Results 151 to 160 of about 244,346 (227)

IHH–GLI-1–HIF-2α signalling influences hypertrophic chondrocytes to exacerbate osteoarthritis progression

open access: yesJournal of Orthopaedic Translation
Background: Chondrocyte hypertrophy is a potential target for osteoarthritis (OA) treatment, with Indian hedgehog (IHH), glioma-associated oncogene homolog (GLI), and hypoxia-inducible factor-2α (HIF-2α) being closely associated with chondrocyte ...
Chengming Zhang   +12 more
doaj   +1 more source

miR-892b Inhibits Hypertrophy by Targeting KLF10 in the Chondrogenesis of Mesenchymal Stem Cells

open access: yesMolecular Therapy: Nucleic Acids, 2019
We investigated the functional role of miR-892b as a novel inhibitor of chondrocyte hypertrophy during TGF-β-mediated chondrogenesis of human mesenchymal stem cells (hMSCs). The expression of miR-892b during TGF-β-mediated chondrogenesis of hMSCs and the
Jong Min Lee   +5 more
doaj   +1 more source

Cordycepin inhibits chondrocyte hypertrophy of mesenchymal stem cells through PI3K/Bapx1 and Notch signaling pathway

open access: yesBMB Reports, 2016
Mesenchymal stem cells (MSCs) are widely used in cartilage tissue engineering to repair articular cartilage defects. However, hypertrophy of chondrocytes derived from MSCs might hinder the stabilization of hyaline cartilage. Thus, it is very important to
Z. Cao   +9 more
semanticscholar   +1 more source

Role of miR-101a in targeting Cox-2 to attenuate chondrocyte hypertrophic differentiation and osteoarthritis progression

open access: yesGenes and Diseases
MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression post-transcriptionally, often playing critical roles in various biological processes.
Rui Mi   +11 more
doaj   +1 more source

Notch signaling indirectly promotes chondrocyte hypertrophy via regulation of BMP signaling and cell cycle arrest

open access: yesScientific Reports, 2016
Cell cycle regulation is critical for chondrocyte differentiation and hypertrophy. Recently we identified the Notch signaling pathway as an important regulator of chondrocyte proliferation and differentiation during mouse cartilage development.
X. Shang   +7 more
semanticscholar   +1 more source

Modulation of TGF-beta signaling by proinflammatory cytokines in articular chondrocytes. [PDF]

open access: yes, 2007
OBJECTIVE: The normal structure and function of articular cartilage are the result of a precisely balanced interaction between anabolic and catabolic processes.
Jimenez, Sergio A.   +2 more
core   +1 more source

Cell hypertrophy and type X collagen synthesis in cultured articular chondrocytes

open access: yesExperimental Cell Research, 1991
Articular cartilage is a permanent tissue whose cells do not normally take part in the endochondral ossification process. To determine whether articular chondrocytes possess the potential to express traits associated with this process such as cell hypertrophy and type X collagen, chondrocytes were isolated from adult chicken tibial articular cartilage ...
M, Pacifici   +3 more
openaire   +2 more sources

Osteocyte dysfunction promotes osteoarthritis through MMP13-dependent suppression of subchondral bone homeostasis. [PDF]

open access: yes, 2019
Osteoarthritis (OA), long considered a primary disorder of articular cartilage, is commonly associated with subchondral bone sclerosis. However, the cellular mechanisms responsible for changes to subchondral bone in OA, and the extent to which these ...
Acevedo, Claire   +12 more
core  

Salmon calcitonin inhibited chondrocyte hypertrophy ex vivo [PDF]

open access: yesOsteoarthritis and Cartilage, 2012
Chen-An, P.   +6 more
openaire   +1 more source

Golgi proteomics : Identification of a novel cartilage-specific Golgi protein GoPro49 [PDF]

open access: yes, 2009
The Golgi complex is a central organelle of the secretory pathway, responsible for a range of post-translational modifications, as well as for membrane traffic to the plasma membrane and to the endosomal-lysosomal pathway. In addition, this organelle has
Takatalo, Maarit
core  

Home - About - Disclaimer - Privacy