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At least 181 records · Page 10Linked to original sources
PubMed1981

Age-dependent mitogenesis in normal connective tissue cells.

We have previously described ways to use the mesentery for studies of proliferation in intact tissue. Here we have studied a weak and a strong mitogenic response in the mesentery of rats aged 6--42 weeks, induced by a single intraperitoneal injection of saline or the mast-cell-degranulating drug 48/80. Proliferation was measured by the specific DNA activity, the fraction of fibroblast- and mesothelial-like cells in the S+G2 cell-cycle-phases, and the mitotic index. We also counted the relative number of mast cells in the tissue (normalized to 5,000 fibroblast-like and mesothelial-like cells), since this might influence 48/80-induced mast-cell-mediated proliferation. In old animals there was a decline in the proliferative response and the time required to initiate DNA synthesis was prolonged. This appears to be the first report of such an age-dependent proliferation characteristic in the mesentery, and probably in any connective tissue. The normalized number of mast cells in the mesentery also declined with increasing age.

Age Factors↗
PubMed1982

Immunological challenge causes mitogenic stimulation in normal connective tissue cells.

Because polyamine-induced mast-cell secretion causes mitogenesis in surrounding tissue cells in the rat mesentery, we studied whether an immunological challenge in guinea-pig and rat that normally involves mast-cell secretion caused mitogenesis in adjacent normal tissue cells. The appropriate antigen was injected intraperitoneally into pre-sensitized animals. Mast-cell secretion was assessed as histamine release and proliferation by estimating DNA synthesis and mitotic index in the mesentery of the intact animals. In both species the immunological challenge causing significant release of mast-cell histamine was followed by a marked mitogenic response in fibroblasts and mesothelial cells of the mesentery. Although the present study was not primarily designed to study the molecular mechanisms for stimulating cell proliferation, the results suggest that the role of primary mast-cell products on a quantitative basis is significantly different in the mitogenesis following immunological challenge than in polyamine-induced mast-cell mediated mitogenesis in the rat.

Animals↗
PubMed2004

Proliferative activities of epithelial and connective tissue cells in the rat periodontal regeneration using argyrophilic nucleolar organizer regions staining.

BACKGROUND AND OBJECTIVE: It is still an open question why long junctional epithelium can proliferate and occupies the root surface following periodontal surgery or experimentally produced periodontitis, and why the epithelium repopulated once on the root surface is replaced by the connective tissue. The aim of this study is to investigate the proliferative activity of the newly formed regenerative connective tissue and long junctional epithelium during wound healing by staining argyrophilic proteins of the nucleolar organizer regions (AgNORs). METHODS: Regenerative connective tissue and long junctional epithelium were experimentally created by insertion of a rubber piece between maxillary molars of rats for 1 week. After removal of the rubber, AgNORs parameters including nuclear area (NA), AgNORs area (AA), AgNORs percentage nuclear area (APNA), AgNORs number (AN) and nuclear number (NN) in regenerative connective tissue and long junctional epithelium were measured and analyzed statistically. RESULTS: APNA in long junctional epithelium after 1 and 4 weeks was over two times greater than that in the regenerative connective tissue. AA in long junctional epithelium was significantly higher than in regenerative connective tissue at 1 and at 4 weeks post-treatment. AN was higher in the central portion than at the root surface except at 20 weeks. APNA and AA decreased remarkably in long junctional epithelium at 12 weeks post-treatment (approximately half at 4 weeks), whereas in regenerative connective tissue, they did not change distinctly. CONCLUSIONS: These results imply that long junctional epithelium cannot supply sufficient epithelial cells because of their significantly low rates of proliferation, consequently long junctional epithelium becomes shorter after 12 weeks, whereas the proliferative activity of regenerative connective tissue maintains the same level of proliferation, and ultimately long junctional epithelium is replaced by regenerative connective tissue.

Animals↗
PubMed1991

The connective tissue cells of human dental pulp: an histologic and immunohistochemical study.

Twenty human healthy teeth were extracted for orthodontic purposes and processed for histological, and immunohistochemical examination. Odontoblasts were pseudostratified in depth of 1-8 cells in pulpward direction showing the zone of Weil and the cell-rich zone in coronal third pulp. In the central part of pulp tissue, fibroblasts were arranged as a network. These cells strongly immunoreacted with an antibody (monoclonal and polyclonal) directed against the intermediate filament vimentin. The product reaction was specifically located in the cytoplasm. Near vessels occasional lymphocytes and mast cells were also present. Collagen fibers formed a plexus below the cell-rich zone in middle and coronal pulp.

Connective Tissue↗
PubMed1992

Expression of 92 kDa phagocyte gelatinase by inflammatory and connective tissue cells.

It is now apparent that multiple proteinases cooperate in the degradation of the collagenous matrix. Among these proteinases are two biochemically related proteinases which were originally identified by their ability to degrade denatured collagens. The higher molecular weight proteinase (M(r) = 92,000) is predominantly expressed by inflammatory cells while the lower molecular weight proteinase (M(r) = 72,000) is secreted constitutively by fibroblasts. To explore the expression of the 92 kDa proteinase, the gelatinase from human neutrophils was purified and characterized and specific immunologic probes developed for its study in other cell types. Studies of leukemic cell lines (U937s and HL60s) which can be differentiated to a monocyte/macrophage phenotype revealed that after differentiation with phorbol myristic acetate the 92 kDa proteinase was the major proteinase produced. Additional studies of human alveolar macrophages and monocytes differentiated in vitro suggest that these cells secrete a proteinase immunologically and biochemically similar to human neutrophil gelatinase. Although the major gelatinase secreted by the fibroblasts is the 72 kDa proteinase, they also produce the 92 kDa proteinase in a regulated manner. These studies suggest that the regulation of these similar gelatinolytic proteinases varies dependent on cell type. Further studies of their regulation will be important to define the roles of these proteinases in physiologic and pathological processes.

Cell Differentiation↗
PubMed1980

Effects of corticosteroids on the proliferation of normal and abnormal human connective tissue cells.

Four corticosteroids were tested in vitro for effect on the proliferation of four strains of fibroblasts from scleroderma skin, four strains from normal adult skin and four strains of rheumatoid synovial cells. Significant effects on fibroblasts occurred only at the highest steroid concentration tested (10 microgram/ml) where the inhibitory ranking of the steriods was clobetasol propionate greater than clobetasone butyrate greater than betamethasone valerate greater than hydrocortisone. Hydrocortisone and betamethasone valerate stimulated proliferation of two normal strains, had no certain effect on the scleroderma group, and inhibited growth of synovial cells. Clobetasone butyrate and clobetasol propionate inhibited growth of all cells. All four steroids substantially reduced acid mucopolysaccharide secretion by scleroderma fibroblasts. These results suggest that fibroblasts from normal and abnormal skin show only small differences in their responses to corticosteroids in vitro, but contrast sharply with the mouse L-929 fibroblasts previously used in some assays of topical corticosteroid potency.

Adrenal Cortex Hormones↗
PubMed1991

In vitro clonal analysis of quail cardiac neural crest development.

The developmental potentials of cardiac neural crest cells were investigated by in vitro clonal analysis. Five morphologically distinct types of clones were observed: (1) "pigmented" clones contained melanocytes only; (2) "mixed" clones consisted of pigmented and unpigmented cells; (3) "unpigmented dense" clones consisted of flattened, closely aligned unpigmented cells; (4) "unpigmented loose" clones consisted of a few loosely arranged, flattened cells; and (5) "unpigmented large" clones included a large number of small, stellate cells that were highly proliferative. The binding patterns of antibodies against lineage-specific markers showed that cells in the different clones expressed characteristic phenotypes. The following phenotypes were expressed in addition to pigment cells: smooth muscle cells, connective tissue cells, chondrocytes, and cells in the sensory neuron lineage. Mixed clones expressed all five phenotypes. Unpigmented dense clones contained smooth muscle cells, connective tissue cells, chondrocytes, and sensory neurons. Unpigmented loose clones exclusively consisted of smooth muscle cells, whereas unpigmented large clones contained chondrocytes and sensory neuron precursors. Based on these results, the following conclusions can be drawn: (1) Pigmented and unpigmented loose clones are most likely formed by precursors that are committed to the melanogenic and myogenic cell lineages, respectively. (2) Mixed and unpigmented dense clones are derived from pluripotent cells with the capacity to give rise to four or five phenotypes. (3) Unpigmented large clones originate from progenitor cells that appear to have a partially restricted developmental potential, that is, these cells are capable of generating two phenotypes in clonal cultures. Thus, the data indicate that the early migratory cardiac neural crest is a heterogeneous population of cells, consisting of pluripotent cells, cells with a partially restricted developmental potential, and cells committed to a particular cell lineage.

Animals↗
PubMed1975

The relation between connective tissue cells and intercellular substances, including basement membranes.

Basement membranes are distributed widely in the body forming an extracellular matrix for epithelial and endothelial cells. The collagenous and glycoprotein constituents of basement membranes are synthesized by these two cell types. Disturbance of the interactions between basement membranes and their associated epithelial and endothelial cells can lead to the pathological changes seen in diseases involving basement membranes. These changes are illustrated here by reference to glomerulonephritis induced by the deposition of immune complexes in the glomerulus of the kidney, and chronic inflammatory changes occurring in the lung after inhalation of asbestos. In these diseases basement membrane changes can occur in several ways. Hydrolytic enzymes released from inflammatory cells degrade basement membranes while other constituents by epithelial and endothelial cells. Alternatively the physical separation of epithelial and endothelial cells from their basement membrances by space-occupying substances such as immune complexes can interfere with feedback mechanisms leading to synthesis of basement membrane constituents and cell proliferation. Studies of these pathological changes at a cellular level should shed new light on the ways in which cells interact with their pericellular environment.

Asbestos↗
PubMed2000

Dynamics of nuclei of muscle fibers and connective tissue cells in normal and denervated rat muscles.

The mitotic activity in muscles of growing rats and the effect of denervation were studied by means of continuous infusion of 5-bromo-2-deoxyuridine (BRDU). Denervated muscles after 10 weeks contained 20 to 60% fewer muscle nuclei than normal; BRDU labeled about 25% of the nuclei of normal soleus and extensor digitorum longus (EDL) and of denervated EDL muscles but only 5% in the denervated soleus muscle. Labeled nuclei persisted in denervated but not in normal muscles. After the main growth period, the turnover of myonuclei was at most 1 to 2% per week. The behavior of connective tissue nuclei was similar to that in muscle fibers. Infusion of BRDU had no effect on contractile properties. It is suggested that the exceptionally rapid atrophy of the denervated rat soleus associated with loss of satellite cells was due to loss of myonuclei and differentiation and fusion of satellite cells. The cause may possibly be that the phase of postdenervation fibrillation is shorter than in other muscles.

Animals↗
PubMed1984

Multiple responses of connective tissue cells to mitogenic stimulation with platelet-derived growth factor.

A number of important properties are held by mitogenic substances such as platelet derived growth factor for cells that can respond to such a mitogen. These include responses that occur early after exposure of the cells to the mitogens. Such responses include increases in endocytosis, binding of low density lipoprotein to high affinity cell surface receptors and increased uptake and degradation of LDL, increases in phospholipid metabolism, sodium and potassium ion flux, increases in protein and RNA synthesis, and chemotaxis. It is not yet clear whether some of these properties can be separated from the stimulus to enter DNA synthesis and mitosis, or whether they are tightly coupled to the latter. Nevertheless, they all precede DNA synthesis by many hours before the cells enter into S and go on to divide. It is highly probable that a number of other biological events will be found to be stimulated by exposing cells to mitogens, such as the platelet derived growth factor. Elucidation of these events and determination of the interrelation of each of these biological responses to the subsequent multiplication of the cells in a given set of circumstances will help to provide a basis for understanding how these mitogens work, and potentially how it may be possible to prevent some of the proliferative responses that represent such an inherent part of many disease processes.

Chemotaxis↗