Chondrocytes play a critical role in the repair process of osteoarthritis, which is also known as degenerative arthritis. Integrins, as the key family of cell surface receptors, are responsible for the regulation of chondrocyte proliferation, differentiation, survival and apoptosis through the recruitment and activation of downstream adaptor proteins. Moreover, G-protein-coupled receptor kinase interacting protein-1 (GIT1) exerts its effects on cell proliferation and migration through interaction with various cytokines. It has been previously suggested that GIT1 acts as a vital protein downstream of the integrin-mediated pathway. In the present study, we investigated the effects of integrin-β1 on cell proliferation and apoptosis, as well as the underlying mechanisms in chondrocytes in vitro. Following transfection with a vector expressing integrin-β1, our results revealed that the overexpression of integrin-β1 enhanced GIT1 expression, whereas the knockdown of integrin-β1 by siRNA suppressed GIT1 expression. However, no significant effect was observed on integrin-β1 expression following the enforced overexpression of GIT1, which suggests that GIT1 is localized downstream of integrin-β1. In other words, integrin-β1 regulates the expression of GIT1. Furthermore, this study demonstrated that integrin-β1 and GIT1 increased the expression levels of aggrecan and type II collagen, thus promoting chondrocyte proliferation; however, they inhibited chondrocyte apoptosis. Taken together, our data demonstrate that integrin-β1 plays a vital role in chondrocyte proliferation, differentiation and apoptosis. GIT1 exerts effects similar to those of integrin-β1 and is a downstream target of integrin-β1.
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http://dx.doi.org/10.3892/ijmm.2015.2114 | DOI Listing |
Aim: This study was conducted to evaluate the in vitro effects of hydroxychloroquine (HCQ) on histone deacetylase (HDAC) enzyme activity and interleukin (IL)-6, IL-10, and tumor necrosis factor-alpha (TNF-α) expression. HDAC enzyme activity and the expression of inflammation markers were tested, with the presence of the HDAC inhibitor valproic acid, in human primary cell cultures prepared from two different tissues.
Material And Methods: Primary cell cultures were prepared.
Mater Today Bio
February 2025
Institute of Orthopedics, The Fourth Medical Center of Chinese PLA General Hospital, Beijing Key Lab of Regenerative Medicine in Orthopedics, Key Laboratory of Musculoskeletal Trauma & War Injuries PLA, No. 51 Fucheng Road, Beijing, 100048, PR China.
Due to its unique structure, articular cartilage has limited self-repair capacity. Microtissues are tiny tissue clusters that can mimic the function of target organs or tissues. Using cells alone for microtissue construction often results in the formation of necrotic cores.
View Article and Find Full Text PDFInt J Rheum Dis
January 2025
Department of Orthopaedics, Shaanxi Rehbilitation Hospital, Xi'an, Shaanxi, China.
Background: Osteoarthritis (OA) is one of the most common bone disorders and has a serious impact on the quality of life of patients. LncRNA-HCP5 (HCP5) is downregulated in OA tissues. However, the latent function and regulatory mechanisms of HCP5 in OA are unclear.
View Article and Find Full Text PDFACS Biomater Sci Eng
January 2025
Chair and Department of Biochemistry and Biotechnology, Medical University of Lublin, Chodzki 1 Street, 20-093 Lublin, Poland.
The aim of this work is to provide a comprehensive set of biological tests to assess the biomedical potential of novel osteochondral scaffolds with methods proposed to comply with the 3Rs principle, focusing here on a biphasic Curdlan-based osteochondral scaffold as a promising model biomaterial. experiments include the evaluation of cytotoxicity, mutagenicity, and genotoxicity referring to ISO standards, the assessment of the viability and proliferation of human chondrocytes and osteoblasts, and the estimation of inflammation after direct contact of biomaterials with human macrophages. experiments include assessments of the response of the surrounding osteochondral tissue after incubation with the implanted biomaterial.
View Article and Find Full Text PDFRegen Ther
June 2024
Center for Regenerative Medicine, National Center for Child Health and Development Research Institute, Tokyo, Japan.
Introduction: Repairing damaged cartilage poses significant challenges, particularly in cases of congenital cartilage defects such as microtia or congenital tracheal stenosis, or as a consequence of traumatic injury, as the regenerative potential of cartilage is inherently limited. Stem cell therapy and tissue engineering offer promising approaches to overcome these limitations in cartilage healing. However, the challenge lies in the size of cartilage-containing organs, which necessitates a large quantity of cells to fill the damaged areas.
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