PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 2011834

[Arthritis from a biochemical aspect].

A Baici
View original source ↗Export metadata ↓

Abstract

The dynamic processes of remodeling and cartilage destruction occurring in osteoarthritis are associated with an altered metabolism of the chondrocytes. Two mechanisms can be made responsible for chondrocyte activation: Stimulation by cytokines (mainly interleukin-1) and phenotypic modulation. Remodeling of osteoarthritic joint structures is associated with cell proliferation and neovascularization, while erosion of the articular cartilage is promoted by a variety of endopeptidases of chondrocytic origin. These aspects are briefly reviewed in the light of recent findings.

Explore related subjects

Cartilage, ArticularEndopeptidasesHumansInterleukin-1OsteoarthritisPhenotypeEnglish AbstractJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

A Baici. 1991. [Arthritis from a biochemical aspect].. https://pubmed.ncbi.nlm.nih.gov/2011834/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2006

Novel fast semi-automated software to segment cartilage for knee MR acquisitions.

OBJECTIVE: Validation of a new fast software technique to segment the cartilage on knee magnetic resonance (MR) acquisitions. Large studies of knee osteoarthritis (OA) will require fast and reproducible methods to quantify cartilage changes for knee MR data. In this report we document and measure the reproducibility and reader time of a software-based technique to quantify the volume and thickness of articular cartilage on knee MR images. METHODS: The software was tested on a set of duplicate sagittal three-dimensional (3D) dual echo steady state (DESS) acquisitions from 15 (8 OA, 7 normal) subjects. The repositioning, inter-reader, and intra-reader reproducibility of the cartilage volume (VC) and thickness (ThC) were measured independently as well as the reader time for each cartilage plate. The root-mean square coefficient of variation (RMSCoV) was used as metric to quantify the reproducibility of VC and mean ThC. RESULTS: The repositioning RMSCoV was as follows: VC=2.0% and ThC=1.2% (femur), VC=2.9% and ThC=1.6% (medial tibial plateau), VC=5.5% and ThC=2.4% (lateral tibial plateau), and VC=4.6% and ThC=2.3% (patella). RMSCoV values were higher for the inter-reader reproducibility (VC: 2.5-8.6%) (ThC: 1.9-5.2%) and lower for the intra-reader reproducibility (VC: 1.6-2.5%) (ThC: 1.2-1.9%). The method required an average of 75.4min per knee. CONCLUSIONS: We have documented a fast reproducible semi-automated software method to segment articular cartilage on knee MR acquisitions.

Cartilage, Articular↗
PubMed2006

Expression and function of TbetaRII-B, a variant of the type II TGF-beta receptor, in human chondrocytes.

OBJECTIVE: Transforming growth factor-beta (TGF-beta) has profound effects on chondrocyte proliferation and matrix production, and dysregulation of TGF-beta action has been implicated in osteoarthritis. The mechanisms by which the diverse actions of TGF-beta are regulated in chondrocytes are unclear. Although it is well documented that TGF-beta signaling is transduced by types I and II receptors, other TGF-beta receptors may play critical roles by regulating signaling receptor activity. Our objective was to examine the expression of TbetaRII-B, a splice variant of the type II TGF-beta receptor, and to analyze its role in regulating TGF-beta signaling in human chondrocytes. METHODS: TbetaRII-B expression was examined in human cartilage tissue specimens, human chondrocyte cell lines C28/I2 and tsT/AC62, and human primary chondrocytes by Western blot and reverse-transcriptase-polymerase chain reaction. Ligand binding and heteromerization of TbetaRII-B with other TGF-beta receptors on the cell surface were analyzed by affinity labeling, immunoprecipitation, and two-dimensional SDS-PAGE. Regulation of TGF-beta responses by TbetaRII-B was determined by examining Smad2 phosphorylation, Smad3-specific signaling, transcriptional activity, and type II collagen levels. RESULTS: TbetaRII-B is expressed in normal and osteoarthritic human cartilage. Furthermore, it is a dynamic component of the TGF-beta receptor system in human chondrocytes, forming heteromeric complexes with the types I and II TGF-beta receptors, betaglycan and endoglin. Importantly, overexpression of TbetaRII-B leads to enhanced TGF-beta signaling and responses in chondrocytes. CONCLUSIONS: These results suggest that TbetaRII-B may play a key role in the regulation of TGF-beta action in human chondrocytes.

Cartilage, Articular↗