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Results for “Connective Tissue Cells”

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At least 91 records · Page 5Linked to original sources
PubMed1975

Intranuclear silicon detection in a subcutaneous connective tissue cell by energy-dispersive x-ray miscroanalysis using fresh air-dried spread.

Silicon was detected by energy-dispersive x-ray microanalysis in the nucleus of a subcutaneous connective tissue cell of mice fed normally. To eliminate contamination, pieces of connective tissue were spread on copper grids and examined without any treatment by an energy-dispersive spectrometer with a scanning transmission apparatus attached to an electron microscope. Scanning transmission electron microscopy of the spread has demonstrated a well-preserved ultrastructure. Fibrous structures, nuclei and nucleoli of cells and mitochondrial granules were recognized. Electron probe analysis showed peaks for silicon at three spots on the nucleus of a cell in addition to those for phosphorus, sulfur, chlorine, potassium and calcium, whereas no peak of silicon could be detected at the spots on nuclei of other cells, mitochondrial granules and electron-lucent area on the same grid as the above. Silicon appears to play a significant role in the nucleus. Applicability of the technique to know the distribution of easily contaminating elements and diffusible substances is shown.

Air↗
PubMed1981

[Transformation of connective tissue cells by pathological altered synovial fluid as demonstrated by experimental studies (author's transl)].

Joint cavities and tendon sheaths are fissurations in the mesenchyme. The coating synovial lining cell layer is caused through the environment of the synovial fluid. The pathologically altered synovial fluid initiates the transformation and proliferation of the marginal connective tissue cells. Evidence for this thesis are the synovial transformatory processes of the cutaneous connective tissue in the area of a synovial fistula and the formation of synovial like structures in the subcutaneous fatty tissues of the rat following the application of synovial fluid from patients with rheumatoid arthritis.

Animals↗
PubMed2002

The chitinase 3-like protein human cartilage glycoprotein 39 (HC-gp39) stimulates proliferation of human connective-tissue cells and activates both extracellular signal-regulated kinase- and protein kinase B-mediated signalling pathways.

Human cartilage glycoprotein 39 (HC-gp39) is a glycoprotein secreted by articular chondrocytes, synoviocytes and macrophages. Increased levels of HC-gp39 have been demonstrated in synovial fluids of patients with rheumatoid or osteoarthritis. The increased secretion of HC-gp39 under physiological and pathological conditions with elevated connective-tissue turnover suggests its involvement in the homoeostasis of these tissues. We report here that HC-gp39 promotes the growth of human synovial cells as well as skin and fetal lung fibroblasts. A dose-dependent growth stimulation was observed when each of the fibroblastic cell lines was exposed to HC-gp39 in a concentration range from 0.1 to 2 nM, which is similar to the effective dose of the well-characterized mitogen, insulin-like growth factor-1. At suboptimal concentrations, the two growth factors work in a synergistic fashion. The use of selective inhibitors of the mitogen-activated protein kinase and the protein kinase B (AKT) signalling pathways indicates that both are involved in mediating the mitogenic response to HC-gp39. Phosphorylation of both extracellular signal-regulated kinases 1/2 and AKT occurred in a dose- and time-dependent fashion upon addition of HC-gp39. Activation of these signalling pathways could also be demonstrated in human chondrocytes. Thus HC-gp39 initiates a signalling cascade in connective-tissue cells which leads to increased cell proliferation, suggesting that this protein could play a major role in the pathological conditions leading to tissue fibrosis.

Adipokines↗
PubMed1978

Organization of extracellular proteins on the connective tissue cell surface: relevance to cell-matrix interactions in vitro and in vivo.

A model has been developed that proposes a cell surface-associated protein meshwork, composed in part of fibronectin and collagen, for a connective tissue cell attached to a substratum. In support of this model are the observations that collagen and fibronectin interact and that these proteins are similarly distributed on the fibroblast cell surface. We suggest that this external meshwork interacts directly or indirectly with the internal cytoskeleton and with the extracellular matrix and thereby mediates several cellular properties, including adhesion, shape, and motility. Loss of cell surface fibronectin as a result of viral transformation, or due to treatment of normal cells with tunicamycin, an inhibitor of protein glycosylation, may contribute to the reduced adhesion and altered morphology observed in these circumstances. We therefore predict that the changes in these properties observed with virally transformed cells, mitotic cells, and cells treated with proteolytic enzymes are related to alterations in the external protein meshwork.

Animals↗
PubMed1978

Connective tissue activation. XIII. Stimulation of sulfated glycosaminoglycan synthesis in human connective tissue cells by peptide mediators from lymphocytes and platelets.

CTAP-I from lymphocytes and CTAP-III from platelets markedly stimulated 35SO4= incorporation into chondroitin 4/6 sulfate and dermatan sulfate synthesized by human synovial, dermal, and cartilage connective tissue cells in vitro. These agonists promoted synthesis of the GAG carbon chain as well as sulfate incorporation. Both RNA and protein synthesis were required for these mediators to be effective in stimulating synthesis of connective tissue matrix components. A major part of the capacity of normal serum to stimulate sulfate incorporation into GAG's may reside in CTAP-III.

Blood Platelets↗
PubMed1997

Platelet-derived growth factor: a key regulator of connective tissue cells in embryogenesis and pathogenesis.

Studies of PDGF-A, PDGF-B and PDGF receptor-beta knock-out mice have revealed critical functions for the PDGF-PDGF receptor signaling systems in the ontogeny of connective tissue cells: the mesangial cells of kidney glomeruli and the alveolar smooth muscle cells (SMC) of the lung. The phenotypes of the PDGF mutant mice have also shed light on the identity and functions of these cell types, as well as revealed analogies suggesting that common morphogenetic principles have evolved for use in different organs, involving related growth factors and cell types. Although the lethality of PDGF knock-out mice has not allowed an investigation of the role of PDGF in SMC of the vessel wall, regulation of PDGF and its receptors in adult vessels following injury is consistent with a role for PDGF in the fibroproliferative response in the intima that occurs as part of the pathogenesis of atherosclerosis. PDGF modulation of connective tissue synthesis may thus be critical to connective tissue phenotype and proliferation in both embryogenesis and pathogenesis.

Animals↗
PubMed1979

Activation of lung connective tissue cells in vitro.

Guinea pig lung fibroblasts "activated" in vitro by exposure to connective tissue-activating peptides I and III, and guinea pig tissue extracts showed enhanced glycolysis and accelerated glycosaminoglycan synthesis. Formation of hyaluronic acid, and to a lesser extent, chondroitin 4/6-sulfate was stimulated by these agents.

Animals↗
PubMed1987

[Effect of actinomycin D on the survival and recovery capacity of irradiated connective tissue cells in the Chinese hamster].

Simultaneous treatment of Chinese hamster fibroblasts with Actinomycin D and gamma rays under normal aerobic conditions leads to radiosensitization. In contrast to Actinomycin D pretreatment, modification to the effect of radiation is drug dose dependent in the case of post-treatment. No effect of Actinomycin D upon the shape of the radiation cell survival curve is seen under hypoxic conditions. Recovery from radiation damage in split dose experiments is not influenced by the drug.

Anaerobiosis↗
PubMed1989

[Thermolabile inhibiting proliferation of connective tissue cell activity from platelets].

The action of a platelet extract (PE) and a heat-inactivated PE on 3T3 cells proliferation has been investigated. The heat-inactivated PE and platelet poor plasma (PPP) together can promote cell proliferation like fetal calf serum. At the same time PE inhibits proliferation of the cell culture stimulated by 5% fetal calf serum, whereas the heat-inactivated PE does not. Although the actions of 2% PE and 2% heat-inactivated PE on the cells incubated with PPP are equal, the stimulating effect of a 10% heat-inactivated PE is higher than that of a 10% PE. Thus, the inhibitor acts only at high concentrations. The role of the platelet-derived inhibitor in the limiting of extensive cell proliferation during vessel wall injury repair is discussed.

Blood Platelets↗