PubMed Health⌕ Search

Biomedical subjects

F M Desa

Publications and source records attributed to F M Desa.

11 recordsLinked to original sources
PubMed1991

The effects of estrogens on cartilage degradation using in vivo and in vitro models.

We have investigated the effects of estradiol on cartilage breakdown. The model of arthritis used involved the subcutaneous implantation of rat femoral head cartilage (FHCs) into the dorsal region of female mice. The FHCs had been previously wrapped in sterile 5 mg cotton to provoke the growth of granulomatous tissue adjacent to cartilage. Animals were dosed daily, a day after implantation, for 14 days with either 17 beta-estradiol or tamoxifen at different doses. The FHCs were removed and analysed for glycosaminoglycan (GAG) content. The results demonstrated that estradiol accelerated cartilage breakdown in a dose dependent manner, an effect which is blocked by tamoxifen. In addition, estradiol was found to increase cartilage degradation in an in vitro model using FHCs. This effect was enhanced by the addition of fibroblasts.

Animals↗
PubMed1990

The protective effects of cell-free fluid exudate on cartilage degradation in vitro.

In a short-term culture system, polymorphonuclear neutrophils (PMNs) were shown to cause significant loss of glycosaminoglycan (GAG) from cartilage. In addition, a lysate of these cells, and in particular cells stimulated with a phorbol ester, greatly enhanced this loss of GAG. This loss could be partially or completely inhibited by the addition of cell-free fluid exudate to the system. In other long-term culture experiments, IL-1a was shown to enhance fibroblast-induced GAG loss from cartilage. In this system too the breakdown was inhibited by cell-free fluid exudate. Initial characterization of the protective agent or agents shows them to be heat-stable at 56 degrees C and to be non-dialysable. It is proposed that in the chronic inflammatory joint disease, rheumatoid arthritis, the fluid phase of an inflammatory response may have a protective effect against the underlying pathological processes.

Animals↗
PubMed1989

The effect of indomethacin on cartilage breakdown.

The effects of recombinant interleukin-1 alpha (rIL-1 alpha) and indomethacin on the glycosaminoglycan (GAG) content of rat femoral head cartilage (FHC) were studied in vitro. Net GAG loss was observed from cartilage cultured in the presence of indomethacin plus rIL-1 alpha. Indomethacin and rIL-1 alpha alone caused no net loss of GAG from cartilage unless the cartilage was cultured in the presence of fibroblasts.

Animals↗
PubMed1989

Anti-inflammatory effects of endothelin-1.

Endothelin-1 (ET-1), when injected intradermally in rats concurrently with FMLP, did not suppress cell accumulation 6 h later. In view of the fact that ET-1 can antagonize mediators of increased vascular permeability, it is proposed that this is further evidence that fluid and cell accumulation at an inflammatory site are separate processes.

Animals↗
PubMed1989

The effects of heparin and cortisone on an experimental model of pannus.

The effects of heparin and cortisone were investigated in a model of experimental pannus-mediated cartilage degradation. Rat femoral head cartilages were implanted bilaterally (sc.) into female mice either non-wrapped or wrapped in cotton. Animals were treated with tap water (p.o.), heparin 1000 Units (p.o.), cortisone 2 mg/kg (s.c) and heparin-cortisone combined. After 14 days, the implants were removed and analysed for exudate volume, granulation-tissue dry weight and cartilage glycosamino-glycan (GAG) content. In the heparin-treated animals there was a significant (p less than 0.001) increase in the granulation-tissue dry weight, whilst combined treatment significantly (p less than 0.001) reduced both exudate volume and cartilage degradation. It is possible that the effects on angiogenesis may indicate novel treatment for the growth of pannus and cartilage breakdown.

Animals↗
PubMed1989

The chemotactic properties of cartilage glycosaminoglycans for polymorphonuclear neutrophils.

Cartilage breakdown products have been tested for their effects on the locomotion of rat polymorphonuclear neutrophils in vitro. Chondroitin sulphate, keratan sulphate and hyaluronic acid were used in checkerboard migration assays to differentiate chemotaxis from chemokinesis. All test substances showed both chemokinetic and chemotactic activities. The same substances were then injected intradermally to determine their effects on vascular permeability and leukocyte accumulation in vivo. There was no significant effect on vascular permeability 30 minutes after injection as measured by a dye-leakage method. Histological examination of skin sections taken 6 hours after injection showed modest accumulations of polymorphonuclear neutrophils. It is suggested that cartilage breakdown products may account for the persistence of polymorphonuclear neutrophils in some chronic inflammatory joint diseases.

Animals↗
PubMed1989

Myofibroblasts in cotton-induced granulation tissue and the bovine adrenal capsule: morphological aspects.

Ultrastructural studies of one week old cotton-induced granulation tissue revealed the presence of polymorphonuclear neutrophils (PMN), macrophages and mast cells, whilst the granulation tissue from two week old cotton implants contained fibroblasts, myofibroblasts and abundant collagen fibres. Similarly, the bovine adrenal capsule contained both fibroblasts and myofibroblasts. It is proposed that the bovine adrenal capsule and two week cotton-induced granulation tissue could be utilized as in-vitro models to study the mechanism(s) involved in myofibroblast contraction.

Adrenal Glands↗
PubMed1989

Cellular interaction in cartilage degradation.

Rat femoral head cartilages (FHCs) in culture for six days retained their glycosaminoglycan (GAG) content and were not affected by recombinant human interleukin-la (IL-1), conditioned media from concanavalin-A stimulation of sensitized lymphocytes (lymphocyte media), or conditioned media from lymphokine-stimulated macrophages (macrophage media). Similarly FHCs cultured with macrophages in the presence of IL-1, lymphocyte medium or macrophage medium did not suffer a loss of GAG. However, FHCs cultured with fibroblasts showed a substantial loss of GAG. This fibroblast-mediated cartilage degradation was significantly increased by IL-1 and macrophage media respectively. Stimulation of fibroblasts by lymphocyte media failed to increase the loss of GAG. It is proposed that cartilage degradation in inflammatory joint disease is brought about by a sequential cell-to-cell interaction via cytokines leading ultimately to stimulation of fibroblast-mediated cartilage degradation.

Animals↗
PubMed1988

The local modulation of vascular permeability by endothelial cell derived products.

Endothelin has been shown to suppress increased vascular permeability in the rat at doses of 0.01 pmol. The agonists used were nitric oxide and nitroprusside, which have the same activity as endothelial-derived relaxing factor. Histamine, 5-hydroxytryptamine, platelet activating factor and carrageenan were the other agonists used. It is proposed that endothelin and EDRF act as local hormones produced by endothelial cells to control local vascular permeability.

Animals↗