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PubMed1988

Connective tissue remodelling in the ovine cervix during pregnancy and at term.

Cervical ripening and dilation in the ewe has been quantitated in terms of the connective tissue content of the tissue and the biosynthesis of the macromolecular components which make up the extracellular matrix of this tissue. During pregnancy there is a marked increase in the total tissue mass of the cervix along with the total mass of hydroxyproline (collagen) and hexuronate (proteoglycans and hyaluronate). The concentration of hydroxyproline of the cervix based on wet weight of the tissue decreases during pregnancy, however if based on dry weight, the concentration does not change until term. The hexuronate concentration based on both wet and dry weight of the tissue declines with pregnancy. The biosynthesis of collagen does not change during pregnancy but the rate of hyaluronate and proteoglycan synthesis by the cervix is increased in late pregnancy, and at term the rate of proteoglycan biosynthesis is elevated 10-fold. These data suggest that during cervical ripening and dilation a highly dynamic metabolic state exists within the tissue which allows for rapid tissue remodelling.

Animals↗

PubMed1994

Modulation of gap junction-mediated intercellular communication in embryonic chick mesenchyme during tissue remodeling in vitro.

Gap junction-mediated intercellular communication was analyzed in a model system in which tissue necrosis and remodeling could be modulated. This in vitro system, previously used for analysis of epithelial-mesenchymal tissue interaction, was modified to permit analysis of the presence and extent of intercellular communication by monitoring intercellular transfer of the microinjected fluorescent dye, Lucifer Yellow. Light and transmission electronmicroscopy were employed to correlate the presence and degree of gap junctional communication (coupling) with tissue morphology. Digital image analysis was used to determine cell density and mitotic indices within the outgrowths of explants. Our results indicated that cell communication in outgrowths adjacent to necrotic foci within an explant was minimal or absent. Cell-coupling in outgrowths adjacent to a compartment of viable mesenchyme was significantly higher - equivalent to unseparated control cultures. A time-course study demonstrated correlation of increased levels of cell-coupling in outgrowths with the level of tissue remodeling within an explant. Our conclusions from these studies are that embryonic mesenchymal cell populations may be selectively uncoupled as a result of alterations in the microenvironment produced by a proximate impaired cell population. It is proposed that endogenous factors in the microenvironment ("wound signals"), emanating from impaired cell populations, regulate gap junction-mediated intercellular communication in adjacent viable tissue. Normal, unimpaired populations of cells surrounding an area of injury are thereby isolated from the effects of a potentially toxic environment. This could serve as a protective function in development and may represent, in a more general sense, part of the repertoire of events associated with tissue repair and remodeling.

Animals↗

PubMed2005

Peroxisome proliferator-activated receptors (PPARs) and ovarian function--implications for regulating steroidogenesis, differentiation, and tissue remodeling.

The peroxisome proliferator-activated receptors (PPARs) are a family of transcription factors involved in varied and diverse processes such as steroidogenesis, angiogenesis, tissue remodeling, cell cycle, apoptosis, and lipid metabolism. These processes are critical for normal ovarian function, and all three PPAR family members--alpha, delta, and gamma, are expressed in the ovary. Most notably, the expression of PPARgamma is limited primarily to granulosa cells in developing follicles, and is regulated by luteinizing hormone (LH). Although much has been learned about the PPARs since their initial discovery, very little is known regarding their function in ovarian tissue. This review highlights what is known about the roles of PPARs in ovarian cells, and discusses potential mechanisms by which PPARs could influence ovarian function. Because PPARs are activated by drugs currently in clinical use (fibrates and thiazolidinediones), it is important to understand their role in the ovary, and how manipulation of their activity may impact ovarian physiology as well as ovarian pathology.

Animals↗

PubMed1989

Cytokine-mediated proteolysis in tissue remodelling.

Proteolytic enzymes play a key role in a variety of physiological processes in which the degradation of macromolecules is essential: angiogenesis, embryogenesis, bone and tissue remodelling, blood hemostasis and cell migration. The action of these enzymes is also crucial in the development of many pathological conditions such as wound healing, neoplasia, inflammation and arthritic disorders. The activity of proteases is negatively affected by specific protease-inhibitors. Various growth factors and other cytokines modulate the synthesis and secretion of both proteases and protease-inhibitors. The study of this regulation results in a better insight into (patho)physiology at the molecular level and promises to result in alternative treatment strategies.

Animals↗

PubMed2006

Prolonged treatment with the beta3-adrenergic agonist CL 316243 induces adipose tissue remodeling in rat but not in guinea pig: 2) modulation of glucose uptake and monoamine oxidase activity.

Beta3-adrenergic agonists are well-recognited to promote lipid mobilisation and adipose tissue remodeling in rodents, leading to multilocular fat cells enriched in mitochondria. However, effects of beta3-adrenergic agonists on glucose transport are still controversial. In this work, we studied in white adipose tissue (WAT) the influence of sustained beta3-adrenergic stimulation on the glucose transport and on the mitochondrial monoamine oxidase (MAO) activity. As one-week administration of CL 316243 (CL, 1 mg/kg/d) induces beta-adrenergic desensitization in rat but not in guinea pig adipocytes, attention was paid to compare these models. When expressing glucose uptake as nmoles of 2-deoxyglucose/100 mg cell lipids, maximally stimulated uptake was increased in adipocytes of WAT from treated rats but not from treated guinea pigs. However, basal hexose uptake was also increased in CL-treated rats and, as a consequence, the dose-dependent curves for insulin stimulation were similar in control and CL-treated rats when expressed as fold increase over basal. Insulin-induced lipogenesis was unchanged in rat or guinea pig adipocytes after CL-treatment. The glucose carriers GLUT4 and corresponding mRNA were increased in subcutaneous WAT or in brown adipose tissue (BAT) but not in visceral WAT or muscles of CL-treated rats. There was an increase of MAO activity in WAT and BAT, but not in liver, of CL-treated rats while no change was detected in guinea pigs. These findings show that only rat adipocytes, which are beta3-adrenergic-responsive, respond to chronic beta3-AR agonist by an increase of GLUT4 content and MAO activity, despite a desensitization of all beta-adrenoceptor subtypes.

Adipocytes, White↗

PubMed1989

Plasminogen activators in tissue remodeling and invasion: mRNA localization in mouse ovaries and implanting embryos.

To assess in vivo the postulated participation of urokinase-type (u-PA) and tissue-type (t-PA) plasminogen activators in processes involving tissue remodeling and cell migration, we have studied the cellular distribution of u-PA and t-PA mRNAs during mouse oogenesis and embryo implantation. By in situ hybridizations, we detected t-PA mRNA in oocytes and u-PA mRNA in granulosa and thecal cells from preovulatory follicles. These findings are compatible with a role for plasminogen activators in oogenesis and follicular disruption. We demonstrated the presence of u-PA mRNA in the invasive and migrating trophoblast cells of 5.5- and 6.5-d-old embryos. At 7.5 days, u-PA mRNA was predominantly localized to trophoblast cells that had reached the deep layers of the uterine wall, while the peripheral trophoblast cells surrounding the presomite stage embryo were devoid of specific signal. In 8.5-d-old embryos abundant u-PA mRNA expression resumed transiently in the giant trophoblast cells at the periphery of the embryo and in the trophoblast cells of the ectoplacental cone, to become undetectable in 10.5-d-old embryos. These observations establish the in vivo expression of the u-PA gene by invading and migrating trophoblast cells in a biphasic time pattern; they are in agreement with the proposed involvement of the enzyme in the extracellular proteolysis accompanying embryo implantation.

Animals↗

PubMed2004

Patterns of tissue remodeling after placement of ITI dental implants using an osteotome technique: a longitudinal radiographic case cohort study.

The aim of this prospective study was to document radiographically tissue remodeling patterns around ITI implants placed according to an osteotome technique. In 19 consecutive patients from a private practice, 25 implants of the ITI Dental Implant System were placed subjacent to the sinus floor. Implant beds were pre-prepared with pilot drills and/or using the Summers Osteotome Kit. Bio Oss particles were mixed with autologous bone and inserted into the apex area. Implants were placed self-tapping. The sinus floors were thereby pushed up with attempts not to sever the Schneiderian membrane. Healing occurred submerged or semi-submerged and was uneventful in 24/25 implants. At 1 year, all implants had been restored with crowns or short fixed partial dentures. One implant was lost in the first 3 weeks, but was replaced 6 months later in a second attempt. Intraoral radiographs were obtained presurgically and postsurgically at 3 and 12 months. The mean preoperative distance between the sinus floor and the crest was 7.0 mm (range 2.3-10.3 mm). The mean distances between the implant apex and the initial sinus floor were: 3.66 +/- 1.74 mm mesially and 4.44 +/- 1.62 mm distally. The mean height of the new bone reaching apically and mesially to the implants was 1.52 +/- 2.48 mm at surgery, but was reduced significantly to 1.24 +/- 1.30 mm at 3 months and 0.29 +/- 1.91 mm after 12 months (Hotelling's test P< or =0.01). Similar values were obtained at the disto-apical aspects. In an attempt to assess periapical bone/graft remodeling, a novel index was applied: 0=no bone/graft visible, 1=cloudy appearance of new bone/graft, 2=clearly visible new bone/graft disappearing structures of original sinus floor, 3=new bone/graft with new cortical plate and the former boundary of the sinus floor disappearing. This index increased statistically significantly from baseline to 12 months (Hotelling's test P< or =0.02). In conclusion, this study shows that in areas with reduced bone height subjacent to the sinus, an osteotome technique may provide a minimally invasive way to obtain implant abutments predictably. The grafted area apical to the implants undergoes shrinkage and remodeling. The original boundary of the sinus is eventually consolidated and replaced by a new cortical plate. In addition to the linear measurements, the novel index may assist in assessing periapical remodeling at implants placed with an osteotome technique.

Adult↗

PubMed2002

Myofibroblasts and mechano-regulation of connective tissue remodelling.

During the past 20 years, it has become generally accepted that the modulation of fibroblastic cells towards the myofibroblastic phenotype, with acquisition of specialized contractile features, is essential for connective-tissue remodelling during normal and pathological wound healing. Yet the myofibroblast still remains one of the most enigmatic of cells, not least owing to its transient appearance in association with connective-tissue injury and to the difficulties in establishing its role in the production of tissue contracture. It is clear that our understanding of the myofibroblast its origins, functions and molecular regulation will have a profound influence on the future effectiveness not only of tissue engineering but also of regenerative medicine generally.

Actins↗

PubMed2004

Transforming growth factor-beta1, myofibroblasts, and tissue remodeling in the pathogenesis of tracheal injury: potential role of gastroesophageal reflux.

Subglottic stenosis (SGS) is characterized by the obliteration of the tracheal lumen due to excessive deposition of connective tissue. We hypothesize that tracheal injury triggers the early production of transforming growth factor-beta1 (TGF-beta1), a factor implicated in fibroproliferative disorders. In turn, TGF-beta1 stimulates the transformation of tracheal fibroblasts into myofibroblasts with increased matrix production and scar contraction that might be influential in laying the foundation for the development of SGS. Consistent with this hypothesis, histologic analysis of tracheas from humans with SGS and from rats with experimental tracheal injury revealed increased alpha-smooth muscle actin-positive cells as compared to control tracheas, suggesting increased myofibroblast differentiation. Rat tracheal fibroblasts exposed to TGF-beta1 or gastric juice in vitro showed increased expression of alpha-smooth muscle actin, alterations in the expression of matrix molecules, and increased contraction of collagen gels. These findings suggest that gastric juice or other agents of tracheal injury promote tissue remodeling through the stimulation of the differentiation of fibroblasts into myofibroblasts.

Actins↗

PubMed2002

Thyroid hormone regulation of a transcriptional coactivator in Xenopus laevis: implication for a role in postembryonic tissue remodeling.

Thyroid hormone (TH) affects biological processes by regulating gene transcription through TH receptors (TRs). In the presence of TH, TR activates target gene transcription by recruiting one or more transcription coactivators belonging to diverse groups. Here, we demonstrate that during TH-dependent anuran metamorphosis, one such coactivator gene, the Xenopus laevis homolog of human Trip7, is up-regulated by TH. Kinetic studies suggest that Xenopus Trip7 is most likely induced indirectly by TH in a tissue-dependent manner. In the intestine, which undergoes extensive remodeling as the animal changes from being herbivorous to carnivorous, Trip7 is expressed at high levels during but not before or after metamorphosis. It is also up-regulated in other growing or remodeling tissues such as the brain and limb but not in degenerating tadpole tail skin. By using frog oocyte as a model, we show that Trip7 influences basal transcription in a chromatin structure-dependent manner but enhances the function of liganded TR regardless of the chromatin structure of the target promoter. In vitro studies indicate that Trip7 interacts directly with TR. These results suggest that during Xenopus metamorphosis, TH up-regulates, albeit indirectly, Trip7 to enhance TR function during larval-to-adult tissue transformation.

Amino Acid Sequence↗

PubMed2026

Genomic and epigenetic regulatory mechanisms in exercise-based rehabilitation processes: Cellular and tissue remodeling, microvascular adaptation, and circulating biomarkers.

While exercise-based rehabilitation is known to positively impact functionally related parameters, the role of genomic and epigenomic responses coordinated with cellular, extracellular matrix (ECM), mitochondrial, and microvascular adaptations remains insufficiently investigated. This narrative review summarizes mechanistic evidence linking exercise-associated mechanical, metabolic, hypoxia-redox, inflammatory, and hemodynamic stimuli with tissue remodeling and clinically relevant biomarkers. Current findings indicate that integrin-focal adhesion kinase (FAK) signaling and Hippo YAP/TAZ pathways contribute to mechanical signal transduction, cytoskeletal regulation, and gene expression, whereas metabolic adaptation, ATP homeostasis, and protein synthesis are regulated through AMPK-PGC-1α, SIRT1, and mTOR-dependent pathways. Epigenetic mechanisms, including DNA methylation, histone modifications, chromatin remodeling, and noncoding RNA regulation, further influence cell-specific responses in myofibers, satellite cells, fibro-adipogenic progenitors, endothelial cells, pericytes, and immune cells. In addition, VEGF-VEGFR2, eNOS-NO, and KLF2/KLF4 signaling, together with extracellular matrix turnover and inflammation resolution, contribute to tissue repair and microvascular adaptation during rehabilitation. Importantly, acute exercise-induced molecular responses should not be interpreted as direct evidence of sustained tissue adaptation. Circulating microRNAs, extracellular vesicles, cell-free DNA, collagen-related markers, and vascular proteins represent promising approaches for monitoring rehabilitation-related changes; however, their clinical translation remains limited by challenges related to tissue specificity, biomarker kinetics, analytical variability, and the need for standardized validation alongside structural and functional outcomes.

AMPK–PGC-1α signaling↗

PubMed2000

Role of gelatinases MMP-2 and MMP-9 in tissue remodeling following acute lung injury.

Acute lung injury is characterized by a severe disruption of alveolo-capillary structures and includes a variety of changes in lung cell populations. Evidence suggests the occurrence of rupture of the basement membranes and interstitial matrix remodeling during acute lung injury. The dynamic equilibrium of the extracellular matrix (ECM) under physiological conditions is a consequence of the balance between the regulation of synthesis and degradation of ECM components. Matrix metalloproteinases (MMPs) represent a group of enzymes involved in the degradation of most of the components of the ECM and therefore participate in tissue remodeling associated with pathological situations such as acute lung injury. MMP activity is regulated by proteolytic activation of the latent secreted proenzyme and by interaction with specific tissue inhibitors of metalloproteinases. This review details our knowledge of the involvement of MMPs, namely MMP-2 and MMP-9, in acute lung injury and acute respiratory distress syndrome.

Animals↗

PubMed2003

Drosophila matrix metalloproteinases are required for tissue remodeling, but not embryonic development.

The matrix metalloproteinase (MMP) family is heavily implicated in many diseases, including cancer. The developmental functions of these genes are not clear, however, because the >20 mammalian MMPs can be functionally redundant. Drosophila melanogaster has only two MMPs, which are expressed in embryos in distinct patterns. We created mutations in both genes: Mmp1 mutants have defects in larval tracheal growth and pupal head eversion, and Mmp2 mutants have defects in larval tissue histolysis and epithelial fusion during metamorphosis; neither is required for embryonic development. Double mutants also complete embryogenesis, and these represent the first time, to our knowledge, that all MMPs have been disrupted in any organism. Thus, MMPs are not required for Drosophila embryonic development, but, rather, for tissue remodeling.

Animals↗

PubMed2004

Hepatocyte proliferation and tissue remodeling is impaired after liver injury in oncostatin M receptor knockout mice.

Oncostatin M (OSM) is a member of the IL-6 family of cytokines. Mice deficient in the OSM receptor (OSMR(-/-)) showed impaired liver regeneration with persistent parenchymal necrosis after carbon tetrachloride (CCl(4)) exposure. The recovery of liver mass from partial hepatectomy was also significantly delayed in OSMR(-/-) mice. In contrast to wildtype mice, CCl(4) administration only marginally induced expression of tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2 genes in OSMR(-/-) mice, correlating with the increased gelatinase activity of matrix metalloproteinase (MMP)-9 and matrix degradation in injured livers. The activation of STAT3 and expression of immediate early genes and cyclins were decreased in OSMR(-/-) liver, indicating that OSM signaling is required for hepatocyte proliferation and tissue remodeling during liver regeneration. We also found that CCl(4) administration in IL-6(-/-) mice failed to induce OSM expression and that OSM administration in IL-6(-/-) mice after CCl(4) injection induced the expression of cyclin D1 and proliferating cell nuclear antigen, suggesting that OSM is a key mediator of IL-6 in liver regeneration. Consistent with these results, administration of OSM ameliorated liver injury in wildtype mice by preventing hepatocyte apoptosis as well as tissue destruction. In conclusion, OSM and its signaling pathway may provide a useful therapeutic target for liver regeneration.

Animals↗

PubMed1997

Immunohistochemical analysis of tissue remodelling during the anagen-catagen transition of the human hair follicle.

The transition from the growth phase (anagen) to the involution phase (catagen) involves profound morphological changes in the human hair follicle. Club hair and epithelial column formation, for example, are key features of the catagen phase, which result in the disruption of physical interaction between the bulb and the dermal papilla. However, the dynamics and tissue remodelling that occur during this involution process remain largely unknown. Using monoclonal antibodies directed against K14 keratin, trichohyalin, transglutaminase I, desmoglein and Ki67 antigen, we followed the movements of each of the main hair follicle compartments during the onset of catagen. Our results indicate that the inner root sheath is an early target in this process, suggesting a key role for this compartment in the maintenance of hair follicle homeostasis.

Biomarkers↗

PubMed1992

Membrane proteases: roles in tissue remodeling and tumour invasion.

The coordinated control of extracellular matrix degradation on the cell surface involves three crucial elements: secreted proteases and their inhibitors, surface protease receptors and integral membrane proteases. The roles that each of these elements play in cell surface proteolysis are described. The localization of proteases to the cell surface, protease activation, and regulation of cell surface proteolysis by protease inhibitors are key issues for elucidating the role of membrane proteases in tissue remodeling and tumour invasion.

Animals↗

PubMed1993

Granulomatous reaction and tissue remodelling in the cutaneous lesion of chromomycosis.

The cell-mediated immune reaction was studied in the cutaneous lesion of chromomycosis, using monoclonal antibodies against polymorphonuclear neutrophils, macrophage and lymphocyte subsets, endothelial and fibroblast cells. In addition, immunostaining of the main degradative enzymes (neutrophil elastase and interstitial collagenase) and certain important cytokines (transforming growth factor-beta, tumour necrosis factor-alpha and interferon-gamma) suggested an explanation for the granulomatous reaction and the associated tissue remodelling. The distribution pattern of neutrophils and macrophage subsets, observed by computer-aided image analysis, suggests that the in situ persistence of fungi is the main pathological factor.

Antigens, CD↗

PubMed2006

Human peritoneal adhesions show evidence of tissue remodeling and markers of angiogenesis.

PURPOSE: This study was designed to investigate the vascular structure and angiogenic activity of human peritoneal adhesions. METHODS: Adhesions were collected from patients undergoing laparotomy (n=32). Histologic features were documented and the distribution of mature and immature vascular markers were determined by immunolocalization and quantified by image analysis. The three-dimensional organization of blood vessels was investigated by confocal microscopy. Expression of vascular endothelial growth factor A, its receptor flk-1, and proliferating cell nuclear antigen were assessed by immunohistochemistry as indicators of angiogenic activity. RESULTS: Adhesions were found to be vascularized structures comprising bundles of collagen, interspersed with varying amounts of adipose tissue. Functional blood vessels expressed recognized vascular markers (vWF, CD34, alpha-SMA, and CD105) and formed a branching network similar to that of the peritoneum. Those adhesions expressing vascular endothelial growth factor A and its receptor showed significantly higher numbers of immature vessels as defined by expression of CD105. Omental adhesions (n=16) contained significantly more adipose tissue (P<0.05) and displayed a higher microvessel density (P<0.01) but lower cellularity (P<0.05) compared with nonomental adhesions (n=16). CONCLUSIONS: All adhesions contained functional blood vessels and most showed evidence of cell proliferation. The presence of vascular endothelial growth factor A and its receptor in human adhesions suggests ongoing angiogenic activity. This study demonstrates that adhesions are vascular structures with evidence of tissue remodeling and suggests potential for new prevention strategies involving antiangiogenic therapies.

Adipose Tissue↗