Filtered By:
Condition: Osteoarthritis
Procedure: Gastroschisis Repair

This page shows you your search results in order of relevance.

Order by Relevance | Date

Total 26 results found since Jan 2013.

Notch signalling pathways mediate synovial angiogenesis in response to vascular endothelial growth factor and angiopoietin 2
Conclusions Notch-1 mediates VEGF/Ang2-induced angiogenesis and EC invasion in inflammatory arthritis.
Source: Annals of the Rheumatic Diseases - May 10, 2013 Category: Rheumatology Authors: Gao, W., Sweeney, C., Walsh, C., Rooney, P., McCormick, J., Veale, D. J., Fearon, U. Tags: Open access, Immunology (including allergy), Pathology, Radiology, Degenerative joint disease, Musculoskeletal syndromes, Osteoarthritis, Surgical diagnostic tests, Clinical diagnostic tests Basic and translational research Source Type: research

Involvement of ERCC1 in the pathogenesis of osteoarthritis through the modulation of apoptosis and cellular senescence
In this study we investigated the function of ERCC1 in chondrocytes and its association with the pathophysiology of OA. ERCC1 expression in normal and osteoarthritic cartilage was assessed, as were changes in ERCC1 expression in chondrocytes under catabolic stress. Inhibiting ERCC1 in chondrocytes under interleukin‐1β stimulation using small interfering RNA (siRNA) was also evaluated. Finally, cellular senescence and apoptosis were examined in relation to ERCC1 function. ERCC1 expression was decreased in OA cartilage and increased within 4 h of exposure to interleukin (IL)‐1β, but decreased after 12 h. The inhibi...
Source: Journal of Orthopaedic Research - June 25, 2014 Category: Orthopaedics Authors: Koji Takayama, Yohei Kawakami, Sahnghoon Lee, Nick Greco, Mitra Lavasani, Yutaka Mifune, James H. Cummins, Takashi Yurube, Ryosuke Kuroda, Masahiro Kurosaka, Freddie H. Fu, Johnny Huard Tags: Research Article Source Type: research

Enhanced SOCS3 in osteoarthiritis may limit both proliferation and inflammation.
Abstract Osteoarthritis (OA) is a degenerative joint disease that is characterized by localized inflammatory and secondary proliferative changes. Suppressor of cytokine signaling 3 (SOCS3) is elevated during OA development. We investigated the effects of this protein on human chondrocyte survival in OA and the inflammatory response together with the mechanisms of these effects. Small interfering RNA (siRNA) was used to knock down the expression of SOCS3 in interleukin(IL)-1β-induced primary human osteoarthritic chondrocytes. We found that siRNA-mediated SOCS3 knock-down in human osteoarthritic chondrocytes increa...
Source: Biotechnic and Histochemistry - March 19, 2017 Category: Research Authors: Gui T, He BS, Gan Q, Yang C Tags: Biotech Histochem Source Type: research

Circadian Rhythm Protein Bmal1 Modulates Cartilage Gene Expression in Temporomandibular Joint Osteoarthritis via the MAPK/ERK Pathway
The purpose of this study was to elucidate the role of the circadian gene Bmal1 in human cartilage and its crosstalk with the MAPK/ERK signaling pathway in temporomandibular joint osteoarthritis (TMJ-OA). We verified the periodical variation of the circadian gene Bmal1 and then established a modified multiple platform method (MMPM) to induce circadian rhythm disturbance leading to TMJ-OA. IL-6, p-ERK, and Bmal1 mRNA and protein expression levels were assessed by real-time RT-PCR and immunohistochemistry. Chondrocytes were treated with an ERK inhibitor (U0126), siRNA and plasmid targeting Bmal1 under IL-6 simulation; then, ...
Source: Frontiers in Pharmacology - September 17, 2020 Category: Drugs & Pharmacology Source Type: research

Integrin-β1 regulates chondrocyte proliferation and apoptosis through the upregulation of GIT1 expression.
Abstract 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 th...
Source: International Journal of Molecular Medicine - February 26, 2015 Category: Molecular Biology Authors: Zhang LQ, Zhao GZ, Xu XY, Fang J, Chen JM, Li JW, Gao XJ, Hao LJ, Chen YZ Tags: Int J Mol Med Source Type: research

Role of IFT88 in icariin ‑regulated maintenance of the chondrocyte phenotype.
Role of IFT88 in icariin‑regulated maintenance of the chondrocyte phenotype. Mol Med Rep. 2018 Jan 25;: Authors: Xiang W, Zhang J, Wang R, Wang L, Wang S, Wu Y, Dong Y, Guo F, Xu T Abstract Maintenance of the chondrocyte phenotype is crucial for cartilage repair during tissue engineering. Intraflagellar transport protein 88 (IFT88) is an essential component of primary cilia, shuttling signals along the axoneme. The hypothesis of the present study was that IFT88 could exert an important role in icariin‑regulated maintenance of the chondrocyte phenotype. To this end, the effects of icariin on prolife...
Source: Molecular Medicine Reports - February 4, 2018 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

Exosomal KLF3-AS1 from hMSCs promoted cartilage repair and chondrocyte proliferation in osteoarthritis.
This study was designed to explore whether exosomal lncRNA-KLF3-AS1 derived from human mesenchymal stem cells (hMSCs) can serve as a positive treatment for osteoarthritis (OA). hMSCs and MSC-derived exosomes (MSC-exo) were prepared for morphological observation and identification by transmission electron microscopy (TEM) and flow cytometry. IL-1β-induced OA chondrocytes and collagenase-induced rat model of OA were established for the further experiments. Lentivirus mediated siRNA targeting KLF3-AS1 was transfected into MSCs for silencing KLF3-AS1. The real-time quantitative PCR (qRT-PCR) and western blotting analysis were...
Source: The Biochemical Journal - October 19, 2018 Category: Biochemistry Authors: Liu Y, Zou R, Wang Z, Wen C, Zhang F, Lin F Tags: Biochem J Source Type: research

Exosomal KLF3-AS1 from hMSCs promoted cartilage repair and chondrocyte proliferation in osteoarthritis
The present study was designed to explore whether exosomal lncRNA-KLF3-AS1 derived from human mesenchymal stem cells (hMSCs) can serve as a positive treatment for osteoarthritis (OA). hMSCs and MSC-derived exosomes (MSC-exo) were prepared for morphological observation and identification by transmission electron microscopy and flow cytometry. IL-1β-induced OA chondrocytes and collagenase-induced rat model of OA were established for the further experiments. Lentivirus-mediated siRNA targeting KLF3-AS1 was transfected into MSCs for silencing KLF3-AS1. The real-time quantitative PCR and western blotting analysis were perf...
Source: Biochemical Journal - November 28, 2018 Category: Biochemistry Authors: Liu, Y., Zou, R., Wang, Z., Wen, C., Zhang, F., Lin, F. Tags: Research Articles Source Type: research

Heparan Sulfate Proteoglycan Synthesis is Dysregulated in Human Osteoarthritic Cartilage.
Abstract Osteoarthritis (OA) is a common degenerative joint disease, characterized by cartilage loss and subchondral bone remodelling in response to abnormal mechanical load. Heparan sulfate (HS) proteoglycans bind to many proteins that regulate cartilage homeostasis, including growth factors, morphogens, proteases, and their inhibitors, and modulate their localization, retention, and biological activity. Changes in HS expression and structure may thus have important consequences for joint health. We analyzed normal and osteoarthritic human knee cartilage, and found HS biosynthesis was markedly disrupted in OA, wi...
Source: The American Journal of Pathology - December 13, 2018 Category: Pathology Authors: Chanalaris A, Clarke H, Guimond SE, Vincent TL, Turnbull JE, Troeberg L Tags: Am J Pathol Source Type: research

FKN Facilitates HK-2 Cell EMT and Tubulointerstitial Lesions via the Wnt/ β-Catenin Pathway in a Murine Model of Lupus Nephritis
In this study, we therefore examined whether FKN could stimulate the process of EMT, NF-kB, TGFβ, CCL22, F4/80, inflammation, and tubulointerstitial fibrosis in a murine model of LN. We also determined whether FKN was involved in the EMT process of Wnt/β-catenin-expressing HK-2 cells. Mechanistically, we ascertained, for the first time, whether FKN up-regulated EMT-related gene signatures (e.g., vimentin, α-SMA), and hence, renal tubulointerstitial fibrogenesis, and the role of the Wnt/β-catenin signaling pathway in this process. Materials and Methods Cell Culture, Stable Infection, and Gr...
Source: Frontiers in Immunology - April 29, 2019 Category: Allergy & Immunology Source Type: research

Pin1-mediated regulation of articular cartilage stem/progenitor cell aging
In this study, we investigated the role of Pin1 in the aging of rat knee joint CSPCs. We isolated CSPCs from rat knee joints and demonstrated that, in long-term in vitro culture, Pin1 protein levels are significantly reduced. At the same time, expression of the senescence-related β-galactosidase and the senescence marker p16INK4A were markedly elevated. In addition, Pin1 overexpression reversed the progression of cellular senescence, as evidenced by the down-regulation of senescence-related β-galactosidase, increased EdU positive cells and diminished levels of p16INK4A. In contrast, Pin1 siRNA incorporation promoted CSPC...
Source: Tissue and Cell - March 1, 2022 Category: Cytology Authors: Xiao Zhang Weiwei Sun Weijie Wu Minhao Chen Tianyi Ji Hua Xu Youhua Wang Source Type: research

Chondroitin sulfate modified chitosan nanoparticles as an efficient and targeted gene delivery vehicle to chondrocytes
In conclusion, CH-CS nanoparticles can be considered as a candidate for gene therapy purposes in cartilage diseases.PMID:36049252 | DOI:10.1016/j.colsurfb.2022.112786
Source: Colloids and Surfaces - September 1, 2022 Category: Biotechnology Authors: Naghmeh Akbari Moghadam Fatemeh Bagheri Mohamadreza Baghaban Eslaminejad Source Type: research