded in a specialized extracellular mat
142                                              Chondrocytes experience a complex mechanical environment
143                                              Chondrocytes experimentally depleted of cell-associated
144 M and non-T2DM patients as well as in murine chondrocytes exposed to high glucose (HG).
145 , particularly in the nuclear fraction, than chondrocytes exposed to normal glucose (NG).
146 ifen indicated that the same Col2 expressing chondrocytes expressed prehypertrophic, hypertrophic, an
147                        As a consequence, LSD chondrocytes fail to properly secrete collagens, the mai
148 tion were observed in HG+IL-1beta-stimulated chondrocytes from Nrf-2(-/-) mice than in chondrocytes f
149               However, cultured hypertrophic chondrocytes from these mice did not exhibit impairment
150 nalysis of primary cultures of TMJ articular chondrocytes from wild-type and Ddr2(slie/slie) mice sho
151 ed chondrocytes from Nrf-2(-/-) mice than in chondrocytes from wild-type mice.
152  Transgenic restoration of Mgp expression in chondrocytes fully corrected the craniofacial anomalies
153 ver, the specific role of Runx2 in articular chondrocyte function and in OA development in adult mice
154 ate gene expression, play important roles in chondrocyte function and in the development of osteoarth
155 beta superfamily are important regulators of chondrocyte function.
156  expression and highlights a novel method of chondrocyte gene regulation involving a lncRNA.
157 n Jun- and Sox9-bound regions throughout the chondrocyte genome, reflecting direct binding of each fa
158               Fractions were added to C28/I2 chondrocytes, grown in micromasses, ions with or without
159  complex 1 (mTORC1) activity is required for chondrocyte growth and proliferation, its inactivation i
160 act chondrocytes compared with animals whose chondrocytes had been killed, suggesting that chondrocyt
161              HG-exposed, IL-1beta-stimulated chondrocytes had lower Nrf-2 levels in vitro, particular
162 ed globally in human chondroblastomas and in chondrocytes harboring the same genetic mutation, due to
163 s characterized by cartilage destruction and chondrocytes have a central role in this process.
164                    With age and inflammation chondrocytes have reduced capacity to synthesize and mai
165 tivated in osteoarthritis, where it promotes chondrocyte hypertrophy and cartilage matrix catabolism.
166 roteinase 13 (MMP13) is also associated with chondrocyte hypertrophy in adult articular cartilage, th
167 uces cell cycle arrest and thereby initiates chondrocyte hypertrophy via BMP/SMAD-mediated up-regulat
168 rkers of immature chondrocytes but inhibited chondrocyte hypertrophy while IHH promoted chondrocyte h
169 d chondrocyte hypertrophy while IHH promoted chondrocyte hypertrophy.
170 ncreased MDZ thickness, as well as increased chondrocyte hypertrophy.
171 lysis of Sox9 binding profiles in developing chondrocytes identified marked enrichment of an AP-1-lik
172 ustained SOX9 in SHP2-deficient hypertrophic chondrocytes impaired their differentiation to osteoblas
173                                              Chondrocytes in injured and diseased situations frequent
174             The loss of Sox9 in growth plate chondrocytes in knee joint and in NP cells in interverte
175 ts guanylyl cyclase activity in growth plate chondrocytes in living bone.
176 f diphtheria toxin to kill articular surface chondrocytes in mice and determined that chondrocyte dea
177 gen, we cultured 3D pellets of human primary chondrocytes in normoxia (20% oxygen) and hypoxia (2.5%
178 A composition of the miRISC in primary human chondrocytes in response to IL-1beta treatment.
179 livery of therapeutic agents to the resident chondrocytes in the avascular cartilage.
180  assay showed a marked increase in apoptotic chondrocytes in the calcified nasal septum.
181 ealed that Sox9 and Col2 expressing immature chondrocytes in the epiphysis transition into prehypertr
182 and loss of FlnA enhances FlnB expression of chondrocytes in the growth plate (and vice versa), sugge
183                                 Hypertrophic chondrocytes in the TZ activate expression of the plurip
184 e similar increases in cilia length in human chondrocytes in vitro and after administration of dietar
185 tochondrial pathway that is not specific for chondrocytes in vitro or joint tissues in vivo.
186             Differentiation of stem cells to chondrocytes in vitro usually results in a heterogeneous
187               Treatment of primary articular chondrocytes, in vitro, with IOX2, a specific inhibitor
188  was secreted and it bound to osteoarthritic chondrocytes inhibitable by cognate sugar.
189                                        Since chondrocyte injury and subsequent cell death are the ear
190 feration and migration, but plays no role in chondrocyte intercalation.
191 nstrated the direct cell transformation from chondrocytes into bone cells in postnatal bone growth.
192 emonstrate that the direct transformation of chondrocytes into bone cells is common in both long bone
193         Transdifferentiation of hypertrophic chondrocytes into bone-forming osteoblasts has been repo
194 ontrol the transit of proliferating immature chondrocytes into mature hypertrophic chondrocytes to be
195 hat the abnormal MMP13 gene expression in OA chondrocytes is controlled by changes in the DNA methyla
196 ogical process, in which Bmpr1a signaling in chondrocytes is necessary for the formation of a pool or
197 EK1/2-ERK1/2 phosphorylation in hypertrophic chondrocytes is required for phosphate-mediated apoptosi
198 emoval of the SnCs from in vitro cultures of chondrocytes isolated from patients with OA undergoing t
199 P1A with specific mAbs resulted in increased chondrocyte killing.
200 AMP to adenosine) develop spontaneous OA and chondrocytes lacking A2AR develop an 'OA phenotype' with
201 etrant to human OA cartilage, and persist in chondrocyte lacunae for at least 2 wk.
202 -ERK1/2 immunoreactivity in the hypertrophic chondrocyte layer and impaired vascular invasion.
203  a significant expansion of the hypertrophic chondrocyte layer of the growth plate, accompanied by de
204 o studies demonstrated that loss of c-Raf in chondrocytes leads to expansion of the hypertrophic laye
205     Articular cartilage injury can result in chondrocyte loss and diminishment of specialised extrace
206 faces and in cortical osteocytes, epiphyseal chondrocytes, marrow adipocytes and mesenchymal stem cel
207 lar matrix deposition; this in turn promotes chondrocyte-matrix adhesion and cell proliferation.
208 e and Ddr2(slie/slie) mice showed defects in chondrocyte maturation and mineralization in the absence
209 development, which involves proper timing of chondrocyte maturation and perichondrial cell differenti
210                       Cartilage homeostasis, chondrocyte maturation, and terminal differentiation mar
211 2) is critical for bone formation as well as chondrocyte maturation.
212 ity and is required for joint patterning and chondrocyte maturation.
213 odel of endochondral ossification holds that chondrocytes mature to hypertrophy, undergo apoptosis an
214 ion channels are of functional importance in chondrocyte mechanotransduction; however, direct evidenc
215 tes promotes TMJ degenerative remodelling by chondrocyte-mediated pro-catabolic activities.
216  characterized the dynamic repertoire of the chondrocyte miRNome and miRISC-associated miRNome by dee
217 n of growth plate chondrocytes and articular chondrocytes, not only for long bone growth, but also fo
218 (Vegfa) immunoreactivity in the hypertrophic chondrocytes of c-Raf(f/f);ColII-Cre(+) mice was signifi
219 onsequence of disruption of the Phd2 gene in chondrocytes on the articular cartilage phenotype in mic
220 e, in which the Smpd3 gene is knocked out in chondrocytes only, recapitulate the fro/fro mouse cartil
221                                              Chondrocytes or cartilage can also be activated by treat
222 letion did not give rise to an activation of chondrocytes or cartilage.
223 ivo In addition, target transgene of ECM1 in chondrocytes or osteoblasts in mice leads to striking de
224 ed dental cells ( Col1a1-cKO) or deletion in chondrocytes, osteoblasts, and craniofacial mesenchyme (
225  bone and involves a dynamic interplay among chondrocytes, osteoblasts, and endothelial cells.
226 iate along diverse lineages into adipocytes, chondrocytes, osteoblasts, fibroblasts, and myofibroblas
227 ict cartilage matrix formation and alter the chondrocyte phenotype.
228 h live imaging, the results show that single chondrocyte precursors can generate both single-column a
229 ide new insights into the effects of LiCl on chondrocyte primary cilia and Hedgehog signaling and sho
230 ic lineage tracing experiments have revealed chondrocyte progenitors at the articular surface.
231          Superficial cells are self-renewing chondrocyte progenitors, which form the articular cartil
232 led mTORC1 activity is crucial to coordinate chondrocyte proliferation and differentiation partially
233 t proteoglycans are essential components for chondrocyte proliferation and differentiation.
234 ed bone growth was associated with increased chondrocyte proliferation and expansion of the different
235 e for H3K27 methylation in the regulation of chondrocyte proliferation and hypertrophy in the growth
236  tissue growth factor (CTGF/CCN2) stimulates chondrocyte proliferation and maturation.
237 vement alters limb proportions and regulates chondrocyte proliferation in only specific growth plates
238  kyphosis and a growth defect with decreased chondrocyte proliferation, accelerated hypertrophic diff
239 growth plate chondrocytes and suppression of chondrocyte proliferation.
240 t activation of alpha2A-adrenergic signal in chondrocytes promotes TMJ degenerative remodelling by ch
241 he KBD articular cartilage (average positive chondrocyte rate = 47.59 +/- 7.79%) compared to healthy
242 ealthy articular cartilage (average positive chondrocyte rate = 64.73 +/- 5.05%).
243 lage destruction; however, the mechanisms of chondrocyte recognition by NK cells remain poorly unders
244 A sequencing we identified a human articular chondrocyte repertoire of lncRNAs from normal hip cartil
245                     To better understand the chondrocyte's behavior in response to oxygen, we culture
246 w that the combined loss of Ezh1 and Ezh2 in chondrocytes severely impairs skeletal growth in mice.
247 form expressed in hypertrophic chondrocytes, chondrocyte-specific c-Raf knockout mice (c-Raf(f/f);Col
248                               They show that chondrocyte-specific deletion of BMAL1 leads to cartilag
249       IL-3 increases the expression of mouse chondrocyte-specific genes, Sox9 and collagen type IIa,
250 e development by directing the expression of chondrocyte-specific genes.
251              Our work sheds further light on chondrocyte-specific SOX9 expression and highlights a no
252 istinct mechanical stimuli to primary murine chondrocytes, stretch of the membrane and deflection of
253 urse of chondrogenesis and its expression in chondrocytes strictly depends on parathyroid hormone-rel
254                               VEGF is also a chondrocyte survival factor during development and essen
255 ting Ucn1 acts through CRF-R1 when promoting chondrocyte survival.
256 this IL-6 inflammatory response, mediated by chondrocyte-synovial fibroblast cross-talk, was enhanced
257 that mark OA progression in isolated primary chondrocytes taken from paired intact versus degraded ar
258                          Tamoxifen-inducible chondrocyte-targeted glucocorticoid receptor-knockout (c
259  factor induced by inflammatory cytokines in chondrocytes that increases gene expression of catabolic
260 ation and consequent activation of mTORC1 in chondrocytes, the cells devoted to bone elongation.
261                                    In mutant chondrocytes, the mutations led to low levels of IFT81 a
262 yet down-regulates the HIF-1alpha pathway in chondrocytes, thereby promoting the demise of these cell
263 pothyroid mice, thus providing evidence that chondrocyte to osteoblast transdifferentiation is TH-dep
264 mature chondrocytes into mature hypertrophic chondrocytes to become osteoblasts at the epiphysis.
265 ut the mechanisms controlling the ability of chondrocytes to form columns.
266 show that susceptibility of normal articular chondrocytes to lysis by NK cells is modulated by NKR-P1
267 ntribute to Sox9 action in the transition of chondrocytes to the hypertrophic program.
268  interest are lncRNAs upstream of the master chondrocyte transcription factor SOX9 locus.
269        However, recent data demonstrate that chondrocytes transdifferentiate to osteoblasts in the gr
270 ersely, MMP13 gene expression was reduced in chondrocytes transfected with SIRT1 siRNA or treated wit
271                                           OA chondrocytes treated with F4 in the presence of IL-1beta
272                       Furthermore, articular chondrocytes treated with OA derived extracellular vesic
273                                              Chondrocyte treatment with IL-1alpha resulted in their i
274                             However, loss of chondrocyte TRPV4 did not prevent OA development followi
275 siological oxygen levels (19-21%), culturing chondrocytes under hypoxic oxygen levels (</=8%) promote
276 and sequestration of COX-2 mRNAs in human OA chondrocytes under pathological conditions.
277  of c-Fos/AP-1 expression and activity in OA chondrocytes under pathological conditions.
278  formation postulates that most hypertrophic chondrocytes undergo programmed cell death prior to bone
279 f Hif-1alpha expression in primary articular chondrocytes using lentiviral vectors containing Hif-1al
280 predominantly proliferating and hypertrophic chondrocytes, using "Cre-loxP"-mediated gene excision.
281 g exudate displayed protective activities on chondrocytes, using multiple readouts: these effects wer
282  mesenchymal stem cell markers, and generate chondrocytes via both asymmetric and symmetric different
283 ism for TGF-beta-mediated gene regulation in chondrocytes via p38 and phosphorylation and stabilizati
284 tructure, proteoglycan or collagen contents, chondrocyte viability or RNA expression levels were dete
285 on of the actin cytoskeleton in growth plate chondrocytes was disrupted.
286           Cell-mediated cytotoxicity against chondrocytes was evaluated by means of 18-h (51)Cr-relea
287 and protein expression data in human primary chondrocytes, we identified consistent molecular players
288 atrix metalloproteinases (MMPs) and RANKL by chondrocytes were evaluated.
289                           Human OA articular chondrocytes were examined for miR-146b expression.
290 osis, mice lacking all three Raf isoforms in chondrocytes were generated.
291                                              Chondrocytes were isolated from articular cartilage obta
292                  Human cartilage tissues and chondrocytes were obtained at autopsy from normal knee j
293                                              Chondrocytes were stimulated by norepinephrine to invest
294 gly, these effects could not be detected for chondrocytes which were pretreated with the nanocapsules
295  time that SIRT1 represses MMP13 in human OA chondrocytes, which appears to be mediated, at least in
296 ression of MMP-13 was determined by treating chondrocytes with recombinant IL-6 or by IL6 knockdown u
297 AC6 or following treatment of fibroblasts or chondrocytes with small molecule inhibitors of HDAC6.
298 e conclude that mechanical load and force on chondrocytes within the growth plate regulate postnatal
299 obe accumulation and the number of apoptotic chondrocytes within the injured xiphoid cartilage, which
300 ctopic expression in primary human articular chondrocytes, Wnt7a inhibited IL-1beta-induced MMP and i

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