Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Interleukin-1β and tumor necrosis factor-α increase stiffness and impair contractile function of articular chondrocytes.

Acta biochimica et biophysica Sinica - 1 Feb 2015

Chen Cheng, Xie Jing, Rajappa Ravikumar, Deng Linhong, Fredberg Jeffrey, Yang Liu

Abstract excerpt

Interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) are major proinflammatory cytokines involved in osteoarthritis (OA). These cytokines disturb chondrocyte metabolism by suppressing the synthesis of extracellular matrix proteins and stimulating the release of catabolic proteases, but little is known about their role in chondrocyte mechanics. Thus, the aim of this study was to measure the effects of IL-1β...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Chondrocytes
Share to Elasticity

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Histamine

Share to Interleukin-1beta

Share to Osteoarthritis

Share to Peptide Hydrolases

Share to Stress, Mechanical

Source

Open in PubMed Open full text

Identifiers

PMID: 25520178
DOI: 10.1093/abbs/gmu116
PMCID: PMC4351355

Genes

TNF

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Interleukin-1β and tumor necrosis factor-α increase stiffness and impair contractile function of articular chondrocytes.PMID 25520178Read ↗

Articular Chondrocyte Phenotype Regulation through the Cytoskeleton and the Signaling Processes That Originate from or Converge on the Cytoskeleton: Towards a Novel Understanding of the Intersection between Actin Dynamics and Chondrogenic Function.Semantic proximity Read ↗

IL-6, IL-1β and TNF-α regulation of the chondrocyte phenotype: a possible mechanism of haemophilic cartilage destruction.Semantic proximity Read ↗

IL-1β Regulates FHL2 and Other Cytoskeleton-Related Genes in Human ChondrocytesSemantic proximity Read ↗

Regulation of Chondrocytic Gene Expression by Biomechanical SignalsSemantic proximity Read ↗

Osteoarthritis: articular chondrocyte inflammatory signaling leads to enhanced gene expression and function of mechanotransduction channel Piezo1 as a pathogenic feed-forward mechanismSemantic proximity Read ↗

Transforming growth factor alpha suppression of articular chondrocyte phenotype and Sox9 expression in a rat model of osteoarthritis.Semantic proximity Read ↗

Mechanotransduction and Stiffness-Sensing: Mechanisms and Opportunities to Control Multiple Molecular Aspects of Cell Phenotype as a Design Cornerstone of Cell-Instructive Biomaterials for Articular Cartilage Repair.Semantic proximity Read ↗

PTHrP overexpression partially inhibits a mechanical strain-induced arthritic phenotype in chondrocytes.Semantic proximity Read ↗

Cell geometry dictates TNFα-induced genome responseSemantic proximity Read ↗

Viscoelastic Hydrogel Modulates Phenotype of Macrophage-Derived Multinucleated Cells and Macrophage Differentiation in Foreign Body Reactions.Semantic proximity Read ↗

Catabolic cytokines disrupt the circadian clock and the expression of clock-controlled genes in cartilage via an NFкB-dependent pathwaySemantic proximity Read ↗

Effect of Micro-strain Stress on in Vitro Proliferation and Functional Expression of Human Osteoarthritic ChondrocytesSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.