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PubMedDate not supplied

[Reaction of cells of subcutaneous connective tissue to the activation and blockade of the peptidergic system].

Changes in the quantitative composition of subcutaneous connective tissue cells were examined after activation and blockade of the peripheral peptidergic system with capsaicin. The activating dose (5 mg/kg) of the agent was found to increase the quantity of mast cells in the subcutaneous connective tissue. Its toxic dose (200 mg/kg) elevated the histiocytic and fibroblastic index while the number of mast cells reduced. The same reaction was seen in surgically impaired tissue innervation. It is concluded that peptidergic capsaicin-sensitive neurons play a role in the development of neurogenic dystrophy and this process involves connective tissue cell elements.

Animals↗
PubMed1998

Cellular proliferation in bovine luteal tissues of different reproductive states as demonstrated by Ki-67 immunocytochemistry.

Luteal tissue specimens of corpora lutea of oestrous cycle and pregnancy, post partum corpora lutea, and of luteinised follicular cysts of cows were harvested at slaughter. Cellular proliferation was examined employing Ki-67 immunocytochemistry. Ki-67 immunoreactivities could mainly be demonstrated within the nuclei of the theca interna and theca externa derived cell populations of cyclic corpora lutea. These cells obviously differentiated into vascular cells, connective tissue cells and small luteal cells. Proliferative activity was strongest in young corpora lutea and markedly reduced in the mature ones. During involution of corpora lutea of oestrous cycle Ki-67-positive cells were mainly found in vascular walls and connective tissue districts. Luteinised follicular cysts closely resembled cyclic corpora lutea. Corpora lutea of pregnancy exhibited foci of immunopositive cells close to blood vessels and connective tissue septae during whole gestation. Post partal luteal involution was characterised by Ki-67-positive cells within vascular walls and the surrounding stroma. Results suggest that luteal cellular proliferation is restricted mainly to theca interna-derived cells, which may differentiate to stromal cells and parenchymal cells.

Animals↗
PubMedDate not supplied

In vitro uptake 153gadolinium and gadolinium complexes by hyaline articular cartilage.

This in vitro study evaluated whether Gadolinium (Gd) penetrates into hyaline cartilage and would be incorporated into vital chondrocytes. Hyaline joint cartilage of rabbits was exposed to radioactive 153GdCl3 and to a radioactive 153Gd-DTPA-BSA-complex (DTPA, diethylene-triaminepentaacetic acid; BSA, bovine serum albumine). In addition an exchange experiment with radioactive 153GdCl3 versus Gd-DTPA-di-N-methylglucamine (Magnevist) was performed. Incorporation of 153GdCl3 into neuroblastoma cells, connective tissue cells and chondrocytes was tested. The results showed that the depth and extent of incorporation of Gd depends on the molecular mass and time of exposure. 153Gd-DTPA-BSA complexes exhibited an incorporation rate of maximal 11% +/- 2.8% up to the middle third of the cartilage within 24 h with almost no incorporation (2 +/- 1.9%) for the deep layer. The exchange experiment revealed no uptake of Gd for the deep layer. The maximal incorporation rate of 153GdCl3 into vital chondrocytes was 6.3%. These data indicate that under the condition of MR-arthrography, Gd-DTPA-di-N-methylglucamine will not be absorbed into the deep layers of hyaline cartilage and will not be incorporated into vital chondrocytes.

Animals↗
PubMed1978

Identity of a population of progenitor cells in gingival connective tissue of the mouse incisor.

In the gingiva of the mouse incisor, connective tissue cells were observed which were undergoing mitosis and contained collagen fibrils enclosed in vacuoles in their cytoplasm. The presence of intracellular collagen was noted in the majority of the dividing cells. On the basis of this observation it is suggested that renewal of the fibroblast population in the gingiva occurs preferentially by division of differentiated fibroblasts rather than by division of cells with a lower degree of differentiation.

Animals↗
PubMed1991

Calcium antagonists in experimental atherosclerosis. Use-dependence of isradipine: a potential explanation for enhanced action in atherosclerotic animals and tissue selectivity.

In the context of atherosclerosis, calcium antagonists should be evaluated from two points of view: their hemodynamic action on the atherosclerotic cardiovascular system, and their preventive action on atherosclerosis. Contraction of atherosclerotic vessels in response to vasoconstrictors, especially serotonin and acetylcholine, is enhanced mainly because of endothelial dysfunction. Due to their antivasoconstrictor effect, calcium antagonists partly compensate for this endothelial dysfunction. Agents which show a pronounced 'use-dependence', such as isradipine, are of particular interest as their action increases with the intensity of contraction. Therefore, their action is most prominent where it is most needed. Nevertheless, experiments in atherosclerotic animals indicate that the dose has to be chosen more cautiously than for young animals, as the dose-response curve for several effects is bell-shaped. Calcium antagonists also interfere with the process of atherosclerosis. In cholesterol-fed rabbits, lesion development is reduced, and regression after reverting to a normal diet is modestly enhanced. Calcium antagonists do not lower blood lipid levels. However, they attenuate proliferative lesions following endothelial damage due to a balloon catheter or electrical stimulation. The mechanism of these effects is still not clear. Blockade of the potential-sensitive L-type calcium channel is probably the important mechanism. Many types of cells (macrophages, other leukocytes and platelets, smooth muscle cells, connective tissue cells, endothelium, etc.) are involved in the genesis of atherosclerotic plaques, but it is not known which of these are the important targets of calcium antagonists. Calcium antagonists are most effective when administered at the onset of atherosclerosis, as they probably inhibit events occurring during the initiation of the atherosclerotic process.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2000

The lack of compound 48/80-induced contraction in isolated trachea of mast cell-deficient Ws/Ws rats in vitro: the role of connective tissue mast cells.

In the rat trachea, two types of mast cells have been identified, connective tissue mast cells and mucosal mast cells. Their different characteristics may account for their different biological functions. The role of connective tissue mast cells in tracheal contraction as one feature of the immediate reaction of asthma was studied in vitro in isolated trachea, using tissue derived from mast cell-deficient (Ws/Ws) rats, heterozygous (Ws/+) rats and control (+/+) rats, and compound 48/80 as a potent inducer of mast cell degranulation. The contractile response of tracheas from the three types of rats was also studied upon exposure to the following spasmogens: histamine, 5-hydroxytryptamine (5-HT), and carbachol. Histamine content in tissues reflected the differing mast cell numbers in strips from the three rat types. It was found that carbachol and 5-HT elicited tracheal contraction in a similar manner in strips from the three types of rats. Histamine had no contractile effect. Compound 48/80, at a dose of 25 microg/ml, elicited contraction in tracheas from both control (+/+) and heterozygous (Ws/+), but not in trachea from Ws/Ws rats. Compound 48/80-induced contractions in tracheas from +/+ rats were inhibited by 0.1 microM ketanserin and 0.1 microM nedocromil, but not by 0.1 microM mepyramine. Enzyme histochemistry confirmed that the degranulation occurred in connective tissue mast cells, but not in mucosal mast cells. We concluded that connective tissue mast cells play an important role in rat tracheal contraction via 5-HT release induced by compound 48/80. In addition, the specific mast cell-deficient (Ws/Ws) rats provide a good tool for studying the roles of mast cells in airway system.

Animals↗
PubMed2007

Patent foramen ovale: standards for a preclinical model of prevalence, structure, and histopathologic comparability to human hearts.

BACKGROUND: This study evaluated and standardized a Patent Foramen Ovale (PFO) preclinical model in gross anatomic and histopathologic features. METHODS: We examined 150 necropsy-derived domestic porcine hearts, age 4-6 months for PFO prevalence, appearance, and size. Histopathologic preparations were standardized and processed identically to 24 post-mortem human hearts aged 16-62 years. A measurement scheme was developed for PFO atrial openings, tunnel length, and histopathologic features to compare porcine and patient hearts. RESULTS: PFO was found in 32 of the 150 porcine hearts (prevalence 21.3%). Twenty-five porcine PFO underwent standard characterization by tunnel length, and right, and left atrial orifice diameters. Logarithmic regression analysis between porcine PFO tunnel length and left atrial orifice area demonstrated a significant positive relationship (P = 0.0162, R(2) = 0.227). The porcine PFO tunnel length was significantly longer than in humans (12.0 +/- 4.0 mm vs. 7.1 +/- 3.1 mm respectively, P < 0.0001). Histopathologic comparison was made using serial sections perpendicular to the atrial septum and the tunnel long axis. Human and porcine PFO lesions demonstrated strong similarities in tissue cells, connective tissue, and matrix composition. CONCLUSIONS: PFO assessment was standardized in both macroscopically and histopathologically, with quantitative and qualitative comparisons feasible using a porcine preclinical model. PFO prevalence in domestic swine is identical to humans, and microscopic structures very similar to humans. The domestic swine PFO model appears useful to evaluate new interventional closure technologies due to comparability in microscopic features. Tunnel length should be carefully evaluated due to differences across pigs and patients.

Adolescent↗
PubMedDate not supplied

[Mediator aspects of the inflammatory process].

Signal sequences of inflammation and regeneration are presented. The number of factors such as sensor neuropeptides, lipid mediators, interleukins and factors of growth are shown to participate in the initiation and regulation of inflammation. These factors are produced in a certain sequence by various structures: cells-object of damage, opsonocytophagic and immune cells, connective tissue cells. This results in the stimulation of adhesion proteins, processes of migration, chemotaxis, interaction with components of the intercellular matrix and parenchyma cells of the viscera. Fibroblast is considered to be the central figure in the resolution of inflammation and its chronization. The regulation of the process occurs with the help of autocrine regulation and apoptosis of functionally exhausted cells.

Apoptosis↗
PubMed2002

Effects and regulation of connective tissue growth factor on hepatic stellate cells.

Connective tissue growth factor (CTGF) is a 38-kd protein involved in several human fibrotic disorders including atherosclerosis and skin and renal fibrosis. Although it has been shown that human and experimental liver fibrosis is associated with CTGF expression through up-regulation of CTGF mRNA by hepatic stellate cells (HSC), the role of CTGF in the liver has not yet been determined. The aim of the present study was to assess the effects of CTGF on rat primary HSC and its regulation in a well-established model of in vitro liver fibrogenesis. Incubation of primary HSC with recombinant CTGF induced a significant migratory (2.3-fold, 50 ng/ml CTGF) and proliferative effect (1.8-fold, 100 ng/ml CTGF). Type I collagen mRNA expression, as assessed by a real-time RT-PCR procedure, was also increased when cells were incubated in the presence of CTGF (2-fold, 50 ng/ml). Transforming growth factor-beta1 (TGF-beta1) strongly stimulated CTGF mRNA expression, a direct mechanism observed in the absence of any intermediate protein synthesis. Furthermore, spontaneous activation of HSC plated on plastic and stimulation by vascular endothelial growth factor, lipid peroxidation products (HNE, MDA), acetaldehyde, and platelet-derived growth factor (PDGF)-BB significantly up-regulated CTGF mRNA expression in HSC. PDGF-induced CTGF stimulation might be related in part to TGF-beta1 secretion because CTGF mRNA up-regulation observed after PDGF-BB stimulation was abrogated in the presence of neutralizing TGF-beta1 antibody. In conclusion, this study extends the role of CTGF in HSC activation and suggests that CTGF up-regulation might be a central pathway during HSC activation.

Animals↗
PubMed2004

Adult bone marrow-derived stem cells in muscle connective tissue and satellite cell niches.

Skeletal muscle includes satellite cells, which reside beneath the muscle fiber basal lamina and mainly represent committed myogenic precursor cells, and multipotent stem cells of unknown origin that are present in muscle connective tissue, express the stem cell markers Sca-1 and CD34, and can differentiate into different cell types. We tracked bone marrow (BM)-derived stem cells in both muscle connective tissue and satellite cell niches of irradiated mice transplanted with green fluorescent protein (GFP)-expressing BM cells. An increasing number of GFP+ mononucleated cells, located both inside and outside of the muscle fiber basal lamina, were observed 1, 3, and 6 months after transplantation. Sublaminal cells expressed unambiguous satellite cell markers (M-cadherin, Pax7, NCAM) and fused into scattered GFP+ muscle fibers. In muscle connective tissue there were GFP+ cells located close to blood vessels that expressed the ScaI or CD34 stem-cell antigens. The rate of settlement of extra- and intralaminal compartments by BM-derived cells was compatible with the view that extralaminal cells constitute a reservoir of satellite cells. We conclude that both muscle satellite cells and stem cell marker-expressing cells located in muscle connective tissue can derive from BM in adulthood.

Animals↗
PubMed2003

Generation of a large number of connective tissue type mast cells by culture of murine fetal skin cells.

We describe a novel culture system for generating large numbers of murine skin-associated mast cells and distinguish their characteristics from bone marrow-derived cultured mast cells. Culture of day 16 fetal skin single cell suspensions in the presence of interleukin-3 and stem cell factor allowed expansion and maturation of mast cells in the presence of stromal cells. The average yield of mast cells after 2 wk was 7.3 million cells per fetus at a purity of 96%. These fetal skin-derived cultured mast cells increased their histamine content in a time-dependent manner to 3.6 pg per cell after 2 wk and 6.7 pg per cell after 4 wk. Phenotypic analyses revealed much greater expression of CD49b and CD81 and lesser expression of CD77 and CD102 on fetal skin-derived cultured mast cells as compared with bone marrow-derived cultured mast cells. These findings suggest a close similarity between fetal skin-derived cultured mast cells and freshly isolated cutaneous mast cells. Connective tissue mast cell characteristics of fetal skin-derived cultured mast cells were evidenced by: (1) their greater histamine content than bone marrow-derived cultured mast cells; (2) the presence of heparin; and (3) their degranulation in response to compound 48/80 and substance P. Importantly, fetal skin-derived cultured mast cells secreted greater amounts of interleukin-13 but much less MIP-1beta and interleukin-6 than bone marrow-derived cultured mast cells in response to ionomycin. Thus fetal skin-derived cultured mast cells have many characteristics distinct from bone marrow-derived cultured mast cells and can be used as a model of cutaneous mast cells to discern their functions.

Age Factors↗
PubMed1986

Myocardial DNA content, ploidy level and cell number in geriatric hearts: post-mortem examinations of human myocardium in old age.

A reduced adaptation rate of the myocardium must, in many cases, be made responsible for heart insufficiency of old patients. The present investigations are aimed towards the question whether heart in old age is accompanied by a loss of myocardial cells and whether a polyploidisation of heart muscle cells takes place thus indicating an adaptive process. A total of 40 human hearts obtained from autopsy material were studied, among them 30 geriatric hearts. Following preparation of the hearts, the myocardium was weighed and the total amount of DNA was determined biochemically. By means of Feulgen cytophotometry the ploidy levels of the heart muscle nuclei were detected. We have used a special method for estimating the total number of heart muscle cells and connective tissue cells in the individual hearts. It could be shown that the total amount of DNA in the myocardium is correlated with the myocardial weight and not with the age of the individual. Instead, DNA synthesis occurs in the heart muscle cells of all age groups depending on the functional activity of the heart. The degree of polyploidisation is closely correlated with myocardial hypertrophy without any influence of age. In hypertrophic hearts the number of connective tissue cells increases from normally 4 to 5 X 10(9) to 12 X 10(9) (in hearts weighing more than 700 g); in hearts with interstitial fibrosis these values are even higher. In normal hearts 1.8 to 2.1 X 10(9) heart muscle cells can be estimated; in hearts weighing more than 500 g numerical hyperplasia of the heart muscle cells is produced, reaching a maximum number of 4.8 X 10(9) muscle cells in excessively hypertrophied hearts weighing more than 800 g. No correlation between age and myocardial cell number (i.e. heart muscle cells or connective tissue cells) could be observed. This means that no agespecific changes occur in the myocardium with regard to the DNA content and cell number. The structural changes found in the hearts of old individuals are produced by extracardial influences (i.e. arteriosclerosis, hypertension, etc.) leading to myocardial hypertrophy. Polyploidisation and augmentation of heart muscle cells in cardiac hypertrophy or decrease in the number of heart muscle cells in heart atrophy may occur at any time of life and are not age-specific.

Adult↗
PubMed1997

T cell receptor (V beta) bias in the response of rheumatoid arthritis synovial fluid T cells to connective tissue antigens.

T cell receptor (V beta) use in the response to type II collagen and cartilage proteoglycans was analysed in peripheral blood and synovial fluid T cells from RA patients. T cells from RA patients with an immune response to connective tissue antigens, and paired PB and SF samples were stimulated in vitro with type II collagen, high density aggrecan proteoglycans (PG), and the T cell mitogen concanavalin A. After short term culture, mRNA was extracted from cells and a reverse transcription-polymerase chain reaction was performed, using primers specific for eight TCR V beta determinants. Blood cells stimulated with ConA generated strong bands with virtually all the V beta primers tested, but the TCR (V beta) expression by SF T cells stimulated with mitogen was biased, suggesting a selection process during joint infiltration. The V beta phenotypes of cells responding to PG was restricted in individual RA patients, but the pattern of V beta use in the the RA population was not consistent. In contrast, the V beta phenotypes of SF cells responding to CII was highly biased in both individual patients and the RA population, with V beta 14, V beta 17, and V beta 8 phenotypes predominant. We conclude that the T cell response to connective tissue antigens is restricted compared with mitogen stimulation, with the highest degree of TCR bias seen in the response of SF T cells to stimulation with type II collagen.

Aged↗
PubMed2005

Individual domains of connective tissue growth factor regulate fibroblast proliferation and myofibroblast differentiation.

All members of the Ctgf, Cyr61, and Nov (CCN) family share a high degree of sequence homology and conservation of structural motifs and domains. Here, we present data about a structure function analysis of connective tissue growth factor (CTGF), a prototypic member of the CCN family, which has been shown to be a downstream mediator of transforming growth factor-beta activities on fibroblasts. Our findings demonstrate the two domains of CTGF function to mediate two distinct biological effects. The N-terminal domain of CTGF mediates myofibroblast differentiation and collagen synthesis. The C-terminal domain of CTGF mediates fibroblast proliferation. These data provide a molecular basis for the divergence of CTGF actions on connective tissue cell types and suggest a model for functional analysis of all of the CCN family gene products.

Animals↗
PubMed2004

Connective tissues: signalling by tenascins.

Different connective tissue cells secrete different types of tenascins. These glycoproteins contribute to extracellular matrix (ECM) structure and influence the physiology of the cells in contact with the tenascin containing environment. Tenascin-C expression is regulated by mechanical stress. It shows highest expression in connective tissue surrounding tumors, in wounds and in inflamed tissues where it may regulate cell morphology, growth, and migration by activating diverse intracellular signalling pathways. Thus, integrin and syndecan signalling is influenced by tenascin-C and the levels and/or activies of several proteins involved in intracellular signalling pathways are regulated by its presence. Tenascin-X is important for the proper deposition of collagen fibers in dermis and patients with a tenascin-X deficiency suffer from Ehlers Danlos syndrome. Tenascin-R (and -C) is prominent in the nervous system and has an impact on neurite outgrowth and synaptic functions, and tenascin-W is found in the extracellular matrix of bone, muscle, and kidney. Cell facts:bone: osteoblasts produce tenascin-C, -W cartilage: perichondrial cells produce tenascin-C tendon: fibroblasts produce tenascin-C smooth muscle cells produce tenascin-W, -C skeletal muscle: endo-, peri-, and epimysial fibroblasts produce tenascin-X dermal fibroblasts produce tenascin-X tumors: stromal fibroblasts produce tenascin-C wounds: fibroblasts produce tenascin-C nervous system: glial cells produce tenascin-R, -C, -X.

Cell Shape↗
PubMed1987

Connective tissue activation. XXXII. Structural and biologic characteristics of mesenchymal cell-derived connective tissue activating peptide-V.

Connective tissue activating peptide-V (CTAP-V) is a single-chain, mesenchymal cell-derived anionic protein with large and small molecular forms (Mr of 28,000 and 16,000, respectively), as defined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The proteins have similar specific activities with respect to stimulation of hyaluronic acid and DNA formation in human synovial fibroblast cultures. S-carboxymethylation or removal of sialic acid residues did not modify CTAP-V biologic activity. Rabbit antibodies raised separately against each of the purified CTAP-V proteins reacted, on immunodiffusion and on Western blot, with each antigen and neutralized mitogenic activity. The amino-terminal amino acid sequence of the CTAP-V proteins, determined by 2 laboratories, confirmed their structural similarities. The amino-terminal sequence through 37 residues was demonstrated for the smaller protein. The first 10 residues of CTAP-V (28 kd) were identical to the N-terminal decapeptide of CTAP-V (16 kd). The C-terminal sequence, determined by carboxypeptidase Y digestion, was the same for both CTAP-V molecular species. The 2 CTAP-V peptides had similar amino acid compositions, whether residues were expressed as a percent of the total or were normalized to mannose. Reduction of native CTAP-V protein released sulfhydryl groups in a protein:disulfide ratio of 1:2; this suggests that CTAP-V contains 2 intramolecular disulfide bonds. Clearly, CTAP-V is a glycoprotein. The carbohydrate content of CTAP-V (16 kd) and CTAP-V (28 kd) is 27% and 25%, respectively. CTAP-V may have significance in relation to autocrine mechanisms for growth regulation of connective tissue cells and other cell types.

Acetylglucosaminidase↗