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PubMedDate not supplied

Effect of epidermal growth factor on cell proliferation in normal and wounded connective tissue.

Epidermal growth factor has been previously shown to stimulate connective tissue repair in the perforated rat mesentery. The mechanism by which epidermal growth factor accelerates closure of mesenteric perforations has not been established, but epidermal growth factor may stimulate mitosis, contraction, migration, or angiogenesis. In the present investigation, the effect of epidermal growth factor on connective tissue cell proliferation was studied during the initial phase of repair of mesenteric perforations and in unwounded mesentery. Laparotomies were performed on Sprague-Dawley rats, and standardized perforations were made with a scalpel in the center of the mesenteric "windows," leaving every second window as an internal control. Twice daily for 4 consecutive days, beginning on the day of surgery, the animals received by intraperitoneal injection either 10 microg of epidermal growth factor dissolved in phosphate-buffered saline solution or phosphate-buffered saline solution alone. Cell proliferation was measured by either mitotic index of fibroblasts and mesothelial cells or DNA content of individual fibroblast cell nuclei in the wound area or in unperforated control windows. Laparotomy alone was found to enhance proliferation during the early postoperative period, as shown by increased numbers of S + G2 fibroblasts and a greater mitotic index. Epidermal growth factor treatment increased the mitotic index in perforated windows on the third postoperative day, compared with controls treated with phosphate-buffered saline solution, but did not significantly increase either the number of S + G2 fibroblasts or the mitotic index in unwounded tissue. Also, the proliferative response after epidermal growth factor treatment was significantly higher in wounded tissue. This study shows that epidermal growth factor stimulates proliferation of connective tissue cells in wounded but not unwounded tissue, and such enhancement of fibroblast proliferation might be of importance in epidermal growth factor-stimulated connective tissue repair.

Journal Article↗

PubMed2003

Low density lipoprotein receptor-related protein (LRP) is a heparin-dependent adhesion receptor for connective tissue growth factor (CTGF) in rat activated hepatic stellate cells.

Connective tissue growth factor (CTGF) is a cysteine-rich, extracellular matrix-associated heparin-binding protein implicated in a variety of fibrotic disorders. CTGF is initially synthesized as a mosaic protein containing four discrete structural modules (CTGF(1-4)) but this is susceptible to proteolytic cleavage yielding isoforms comprising modules 3 and 4 (CTGF(3-4)) or module 4 alone (CTGF(4)). In this study, we show that cultured rat hepatic stellate cells (HSCs) produce CTGF(1-4) and CTGF(3-4) following treatment with transforming growth factor-beta and that CTGF is a cell adhesion factor for activated HSCs. Low density lipoprotein receptor-associated protein (LRP) is a receptor for CTGF(1-4) or CTGF(3-4), but not CTGF(4), whereas cell surface heparan sulfate proteoglycans (HSPGs) are binding sites for all CTGF isoforms. Prior occupancy of LRP with other LRP ligands, receptor associated protein, anti-LRP, or a thrombospondin type I peptide (TEWSACSKTCG) resulted in a 50% decrease in the adhesion of activated HSCs to CTGF(1-4) or CTGF(3-4) whereas there was no effect on CTGF(4)-mediated adhesion. Co-incubation of CTGF with heparin or perturbation of cell surface HSPGs with heparinase or sodium chlorate completely blocked adhesion of activated HSCs to all CTGF isoforms. Freshly isolated HSCs demonstrated only weak binding to CTGF but strong binding to fibronectin. Thus HSC adhesion is at least partially promoted by CTGF through its binding to LRP, a process that is heparin-dependent. CTGF-LRP interactions are likely mediated by module 3 and CTGF-heparin interactions occur principally in module 4, although additional motifs may account for the heparin-dependency of LRP binding. These data show that LRP and HSPGs are utilized by HSCs for binding to CTGF and suggest that these cell surface molecules may be involved in mediating CTGF activity or adhesive signaling during the activation process.

Journal Article↗

PubMed1987

Changing processes from bone marrow-derived cultured mast cells to connective tissue-type mast cells in the peritoneal cavity of mast cell-deficient w/wv mice: association of proliferation arrest and differentiation.

Connective tissue-type mast cells (CTMC) and mast cells grown in vitro exhibit many differences in morphology, biochemistry, and function. When cultured mast cells of WBB6F1-+/+ mouse origin were injected into the peritoneal cavity of genetically mast cell-deficient WBB6F1-W/Wv mice, however, the cultured mast cells acquired characteristics similar to CTMC. In this study, we analyzed the changing process. When the density of the cultured mast cells was measured by Percoll density gradient centrifugation, the proportion of dense mast cells increased after injection into the peritoneal cavity. Because the increase in proportion of dense mast cells paralleled the increase in proportion of heparin-containing mast cells, both parameters may be used as an index for differentiation activity of cultured mast cells into CTMC. When proliferation activity of mast cells was estimated by the incorporation of bromodeoxyuridine, the proliferation activity decreased after the i.p. transfer. Moreover, when cultured mast cells were recovered 10 wk after the i.p. transfer, the mast cells almost lost proliferation activity in the same culture condition that had been used for establishment of cultured mast cells from the bone marrow of WBB6F1-+/+ mice. These results demonstrate that the proliferation arrest and the acquisition of CTMC-like characters are associated after i.p. transfer of cultured mast cells.

Animals↗

PubMedDate not supplied

Morphological evidence of vestibular pathology in long-term experimental diabetes mellitus. II. Connective tissue and neuroepithelial pathology.

The influence of long-term experimental diabetes on the saccule and utricle was investigated with light and electron microscopy. Pathological changes involving the connective tissue cells of the subneuroepithelial connective tissue suggest that these cells may play a potentially important role in diabetic pathology of the inner ear. In diabetic animals there was an increased incidence of secondary lysosomes within the connective tissue cells as well as an accumulation of intracellular lipid droplets that increased with the level of hyperglycemia. Five animals with relatively more severe diabetes also had an extensive accumulation of extracellular matrix. Two of these rats with longer diabetes duration had a small number of degenerating type I hair cells scattered through the saccular neuroepithelium, possibly due to chronic stresses from impaired diffusion of oxygen, nutrients and waste material through the dense extracellular matrix. Utricles of these same animals did not have any degenerating hair cells.

Animals↗

PubMed1980

Observations on the histogenesis of bovine ruminal papillae.

Changes in numbers of epithelial and connective tissue cells, thickness of connective tissue, and height and diameter of papillae were quantitated in fetal and postnatal bovine ruminal mucosa. During fetal development, the height of papillae and number of fibroblasts increased, the diameter of papillary base and thickness of subpapillary and interpapillary connective tissue remained constant, and the numbers of basal and superficial cells of the epithelium decreased. During the first 2 months of postnatal development, the height of papillae and numbers of fibroblasts enclosed in the papillary core decreased, and the diameter of the papillary base and the interpapillary distance increased. In consequence, the increase in connective tissue, rather than its redistribution, was involved in papillary development. The epithelial reorganization appeared to follow the changes occurring in the connective tissue, at least during fetal development.

Animals↗

PubMed1985

Differentiation processes of connective tissue mast cells in living mice.

Mice of mutant genotypes were used to investigate the differentiation process of connective tissue mast cells. Mast cell precursors, which are a progeny of the multipotential hematopoietic stem cell, leave the bone marrow, migrate in the bloodstream and enter into connective tissues where they proliferate and differentiate into mast cells. A portion of morphologically identifiable mast cells may function as committed and localized mast cell precursors. When local production of mast cells is demanded, the mast cells with proliferative potentiality respond first. Further demand is met by invasion and differentiation of marrow-derived precursors.

Animals↗

PubMed1979

[Innervation of the small intestinal mucosa of laboratory animals. II. Ultrastructure of neuro-cellular connections].

In addition to our light microscopic contribution (Stach, Hung 1978) giving an insight into the density, architecture, histochemical variety and relations between plexus mucosus and Lieberkühn's glands the herewith presented electron microscopic results reveal mainly neuro-cellular relations from the lamina propria. This means that the plexus mucosus has mainly the function to innervate blood vessels and lymphatics as well as smooth muscle cells and connective tissue cells (mast cells, histiocytes, plasma cells) of the small intestine mucosa.

Animals↗

PubMed1992

Leukotriene formation by mouse connective tissue mast cells.

Stimulation of peritoneal cells from BALB/c, CBA/J or WBB6F1(-)+/+ mice with IgE/antigen caused the release of mast cell granules and leukotriene C4. No leukotriene formation was observed with peritoneal cells from mast cell-deficient WBB6F1-W/Wv mice. Mast cells (greater than 98% purity), separated on metrizamide gradients, did not synthesize detectable amounts of leukotriene C4 when challenged immediately after purification. Co-culture of the mast cells with 3T3 fibroblasts restored the capability of the mast cells to produce leukotrienes. Addition of IL-3 during culture enhanced the synthesis of this eicosanoid. The 5-lipoxygenase inhibitor A-63162 blocked the leukotriene formation. Western blot analysis confirmed the presence of 5-lipoxygenase in connective tissue mast cells. These experiments demonstrate that mouse peritoneal (connective tissue) mast cells can produce significant amounts of leukotrienes.

Acetamides↗

PubMed2006

Effects of human connective tissue growth factor gene transfection on migration of human umbilical vein endothelial cell.

Connective tissue growth factor (CTGF) is a 38-kDa cysteine-rich protein and an important regulator of angiogenesis. In order to study the role CTGF gene playing in angiogenesis, the eukaryotic expression vector of CTGF gene was constructed in this study, and the role of endogenous CTGF on migration of human umbilical vein endothelial cell (HUVECs) was investigated. According to human CTGF cDNA sequence, a pair of specific primers containing digestion sites of Xba I and Hind III on the 5' end respectively were designed. Reverse transcript polymerase chain reaction (RT-PCR) was used to amplify CTGF cDNA from HUVECs. The eukaryotic expression vector pcDNA3.1(-)/CTGF containing the entire coding region was constructed successfully. Compared with CTGF sequence of GenBank, DNA sequence analysis showed that this reformed plasmid contained the same full length of CTGF cDNA. The results of Western blotting demonstrated that CTGF was over-expressed at 48 h after transfection. Migration of HUVECs transfected with CTGF vector increased significantly compared with those transfected with vector control. In conclusion, the eukaryotic expression vector pcDNA3.1(-)/CTGF was constructed successfully and the endogenous CTGF promoted the migration of HUVECs. This study lays a foundation for further study on the role CTGF gene playing in angiogenesis.

Cell Movement↗

PubMed1978

Connective tissue structure: cell binding to collagen.

Established lines of fibroblasts have been shown to adhere to collagen substrates via a serum-derived glycoprotein. The attachment of various other cells to collagen types I-IV is examined here. Cells such as human skin fibroblasts, periosteum, hepatocytes, connective tissue cells, and monocytes required the serum glycoprotein and adhered equally well to all collagens, but attachment of chondrocytes, epidermal cells, and neutrophils was inhibited by the serum glycoprotein. Attachment of 2 tumorigenic cells, an osteosarcoma and a fibrosarcoma, was found to be unaffected by the serum glycoprotein. In addition, the fibrosarcoma and epidermal cells attached preferentially to type IV (basement membrane) collagen.

Animals↗

PubMed2005

Transcriptional regulation of connective tissue growth factor by sphingosine 1-phosphate in rat cultured mesangial cells.

Connective tissue growth factor (CTGF) is induced by transforming growth factor-beta (TGF-beta) via Smad activation in mesangial cells. We recently reported that sphingosine 1-phosphate (S1P) induces CTGF expression in rat cultured mesangial cells. However, the mechanism by which S1P induces CTGF expression is unknown. The present study revealed that S1P-induced CTGF expression is mediated via pertussis toxin-insensitive pathways, which are involved in the activation of small GTPases of the Rho family and protein kinase C. We also showed by luciferase reporter assays and chromatin immunoprecipitation that S1P induces CTGF expression via Smad activation as TGF-beta does.

Animals↗

PubMed1984

Organization of the nervous tissue (hippocampus and septum) developing in the anterior eye chamber. I. General characteristic and non-neural elements.

Hippocampal and septal tissue of the rats' embryos was grafted into anterior eye chamber of the adult rats. After 3-4 months of survival the light and electron microscopy of the grafts was performed. Significant difference in development and organization of septal (SGs) and hippocampal (HGs) grafts was observed. Developed SGs had spherical shape, the area of their contact with host iris was limited, vascularization usually occurred through a narrow tissues talk. HGs often had elongated convex shape, resembling the hippocampus in situ. They contacted the iris by their ventral surface, through which multiple vessels ingrowed. HGs increased in volume significantly more, than SGs. SGs consisted of diffuse aggregates of multipolar neurons, while in HGs pyramidal neurons formed more or less organized layer. The apical dendrites of pyramidal cells were always oriented towards iris. Periferal areas with high number of glial cells and central areas, where nervous cells were concentrated, were distinguished in the grafts. Connective tissue cells were also present in them. Specific clusters of connective tissue cells with tight junctions between them were observed at the interface between a graft and iris. Their intracellular spaces formed tissue capillaries interconnected with perivascular space of blood vessels. Morphology of the clusters indicated that these connective tissue cells had some trophic functions. Two types of organization of limiting superficial glial sheath were observed. Multilayer capsula, consisting of modified oligodendrocytes and their processes was observed in SGs. This glial sheath could be perforated by nervous processes. Monolayer glial membrane formed by fibrous astrocytes was characteristic of HGs. This type of surface organization more closely resembled normal glial limiting membrane of the brain. The capillaries in the grafts were characterized by various degrees of permeability depending on their location. The capillaries of the central "neuronal" areas had all structural features of blood-brain barrier. The capillaries of periferal, "glial" areas had less prominent barrier characteristics. Endothelium of the capillaries in connective tissue aggregates had fenestrae and perforations, which indicates to a higher degree of permeability.

Animals↗

PubMed2006

Novel angiogenic inhibitor DN-9693 that inhibits post-transcriptional induction of connective tissue growth factor (CTGF/CCN2) by vascular endothelial growth factor in human endothelial cells.

Connective tissue growth factor (CTGF/CCN2) is a potent angiogenic factor. In this report, we describe for the first time that vascular endothelial growth factor (VEGF)-mediated induction of the ctgf/ccn2 gene was a post-transcriptional event that was inhibited by a novel angiogenic inhibitor, DN-9693, in human umbilical vein endothelial cells. Steady-state mRNA levels of ctgf/ccn2 were remarkably increased by VEGF in a concentration-dependent manner, whereas the activity of the ctgf/ccn2 promoter was not responsive to VEGF as confirmed by a reporter gene assay and quantitative real-time PCR analysis. By employing a RNA degradation assay, we eventually found that the observed increase in the ctgf/ccn2 mRNA level was due to an increased stability of the mRNA induced by VEGF. DN-9693 at a dose of 0.1 to 2 ng/mL did not affect basal levels of ctgf/ccn2 mRNA; however, enhancement of ctgf/ccn2 mRNA expression by VEGF was specifically inhibited by DN-9693. Of importance, the inhibitory effects could be also ascribed to post-transcriptional regulation, because the VEGF-mediated increase in stability of ctgf/ccn2 mRNA was suppressed by DN-9693. Furthermore, we investigated the effects of DN-9693 on VEGF-induced activation of three subgroups of mitogen-activated protein kinase pathways and found that DN-9693 blocked the activation of these pathways by VEGF. These results suggest that VEGF increases ctgf/ccn2 mRNA stability through mitogen-activated protein kinase-mediated intracellular signaling cascade(s), which can be inhibited posttranscriptionally by a novel angiogenic inhibitor, DN-9693, in human umbilical vein endothelial cells.

Angiogenesis Inhibitors↗

PubMed2006

Lipoxin A4 inhibits connective tissue growth factor-induced production of chemokines in rat mesangial cells.

Connective tissue growth factor (CTGF) is involved in mitogenesis, matrix production, and chemotaxis in mesenchymal cells. The effects of CTGF on the production of chemokines remain unclear. The present studies investigate the regulatory role of CTGF in the production of fractalkine, monocyte chemoattractant protein-1 (MCP-1), and RANTES (regulated upon activation, normal T cell expressed and secreted) in cultured mesangial cells of rats, and the modulatory effects of lipoxin A(4) (LXA(4)) on actions of CTGF. CTGF enhanced the mRNA expression and protein release of fractalkine, MCP-1, and RANTES, the expression of phospho (P)-p42/44 mitogen-activated protein kinase (MAPK), P-phosphoinositide 3-kinase (PI3-K), P-Akt, and activity of nuclear factor-kappaB (NF-kappaB) in mesangial cells. P-p42/44 MAPK blockade inhibited the CTGF-induced expression of P-p42/44 MAPK but not NF-kappaB, and partially decreased the levels of the above chemokines in supernatants. P-PI3-K blockade downregulated the CTGF-stimulated expression of P-PI3-K, P-Akt, and NF-kappaB but not P-p42/44 MAPK, and partially decreased the release of the above chemokines. NF-kappaB blockade abrogated the CTGF-activated NF-kappaB and partially decreased the secretion of the above chemokines. LXA(4) dose-dependently inhibited the CTGF-stimulated mRNA expression and protein release of the above chemokines, and the expression of P-p42/44MAPK, P-PI3-K, P-Akt, and NF-kappaB. In conclusion, these results demonstrate that CTGF induces production of fractalkine, MCP-1, and RANTES via the p42/44 MAPK-, PI3-K/Akt-, and NF-kappaB-dependent signal pathway, and LXA(4) downregulates the above effects of CTGF on rat mesangial cells.

Animals↗

PubMed1986

Fluorescent microscopy of hematoporphyrin derivative in the nude mouse tumor model.

Mechanisms for localization of hematoporphyrin derivative (HPD) within malignant tissue and for tumor necrosis after photodynamic therapy have not yet been established with certainty. We describe a modified freeze-drying technique to study these mechanisms. Normal tissues and squamous cell carcinoma xenografts were examined in nude mice after administration of HPD. Skin reveals marked fluorescence in connective tissue cells. No fluorescence is visible in surface epithelial cells or keratin. Liver shows diffuse fluorescence only in cells lining sinusoids. In tumor, malignant cells do not fluoresce and connective tissue cells fluoresce brilliantly. This technique provides a clear view of HPD fluorescence, frozen instantaneously in location and time. Fluorescence from connective tissue cells in skin and tumor suggests that localization and photodynamic action may be targeted in part at cells that critically support malignant epithelial cell growth as well as at malignant epithelial cells directly.

Animals↗

PubMed1992

Appearance of adipose cells in connective tissue at the implantation site of bone matrix gelatin and bupivacaine injection.

Two types of adipose cells were found in the connective tissue on day 7 after bone matrix gelatin (BMG) implantation and an injection of bupivacaine: mature adipose cells with a large lipid droplet (2-140 microns) and immature adipose cells with many small lipid droplets (0.1-2 microns). On day 10 after BMG implantation, typical adipose tissue was observed near the implant. The immature adipose cells had small, spherical mitochondria, glycogen granules and cytoplasmic microvesicles, and they might differentiate from undifferentiated mesenchymal cells in the connective tissue or the peripheral cells around the vessels as a white adipose tissue. These findings suggest that the differentiation of adipose cells in the connective tissue near heterotopic bone formation might be induced not only by mechanical and/or bupivacaine injury, but also by some factor or factors of the BMG.

Adipocytes↗

PubMed1977

Dispersed mammary gland epithelial cells. I. Isolation and separation procedures.

The mammary gland from midpregnant rabbits has been dissociated into individual cells by enzymatic digestion, divalent cation chelation, and gentle shearing. A heterogeneous cell population is obtained, comprising approximately 60% parenchymal cells, approximately 10% myoepithelial cells, and approximately 30% connective tissue cells, including fibroblasts, plasma cells, and microphages. The epithelial cells are characterized by the presence of fat droplets, which in 65% of the cells form large supranuclear vacuoles. Their buoyant density is less than 1.045, allowing their separation from myoepithelial cells and connective tissue cells by isopycnic centrifugation in a density gradient. The homogeneity of the epithelial cell fraction has been assessed by light and electron microscopy. The cells are viable and functionally active as indicated by their ability to exclude vital dyes, incorporate labeled precursors, consume oxygen, maintain intracellular Na+ and K+ concentrations, and retain their structural integrity. In addition, when cultured in Petri dishes, the cells grow as a monolayer, reestablish junctional complexes and retain cell polarity.

Animals↗

PubMed1978

[New results on ageing of connective tissue (author's transl)].

Some new results on ageing of connective tissue are demonstrated, regarding not only mesenchymal, but also parenchymal organs of human and rat (both sexes). These results show that ageing of connective tissue is more a dynamic process (with measurable metabolic parameters of the several connective tissue cells and their products) than a passive or so-called degenerative connective tissue process. The bradytrophy concept of connective tissue cannot be accepted any longer. Then connective tissue cells can produce metabolic rates of the same level like parenchymal cells. The different organs possess partly common basic processes partly differences in connective tissue ageing, dependent on the composition and patterns of proteoglycans resp. of GAG and collagen types, furthermore dependent on localisation, structure and function. The results on ageing of connective tissue are useful for better understanding of ageing processes of parenchymal organs. Then their ageing is influenced essentially by the ageing of the own connective tissues. The turnover, more than the number of mesenchymal and parenchymal cells, decreases with ageing. More old than young cells seem to exist in old tissues and organs. The performance of ageing connective tissue cells can be constant or increase or decrease. Many mesenchymal and parenchymal organs develop a so-called "ageing-fibrosis".

Aged↗