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At least 109 records · Page 6Linked to original sources
PubMed2004

The effect of eosinophils on collagen gel contraction and implications for tissue remodelling.

Asthma is characterized by an eosinophilic inflammation and a subepithelial fibrosis in the airways. Eosinophils contain several cytotoxic substances, such as eosinophil cationic protein (ECP), which can promote inflammation and cause tissue damage. This has generated the hypothesis that eosinophils may drive remodelling of extracellular matrix (ECM). To investigate the role of eosinophils we used an in vitro model for remodelling, the three-dimensional collagen gel contraction assay. Two sources of eosinophils were used in this study, isolated human peripheral eosinophils (purity > 95%) and stimulated [interleukin (IL)-5, IL-3 and granulocyte macrophage-colony stimulating factor (GM-CSF)] HL-60 clone 15 cells. Human eosinophils or HL-60 cells were cast together with human lung fibroblasts (HFL1) in type I collagen gels. Both types of eosinophils augmented fibroblast-mediated collagen gel contraction in a time and concentration-dependent manner. At 48 h, the gel area in HFL1/eosinophil co-culture was 46.5% +/- 0.5 (mean +/- s.e.m.) of initial area and in HFL1 culture 52.3% +/- 0.1 (P < 0.001). Respective figures for HFL1/stimulated HL-60 co-culture and HFL1 culture only were 44.1% +/- 0.5 and 52.4% +/- 0.4 (P < 0.001). The release of ECP was increased when fibroblasts were cultured with eosinophils compared to eosinophils cultured alone. In addition, native ECP added to fibroblast gel cultures also augmented contraction. Our results suggest that eosinophils may interact with mesenchymal cells, promoting remodelling of ECM and that ECP constitutes one potential eosinophil-derived mediator driving this process. We conclude that this may be one important mechanism by which eosinophil-ECM interactions will lead to airway tissue remodelling in asthma.

Asthma↗
PubMed1991

Second messengers: regulators of mechanically-induced tissue remodelling.

One of the most intriguing aspects of tissue reaction to mechanical forces such as in orthodontic tooth movement is the transduction of force into a meaningful cellular response. The behaviour of all eukaryotic cells is modulated by internal signalling systems which translate a wide array of external stimuli such as hormones or mechanical forces, into a very narrow range of internal signals (second messengers). Classically, the second messenger associated with mechanical force transduction is adenosine 3'5' cyclic monophosphate (cAMP); since it was virtually the only second messenger understood in any detail from 1960 to the late 1970s this is hardly surprising. A great deal more is now known about cell signalling mechanisms and for various reasons outlined in this review, the assumption that cyclic AMP is the sole messenger system in the transduction of mechanical forces is no longer tenable.

Animals↗
PubMed1987

Smooth muscle-mediated connective tissue remodeling in pulmonary hypertension.

Abnormal accumulation of connective tissue in blood vessels contributes to alterations in vascular physiology associated with disease states such as hypertension and atherosclerosis. Elastin synthesis was studied in blood vessels from newborn calves with severe pulmonary hypertension induced by alveolar hypoxia in order to investigate the cellular stimuli that elicit changes in pulmonary arterial connective tissue production. A two- to fourfold increase in elastin production was observed in pulmonary artery tissue and medial smooth muscle cells from hypertensive calves. This stimulation of elastin production was accompanied by a corresponding increase in elastin messenger RNA consistent with regulation at the transcriptional level. Conditioned serum harvested from cultures of pulmonary artery smooth muscle cells isolated from hypertensive animals contained one or more low molecular weight elastogenic factors that stimulated the production of elastin in both fibroblasts and smooth muscle cells and altered the chemotactic responsiveness of fibroblasts to elastin peptides. These results suggest that connective tissue changes in the pulmonary vasculature in response to pulmonary hypertension are orchestrated by the medial smooth muscle cell through the generation of specific differentiation factors that alter both the secretory phenotype and responsive properties of surrounding cells.

Animals↗
PubMed1997

The solid state environment orchestrates embryonic development and tissue remodeling.

Cell interactions with extracellular matrix and with other cells play critical roles in morphogenesis during development and in tissue homeostasis and remodeling throughout life. Extracellular matrix is information-rich, not only because it is comprised of multifunctional structural ligands for cell surface adhesion receptors, but also because it contains peptide signaling factors, and proteinases and their inhibitors. The functions of these groups of molecules are extensively interrelated. In this review, three primary cell culture models are described that focus on adhesion receptors and their roles in complex aspects of morphogenesis and remodeling: the regulation of proteinase expression by fibronectin and integrins in synovial fibroblasts; the regulation of osteoblast differentiation and survival by fibronectin, and the regulation of trophoblast differentiation and invasion by integrins, cadherins and immunoglobulin family adhesion receptors.

Animals↗
PubMed2006

Prevention of high-fat diet-induced adipose tissue remodeling in obese diabetic mice by n-3 polyunsaturated fatty acids.

OBJECTIVE: Obesity is associated with reduced insulin sensitivity and extensive reorganization of adipose tissue. As polyunsaturated fatty acids (PUFA) appear to inhibit diabetes development, we investigated PUFA effects on markers of matrix remodeling in white adipose tissue. METHODS AND PROCEDURE: Male obese diabetic (db/db) mice were treated with either a low-fat standard diet (LF), or high-fat diets rich in saturated and monounsaturated fatty acids (HF/S), n-6 PUFA (HF/6) or the latter including marine n-3 PUFA (HF/3). White adipose tissue was analyzed for gene expression, fatty acid composition and by immunofluorescence. RESULTS: HF/S treatment increased adipose tissue expression of a number of genes involved in matrix degradation including matrix metalloproteinase (MMP)-12, -14 and cathepsin K, L and S compared with LF. MMP-12 gene was expressed in macrophages and adipocytes, and MMP-12 protein colocalized with both cell types. In addition, mean adipocyte area increased by 1.6-fold in HF/S-treated mice. Genes essential for collagen production, such as procollagen I, III, VI, tenascin C and biglycan were upregulated in HF/S-treated animals as well. N-3 PUFA supplementation resulted in enrichment of these fatty acids in adipose tissue. Moreover, n-3 PUFA inhibited the HF/S-induced upregulation of genes involved in matrix degradation and production I restored mean adipocyte area and prevented MMP-12 expression in macrophages and adipocytes. CONCLUSION: N-3 PUFA prevent high-fat diet-induced matrix remodeling and adipocyte enlargement in adipose tissue of obese diabetic mice. Such changes could contribute to diabetes prevention by n-3 PUFA in obese patients.

Adipocytes↗
PubMed1976

Changes in the tail of Ambystoma maculatum at different stages of metamorphosis: observations on tissue remodeling and its relationship to hydrolytic enzymes.

A system for staging A. maculatum during growth and metamorphosis was devised, based on several parameters of body size; body length, tail length and tail width. Animals at various stages of metamorphosis were employed to study the relationship between specific biochemical and histological changes that occur in the tail of this urodele during metamorphosis. The specific and total activity of two hydrolytic enzymes, acid phosphatase and beta-N-acetyl-glucosaminidase, were measured in tail tissues at progressive stages of development. The activities of these enzymes increased in both the fins and muscular portion of the tail during metamorphosis. These activities can be correlated with resorption of the tail fins and the remodeling of tissues in the muscular portion of the tail.

Acetylglucosaminidase↗
PubMed1999

Extracellular matrix-integrin interactions in osteoblast function and tissue remodeling.

Previous work with cultured primary cells, from our group and from other laboratories, has shown that signals from extracellular matrix, transduced by integrins, play critical roles in regulating gene expression, tissue-specific differentiation, and survival of primary osteoblasts and fibroblasts. This summary will focus on our most recent work, dealing with the role of cell-extracellular matrix interactions and focal adhesion kinase in regulating cell survival in osteoblasts and fibroblasts, and the role of beta1 integrins in tissue organization and remodeling in bone.

Bone Remodeling↗
PubMedDate not supplied

Scaffold seeded with cells is essential in urothelium regeneration and tissue remodeling in vivo after bladder augmentation using in vitro engineered graft.

OBJECTIVE: Tissue-engineering methods using synthetic biodegradable scaffolds seeded with cells have potential to induce regeneration to a functional bladder wall. The aim of the study was to induce in vivo urothelial growth on implanted scaffolds previously seeded with stromal cells as compared with matrices implanted without cells for rat cystoplasty augmentation. MATERIALS AND METHODS: 3T3 mouse fibroblasts were multiplied up to total of 10(8) cells. Cells were grown on Dulbecco's modified essential medium supplemented with 10% of fetal bovine serum and antibiotics in CO(2) chambers. Cells were seeded on biodegradable polyglycolic acid (PGA) scaffolds in eight rats: four bladders were augmented with cell-seeded grafts and the other four with acellular scaffolds. Rats were sacrificed after 4 months in preparation for hematoxylin and eosin staining. RESULTS: One death in the acellular cystoplasty group was observed after 3 weeks. No epithelial layer was observed in the central part of the acellular graft. The cell-seeded grafts showed good visible multilayered epithelium with at least five layers of epithelial cells in the central part. The epithelium resembled rat native urothelium. The cell-seeded grafts showed a high degree of implanted 3T3 cells infiltration with good degradation of PGA fibers. CONCLUSIONS: Our data indicated that urothelial proliferation on PGA grafts was intensified using a "feeder layer" of fibroblasts.

3T3 Cells↗
PubMed1996

Differentiation of the bone-tissue remodeling response to axial and torsional loading in the turkey ulna.

The ability of bone tissue to differentiate between axial and torsional loading was determined with use of a functionally isolated turkey-ulna model of bone adaptation. Surface modeling and intracortical remodeling were quantified after four weeks of 5000 cycles per day of axial loading sufficient to cause 1000 microstrain normal to the long axis of the bone (five ulnae), 5000 cycles per day of torsional loading sufficient to cause 1000 microstrain of shear strain (five ulnae), or disuse (six ulnae). Of these three distinct regimens, only disuse caused a significant change in gross areal properties (12 per cent loss of bone; p < 0.05) as compared with those in the contralateral, intact control ulnae (sixteen ulnae). This finding suggested that both axial and torsional loading conditions were suitable substitutes for functional signals normally responsible for bone homeostasis. However, the intracortical response was strongly dependent on the manner in which the bone was loaded. Axial loading increased the number of intracortical pores by a factor of seven as compared with that in the controls (246 +/- 40.5 compared with 36 +/- 8.5 pores); it also increased the area lost because of porosis as compared with that in the controls (1.39 +/- 0.252 compared with 0.202 +/- 0.062 square millimeter); however, the mean size of the individual pores was similar to that in the controls (0.00565 +/- 0.0019 compared with 0.00561 +/- 0.0029 square millimeter). Conversely, torsional loading failed to increase substantially the number of pores (67 +/- 22.6 pores), the area of bone lost because of porosis (0.352 +/- 0.114 square millimeter), or the size of the pores (0.00525 +/- 0.0035 square millimeter) as compared with those in the controls. Although disuse failed to increase substantially the number of intracortical pores (59 +/- 22.4 pores), significant area (1.05 +/- 0.35 square millimeters; p < 0.05) was lost within the cortex because of a threefold increase in the mean size of each pore (0.0178 +/- 0.0126 square millimeter). It appears that bone tissue can readily differentiate between distinct components of the strain environment, with strain per se necessary to retain coupled formation and resorption, shear strain achieving this goal by maintaining the status quo, and axial strain increasing intracortical turnover but retaining coupling. While it is clear that load influences bone mass and morphology, it is also clear that specific parameters within the strain environment have distinct strategic roles in defining this architecture.

Adaptation, Physiological↗
PubMed2001

Correlation of gene expression with physiological functions: Examples of pulmonary blood vessel rheology, hypoxic hypertension, and tissue remodeling.

Microarray gene chip technology is a powerful invention looking for applications. A general principle is proposed here to direct the power of the technology toward physiology, medicine, and pharmacology. Our principle is to match quantitative measures of gene expression with the trend of mathematical parameters that describe biological functions. Mathematical parameterization is the heart. The procedure is illustrated by lung physiology, including the hypoxic hypertension, rheological properties of the tissues, and the remodeling of the pulmonary arterial wall under hypertensive stress. We show first how to reduce the experimental results on these physiological functions into mathematical formulas, and how the parameters of these formulas describe the functional trends precisely. Then under the assumption that the microarray reveals gene activities quantitatively, we match the trends of the gene activity with the trends of the functional parameters. Genes whose trends do match are interpreted as relevant to the functions. Those that do not match are considered irrelevant to the functions. The more functions we consider, the fewer will be the number of genes that are relevant to all functions. Thus we learn about the generality and specificity of the influence of genes on physiology.

Animals↗
PubMed1984

The propagation of cancer, a process of tissue remodeling. Studies in histophysiologic gradient culture.

Effective study of the malignant phenotype at the tissue level requires model systems that are intelligible both to cell biologists and to pathologists, and that also observe the spatial imperatives intrinsic to tissues in nature. Malignant cells commonly appear in multicellular units, and growth of tumor tissue is seen as an increase in the number of cells and multicellular units. The supporting stroma frequently has an abnormal appearance, and this component of the tissue also increases in mass as the tumor enlarges and spreads. The direction of invasion is influenced by the direction of available metabolites. Histophysiologic gradient culture complies with nature's spatial rationale, since at the substrate-parenchymal interface three functions coincide. These are anchorage, initiation of epithelial renewal, and complete exchange of metabolites. Our model system provides a setting for reconstructing and manipulating many features of the malignant phenotype seen in cancer tissues in nature, such as abnormalities in the sequence of maturation of stratified epithelium, hyperplasias, dysplasias, interaction between different types of epithelium, aggregate formation, tumor angiogenesis, and neoplastic blockade.

Animals↗
PubMed2000

Tissue remodeling as a feature of persistent asthma.

A chronic inflammatory process is almost invariably associated with tissue damage and healing. Healing results in repair and replacement of dead or damaged cells by viable cells. Repair usually involves 2 distinct processes: regeneration, which is the replacement of injured tissue by parenchymal cells of the same type, and replacement by connective tissue and its eventual maturation into scar tissue. In many instances both processes contribute to the healing response. Chronic inflammatory disease can therefore lead to a wide variety of consequences, from complete or partial restitution of organ structure and function to fibrosis. Asthma is characterized by a chronic inflammatory process of the airways. The ensuing healing process results in structural alterations referred to as a remodeling of the airways. The mechanisms underlying these structural alterations are still largely unknown. They are likely to be heterogeneous, leading-through the highly dynamic process of cell de-differentiation, migration, differentiation, and maturation-to changes in connective tissue deposition and to the altered restitution of airways structure, resulting in mucus gland hyperplasia, neovascularization, fibrosis, and an increase in smooth muscle mass.

Asthma↗
PubMed2006

Extracellular matrix-mediated tissue remodeling following axial movement of teeth.

Tooth eruption is a multifactorial process involving movement of existing tissues and formation of new tissues coordinated by a complex set of genetic events. We have used the model of the unopposed rodent molar to study morphological and genetic mechanisms involved in axial movement of teeth. Following extraction of opposing upper molars, lower molars supererupted by 0.13 mm. Labeled tissue sections revealed significant amounts of new bone and cementum apposition at the root apex of the unopposed side following supereruption for 12 days. Newly apposited cementum and alveolar bone layers were approximately 3-fold thicker in the experimental vs the control group, whereas periodontal ligament width was maintained. Tartrate-resistant acid phosphatase staining indicated bone resorption at the mesial alveolar walls of unopposed molars and provided in tandem with new bone formation at the distal alveolar walls an explanation for the distal drift of molars in this model. Microarray analysis and semiquantitative RT-PCR demonstrated a significant increase in collagen I, integrin beta5, and SPARC gene expression as revealed by comparison between the unopposed molar group and the control group. Immunohistochemical verification revealed increased levels of integrin beta5 and SPARC labeling in the periodontal ligament of the unopposed molar. Together our findings suggest that posteruptive axial movement of teeth was accomplished by significant formation of new root cementum and alveolar bone at the root apex in tandem with upregulation of collagen I, integrin beta5, and SPARC gene expression.

Acid Phosphatase↗
PubMed2002

Ovarian tissue remodeling: role of matrix metalloproteinases and their inhibitors.

Follicular formation, growth or atresia, and ovulation as well as luteal formation and subsequent regression are dependent upon cyclical remodeling of the extracellular matrix (ECM). The proteinaceous and nonproteinaceous components of the ECM provide the tissue specific, extracellular architecture to which cells attach. Furthermore, the ECM modulates cellular activities through cellular surface receptors and serves as a reservoir for specific growth factors, cytokines, and binding proteins. The ability of the ECM to direct the proliferation, differentiation and function of cells implicates ECM remodeling in normal ovarian function. Specific components of the ECM are cleaved by matrix metalloproteinases (MMPs) whose activities are specifically inhibited by tissue inhibitors of metalloproteinases (TIMPs). MMPs are zinc- and calcium-dependent enzymes that collectively degrade proteinaceous components of the ECM. Controlled turnover of ECM by MMPs and TIMPs may be essential for creating and (or) preserving microenvironments conducive to follicular and luteal function and is likely dependent upon the ratio of enzyme to inhibitor. To date, most studies have focused upon correlating ovarian expression of MMPs and TIMPs with various stages of the reproductive cycle. From these studies, many potential key regulators of ovarian ECM remodeling have been identified. This review presents evidence for the involvement of MMPs and TIMPs in ECM remodeling associated with follicular and luteal function.

Animals↗
PubMed2000

Cartilage tissue remodeling in response to mechanical forces.

Recent studies suggest that there are multiple regulatory pathways by which chondrocytes in articular cartilage sense and respond to mechanical stimuli, including upstream signaling pathways and mechanisms that may lead to direct changes at the level of transcription, translation, post-translational modifications, and cell-mediated extracellular assembly and degradation of the tissue matrix. This review focuses on the effects of mechanical loading on cartilage and the resulting chondrocyte-mediated biosynthesis, remodeling, degradation, and repair of this tissue. The effects of compression and tissue shear deformation are compared, and approaches to the study of mechanical regulation of gene expression are described. Of particular interest regarding dense connective tissues, recent experiments have shown that mechanotransduction is critically important in vivo in the cell-mediated feedback between physical stimuli, the molecular structure of newly synthesized matrix molecules, and the resulting macroscopic biomechanical properties of the tissue.

Animals↗