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Objective: This study was designed to evaluate the combined effects of intermittent hydrostatic pressure (IHP) and TGF-β1 or TNF-α on proteoglycan4 (PRG4) expression in rat temporomandibular synovial fibroblasts (SFs).
Study Design: Rat SFs were isolated and expanded in monolayer cultures and subjected to IHP in the presence of TGF-β1 or TNF-α. Quantitative real-time RT-PCR was applied to analyze the PRG4 expression levels. Enzyme-linked immunosorbent assay was also used for the quantification of PRG4 accumulation in the culture medium while immunofluorescence staining was used to detect intracellular PRG4 protein expression.
Results: The combination of IHP and TGF-β1 induced greater PRG4 expression than either stimulus alone. In contrast, TNF-α inhibited PRG4 expression, and this was partially alleviated by IHP.
Conclusions: Our study demonstrates a beneficial role of IHP, which can be used successfully in combination with TGF-β1 to enhance PRG4 production, and can partially counteract TNF-α-induced PRG4 inhibition in isolated rat SFs.
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http://dx.doi.org/10.1016/j.tripleo.2011.07.001 | DOI Listing |
Cartilage
August 2025
Department of Biological Sciences, University of Delaware, Newark, DE, USA.
BackgroundCell-based therapies to regenerate native-like cartilage are limited by the inability to re-express zone-specific molecules. While monolayer-expanded (passaged) chondrocytes are a clinically approved cell source, the resulting tissues have reduced Proteoglycan-4 (PRG4) expression. This may be due to poor attachment, slow proliferation, and dedifferentiation of superficial zone chondrocytes (SZC) on polystyrene.
View Article and Find Full Text PDFInt J Mol Sci
August 2025
Department of Medicine for Sports and Performing Arts, Graduate School of Medicine, The University of Osaka, Osaka 565-0871, Japan.
Osteoarthritis (OA) is the most common joint disorder worldwide. Autologous chondrocyte implantation (ACI) is an established treatment for articular cartilage defects of the knee, but its effectiveness in OA is still under investigation. In this study, we investigated the effects of a newly developed mammalian-derived collagen matrix, NC-Col, on the proliferation, migration, adhesion, and gene expression of human articular cartilage-derived chondrocytes from OA patients in vitro, using proliferation assays, wound healing assays, adhesion assays, RT-qPCR, and RNA sequencing, respectively.
View Article and Find Full Text PDFMod Rheumatol Case Rep
July 2025
Medical Genetics Diagnosis Laboratory, Near East University Hospital, Nicosia, Cyprus.
Camptodactyly-arthropathy-coxa vara-pericarditis syndrome (CACP) is an example of a rare non-inflammatory familial arthropathy inherited in an autosomal recessive manner. The proteoglycan 4 (PRG4) gene, located on chromosome 1q25-q31, is responsible for encoding a lubricating glycoprotein found in the synovial fluid and on the surface of articular cartilage. Pathogenic mutations in the PRG4 gene have been associated with CACP disease.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
August 2025
Department of Orthopaedic Surgery, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104.
Clinically, compromised fracture healing often occurs at sites with less muscle coverage and muscle flaps can provide the necessary healing environment for appropriate healing in severe bone loss. However, the underlying mechanisms are largely unknown. Here, we established a mouse reporter model for studying muscle cell contribution to bone fracture repair.
View Article and Find Full Text PDFComput Biol Chem
December 2025
Artificial Intelligence Center for Health and Biomedical Research (ArCHER), National Institutes of Biomedical Innovation, Health and Nutrition, 17-3 Senrioka-Shinmachi, Settu, Osaka 566-0002, Japan; Institute for Protein Research, The University of Osaka, 3-2 Yamadaoka, Suita, Osaka 565-0871, Japan.
Idiopathic pulmonary fibrosis (IPF) is an independent risk factor for lung cancer, especially squamous cell carcinoma (SCC). The prognosis of patients with both IPF and SCC is poorer than that of patients with only IPF, and preventive measures against SCC in patients with IPF remain elusive. Understanding the distinct mechanisms that induce both diseases is crucial for mitigating SCC onset in patients with IPF.
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