Prolonged use of glucocorticoids (GCs) for the treatment of chronic inflammatory and autoimmune diseases commonly exerts various side-effects, including impairment of skeletal development. However, the effect of GCs on chondrocytes, which play a key role in skeletal development, has been rarely reported. In the present study, autophagy was induced in the ATDC5 chondrocyte cell line following treatment with dexamethasone (Dex) at doses of 1‑100 µM, and that this effect can be inhibited by RU486, a GC antagonist. Autophagy induced by the highest Dex dose (100 µM) was associated with a reduction in ATDC5 cell viability. We conclude that high doses of GC can reduce ATDC5 chondrocyte cell viability by inducing autophagy.
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http://dx.doi.org/10.3892/mmr.2014.1915 | DOI Listing |
Cytokine
January 2025
Department of Emergency, Baotou City Central Hospital, Baotou 014040, China. Electronic address:
Studies have demonstrated that several lncRNAs exhibit abnormal expression levels in patients suffering from osteoarthritis, and in-depth investigation of these aberrantly expressed lncRNAs may pave the way for innovative therapeutic strategies targeting OA. The aim of this study was to examine the expression of glucuronidase beta pseudogene 11 (GUSBP11) in OA patients and to elucidate its potential molecular mechanism. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) was used to detect GUSBP11 levels on cartilage tissues and serum samples obtained from OA patients.
View Article and Find Full Text PDFEnviron Pollut
January 2025
School of Public Health, Health Science Center, Xi'an Jiaotong University, NHC Key Laboratory of Environment and Endemic Diseases, No. 76 Yanta West Road, Xi'an, 710061, Shaanxi, PR China. Electronic address:
T-2 toxin contamination in food and feed is a growing global concern, with its toxic effects on developing cartilage remaining poorly understood. In this study, we constructed an animal model using 4-week-old male Sprague-Dawley rats, which were administered T-2 toxin (200 ng/g body weight per day) by gavage for one month. Histological analysis showed a significant reduction in hypertrophic chondrocytes and increased caspase-3 expression and TUNEL staining in the deep cartilage zone of T-2 toxin-treated rats.
View Article and Find Full Text PDFJ Drug Target
January 2025
Department of Clinical Laboratory, Affiliated Hospital of Nanjing University of Chinese Medicine, Jiangsu Province Hospital of Chinese Medicine, Nanjing, China.
In this study, we developed an intra-articular injectable hydrogel drug depot (SMN-CeO@G) for sustained OA treatment. This hydrogel system, which carries sinomenine-loaded cerium dioxide nanoparticles (SMN-CeO), enhances anti-inflammatory and anti-apoptotic effects within the joint cavity. SMN-CeO@G features a three-dimensional network structure with an approximate pore size of 10 μm, stably encapsulating SMN-CeO nanoparticles (∼75 nm).
View Article and Find Full Text PDFBMC Med Genomics
December 2024
Department of Orthopedics, The Second Affiliated Hospital of Kunming Medical University, 374# Dianmian Road, Kunming, Yunnan, 650101, P.R. China.
Background: Our previous study demonstrated that temperature-related microwave ablation (MWA) can safely modulate growth plates of piglets' vertebrae. Therefore, this study is designed to investigate the effects of different temperatures on chondrocyte viability and the underlying molecular mechanisms in vitro.
Methods: Following a 10-minute treatment at different temperatures (37 °C, 40 °C, 42 °C, 44 °C, 46 °C, 48 °C, and 50 °C), CCK-8 assay was used to examine the viability of ATDC5 cells at 12 h.
Osteoarthritis Cartilage
February 2025
Department of Biomedical Engineering, Vanderbilt University, Nashville, TN 37212, USA; Center for Bone Biology, Vanderbilt University, Nashville, TN 37212, USA; Center for Stem Cell Biology, Vanderbilt University, Nashville, TN 37212, USA. Electronic address:
Objective: Investigational cell therapies have been developed as disease-modifying agents for the treatment of osteoarthritis (OA), including those that inducibly respond to inflammatory factors driving OA progression. However, dysregulated inflammatory cascades do not specifically signify the presence of OA. Here, we deploy a synthetic receptor platform that regulates cell behaviors in an arthritis-specific fashion to confine transgene expression to sites of cartilage degeneration.
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