vitro , using chondrogenic ATDC5 cells. Materials and methods In vivo studies All in vivo experiments were performed on pre-pubertal 24-day-old male Sprague–Dawley rats with an average weight of 50 g (Envigo, Ltd., Jerusalem, Israel
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Majdi Masarwi, Raanan Shamir, Moshe Phillip, and Galia Gat-Yablonski
Shan-Jin Wang, Xin-Feng Li, Lei-Sheng Jiang, and Li-Yang Dai
growth plate chondrocytes has not been fully elucidated. The purpose of this study was to examine how estrogen modulates the expression of Obr in chondrocytes. The study used mouse chondrogenic ATDC5 cells, which are an excellent in vitro model for
T Mushtaq, C Farquharson, E Seawright, and SF Ahmed
Glucocorticoids (GC) are used extensively in children and may cause growth retardation, which is in part due to the direct effects of GC on the growth plate. We characterised the ATDC5 chondrocyte cell line, which mimics the in vivo process of longitudinal bone growth, to examine the effects of dexamethasone (Dex) and prednisolone (Pred) during two key time points in the chondrocyte life cycle - chondrogenesis and terminal differentiation. Additionally, we studied the potential for recovery following Dex exposure. During chondrogenesis, Dex and Pred exposure at 10(-8) M, 10(-7) M and 10(-6) M resulted in a significant mean reduction in cell number (28% vs 20%), cell proliferation (27% vs 24%) and proteoglycan synthesis (47% vs 43%) and increased alkaline phosphatase (ALP) activity (106% vs 62%), whereas the incidence of apoptosis was unaltered. Minimal effects were noted during terminal differentiation with both GC although all concentrations of Dex lowered apoptotic cell number. To assess catch-up growth the cells were incubated for a total of 14 days which included 1, 3, 7, 10 or 14 days exposure to 10(-6) M Dex, prior to the recovery period. Recovery of proteoglycan synthesis was irreversibly impaired following just one day exposure to Dex. Although cell number showed a similar pattern, significant impairment was only achieved following 14 days exposure. Irreversible changes in ALP activity were only noticed following 10 days exposure to Dex. In conclusion, GC have maximal effects during chondrogenesis; Dex is more potent than Pred and cells exposed to Dex recover but this may be restricted due to differential effects of GC on specific chondrocyte phenotypes.
Chanika Phornphutkul, Ke-Ying Wu, Xu Yang, Qian Chen, and Philip A Gruppuso
. For most of our studies, we utilized the ATDC5 cell line ( Atsumi et al. 1990 ), a well-characterized chondrogenic cell line derived from a mouse teratocarcinoma. To assess the broader relevance of our findings, our observations were extended to a
V E MacRae, T Burdon, S F Ahmed, and C Farquharson
differentiation and induce cell death ( Martensson et al. 2004 , MacRae et al. 2006 b ), the direct effects of ceramide on growth plate chondrocytes have yet to be reported. In this study, the ATDC5 chondrogenic cell line was used to characterise and compare
V E MacRae, C Farquharson, and S F Ahmed
complex interplay of proliferative kinetics, size of the proliferative pool matrix synthesis and hypertrophic chondrocyte enlargement ( Atsumi et al. 1990 , Breur et al. 1991 ). The murine ATDC5 chondrocyte cell line has been shown to undergo the
Yan Wang, Mengqi Zhang, Zhikun Huan, Shanshan Shao, Xiujuan Zhang, Dehuan Kong, and Jin Xu
primary chondrocytes and the ATDC5 cell line were used to investigate whether FSH activation could disrupt ECM homeostasis and affect chondrocyte dedifferentiation. In addition, the possible signaling mechanisms underlying FSH-altered dedifferentiation
Hyuck Joon Kwon
hypotheses to elucidate the molecular mechanism underlying ATP oscillations in chondrogenesis. In most experiments, the prechondrogenic cell line ATDC5 that differentiates into chondrocyte to form cartilage nodules via prechondrogenic condensation in the
Hiroki Saito, Tomoya Nakamachi, Kazuhiko Inoue, Ryuji Ikeda, Kazuo Kitamura, Naoto Minamino, Seiji Shioda, and Atsuro Miyata
N mbr are expressed in mouse ATDC5 chondrogenic cells, which proliferate in response to NMB ( Saito et al . 2012 ). Bone tissue is primarily made via two mechanisms. During endochondral bone formation in long bones and vertebrae, a
Emin Umit Bagriacik, Melek Yaman, Rauf Haznedar, Gulsan Sucak, and Tuncay Delibasi
) showed that THs enhanced cartilage differentiation in the growth plate in organ-cultured mouse tibias. By doing so, longitudinal bone growth was stimulated. They also found that T 3 exposure increased expression of type II collagen gene in ATDC5 cells, a
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