Effects of transforming growth factor betas and basic fibroblast growth factor on articular chondrocytes obtained from immobilised rabbit knees
Article Abstract:
Transforming growth factor B1 (TGFB1), TGFB2, and basic fibroblast growth factor (bFGF) may play a role in the repair of joint cartilage. Mature cartilage cells called chondrocytes produce these growth factors. Researchers studied the joint tissue of 32 rabbit knees immobilized with a splint for evidence of joint damage 0, four, seven, 14, 28, and 42 days after splinting. They also measured the response of joint chondrocytes to TGFB1, TGFB2, and bFGF at the same time points. Tissue samples showed progressive joint damage over the 42-day study period. Chondrocyte production was 2.5 to 4.5 times higher in the presence of all three growth factors seven days after splinting. This effect decreased 14 days after splinting. At four, seven, and 14 days after splinting, there was an additive effect in stimulating chondrocyte production with TGFB2 and bFGF. There was no response to the growth factors at the 42-day time point.
Publication Name: Annals of the Rheumatic Diseases
Subject: Health
ISSN: 0003-4967
Year: 1996
User Contributions:
Comment about this article or add new information about this topic:
Synergism between muramyl dipeptide and lipopolysaccharide in the inhibition of glycosaminoglycan synthesis in cultured rat costal chondrocytes
Article Abstract:
Muramyl dipeptide may increase the affect of lipopolysaccharide on cartilage breakdown in patients suffering from inflammatory joint diseases such as rheumatoid arthritis. Muramyl dipeptide and lipopolysaccharide are different components of the bacterial cell wall. A study examined the effect of lipopolysaccharide, muramyl dipeptide and interleukin-1 (IL-1) on cartilage degradation in rat chondrocytes, or cartilage cells. Muramyl dipeptide alone did not affect cartilage degradation, but it enhanced the inhibitory affect of lipopolysaccharide on cartilage production. Activated substances similar in structure to muramyl dipeptide also increased the affect of lipopolysaccharide on cartilage production, but the inactivated forms of these substances had no effect. Lipid A may be the one of the three subunits that compose lipopolysaccharide that causes cartilage degradation.
Publication Name: Annals of the Rheumatic Diseases
Subject: Health
ISSN: 0003-4967
Year: 1993
User Contributions:
Comment about this article or add new information about this topic:
Phenotypic modulation of chondrocytes as a potential therapeutic target in osteoarthritis: a hypothesis
Article Abstract:
A change in the expression of certain types of collagen by cartilage cells called chondrocytes may be responsible for the destruction of cartilage in osteoarthritis. Researchers propose three steps in the destruction of cartilage. First there is an increase in collagen type II and aggrecan synthesis. Then the chondrocyte begins producing collagen type III and finally, the synthesis of aggrecan core protein and collagen types II and III is suppressed. This leads to the loss of extracellular matrix. It also physically damages the collagen network, leading to cartilage destruction.
Publication Name: Annals of the Rheumatic Diseases
Subject: Health
ISSN: 0003-4967
Year: 1997
User Contributions:
Comment about this article or add new information about this topic:
- Abstracts: Effects of disease stage and zidovudine therapy on the detection of human immunodeficiency virus type 1 in semen
- Abstracts: Geriatric medicine. Ultralow-dose micronized 17beta-estradiol and bone density and bone metabolism in older women: a randomized controlled trial
- Abstracts: Diet and blood coagulation factor VII - a key protein in arterial thrombosis. An eight-month controlled study of a low-fat high-fibre diet: effects on blood lipids and blood pressure in healthy young subjects
- Abstracts: Congress in Dallas: focus on the future. Tough issues addressed at congress. Congress Blockbusters explore today's hot issues
- Abstracts: Misconceptions about cancer among Latinos and Anglos. Sudden traumatic death in children: "We did everything but your child didn't survive"