scholarly journals Porta-caval fibrous connections — the lesser-known structure of intrahepatic connective-tissue framework: A unified view of liver extracellular matrix

2021 ◽  
Vol 13 (11) ◽  
pp. 1484-1493
Author(s):  
Leila Patarashvili ◽  
Salome Gvidiani ◽  
Elza Azmaipharashvili ◽  
Keti Tsomaia ◽  
Marom Sareli ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Connective Tissue ◽  
Unified View

scholarly journals A Closer Look at the Cellular and Molecular Components of the Deep/Muscular Fasciae

2021 ◽  
Vol 22 (3) ◽  
pp. 1411
Author(s):  
Caterina Fede ◽  
Carmelo Pirri ◽  
Chenglei Fan ◽  
Lucia Petrelli ◽  
Diego Guidolin ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Connective Tissue ◽  
Treatment Strategies ◽  
Clear Understanding ◽  
Pathological Characteristics ◽  
Appropriate Treatment ◽  
Different Types ◽  
Molecular Components ◽  
Entire Network ◽  
Shed Light

The fascia can be defined as a dynamic highly complex connective tissue network composed of different types of cells embedded in the extracellular matrix and nervous fibers: each component plays a specific role in the fascial system changing and responding to stimuli in different ways. This review intends to discuss the various components of the fascia and their specific roles; this will be carried out in the effort to shed light on the mechanisms by which they affect the entire network and all body systems. A clear understanding of fascial anatomy from a microscopic viewpoint can further elucidate its physiological and pathological characteristics and facilitate the identification of appropriate treatment strategies.

scholarly journals Connective Tissue Metabolism and Gingival Overgrowth

2004 ◽  
Vol 15 (3) ◽  
pp. 165-175 ◽  
Author(s):  
P. C. Trackman ◽  
A. Kantarci
Keyword(s):  
Extracellular Matrix ◽  
Connective Tissue ◽  
Oral Hygiene ◽  
Tissue Specificity ◽  
Gingival Fibroblast ◽  
Drug Induced ◽  
Gingival Overgrowth ◽  
Connective Tissue Metabolism ◽  
Matrix Metabolism ◽  
Systemic Health

Gingival overgrowth occurs mainly as a result of certain anti-seizure, immunosuppressive, or antihypertensive drug therapies. Excess gingival tissues impede oral function and are disfiguring. Effective oral hygiene is compromised in the presence of gingival overgrowth, and it is now recognized that this may have negative implications for the systemic health of affected patients. Recent studies indicate that cytokine balances are abnormal in drug-induced forms of gingival overgrowth. Data supporting molecular and cellular characteristics that distinguish different forms of gingival overgrowth are summarized, and aspects of gingival fibroblast extracellular matrix metabolism that are unique to gingival tissues and cells are reviewed. Abnormal cytokine balances derived principally from lymphocytes and macrophages, and unique aspects of gingival extracellular matrix metabolism, are elements of a working model presented to facilitate our gaining a better understanding of mechanisms and of the tissue specificity of gingival overgrowth.

New insight in the biological integration of polytetrafluoroethylene from an explant used for diaphragm repair

2016 ◽  
Vol 31 (6) ◽  
pp. 844-850 ◽  
Author(s):  
Anne Schneider ◽  
Isabelle Talon ◽  
Eric Mathieu ◽  
Pierre Schaaf ◽  
François Becmeur ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Connective Tissue ◽  
Congenital Diaphragmatic Hernia ◽  
Diaphragmatic Hernia ◽  
Severe Disease ◽  
Central Area ◽  
Prosthesis Failure ◽  
Expanded Polytetrafluoroethylene ◽  
Peripheral Areas ◽  
Diaphragm Replacement

Congenital diaphragmatic hernia is a severe disease requiring diaphragm replacement mostly with expanded polytetrafluoroethylene. Unfortunately, the recurrence rate is high due to prosthesis failure with significant morbidity for the child. To provide a better understanding of the integration and possible failure processes of the biomaterial implanted in humans, we conducted electron microscopical and mechanical assessments on a prosthesis explant from a child with congenital diaphragmatic hernia presenting a recurrence. Our findings show a major penetration of connective tissue into the expanded polytetrafluoroethylene on the rough side, whereas the smooth side presents few tissue colonization. This penetration is more important in the central area (area A) with large collagen bundles and layers, in comparison to the peripheral areas without prosthesis failure (area B), where few extracellular matrix is produced. The connective tissue penetrates the prosthesis in depth. In contrast, the peripheral areas with prosthesis failure (area C) show very few cells and extracellular matrix, with an oriented organization in comparison to areas A and B. Obviously, the forces applied on the implanted material modulate the cellular behavior of the newly developed tissues. Atomic force microscopic measurements of the biomaterials’ surfaces may explain some cellular behaviors according to areas with or without failure.

Connective tissue growth factor and vascular endothelial growth factor from airway smooth muscle interact with the extracellular matrix

2006 ◽  
Vol 290 (1) ◽  
pp. L153-L161 ◽  
Author(s):  
Janette K. Burgess ◽  
Qi Ge ◽  
Maree H. Poniris ◽  
Sarah Boustany ◽  
Stephen M. Twigg ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Vascular Endothelial Growth Factor ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Connective Tissue ◽  
Airway Smooth Muscle ◽  
Connective Tissue Growth Factor ◽  
Tissue Growth ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

Airway remodeling describes the structural changes that occur in the asthmatic airway that include airway smooth muscle hyperplasia, increases in vascularity due to angiogenesis, and thickening of the basement membrane. Our aim in this study was to examine the effect of transforming growth factor-β on the release of connective tissue growth factor and vascular endothelial growth factor from human airway smooth muscle cells derived from asthmatic and nonasthmatic patients. In addition we studied the immunohistochemical localization of these cytokines in the extracellular matrix after stimulating bronchial rings with transforming growth factor-β. Connective tissue growth factor and vascular endothelial growth factor were released from both cell types and colocalized in the surrounding extracellular matrix. Prostaglandin E2 inhibited the increase in connective tissue growth factor mRNA but augmented the release of vascular endothelial growth factor. Matrix metalloproteinase-2 decreased the amount of connective tissue growth factor and vascular endothelial growth factor, but not fibronectin deposited in the extracellular matrix. This report provides the first evidence that connective tissue growth factor may anchor vascular endothelial growth factor to the extracellular matrix and that this deposition is decreased by matrix metalloproteinase-2 and prostaglandin E2. This relationship has the potential to contribute to the changes that constitute airway remodeling, therefore providing a novel focus for therapeutic intervention in asthma.

THE APODEME COMPLEX OF THE FEMORAL CHORDOTONAL ORGAN IN THE METATHORACIC LEG OF THE LOCUST SCHISTOCERCA GREGARIA

1992 ◽  
Vol 163 (1) ◽  
pp. 345-358 ◽  
Author(s):  
P. M.J. SHELTON ◽  
R. O. STEPHEN ◽  
J. J.A. SCOTT ◽  
A. R. TINDALL
Keyword(s):  
Extracellular Matrix ◽  
Connective Tissue ◽  
Direct Observation ◽  
Schistocerca Gregaria ◽  
Chordotonal Organ ◽  
Acid Fuchsin ◽  
Joint Angles ◽  
Direct Continuation ◽  
Loop Shape ◽  
Tissue Cells

The mechanical connections of the metathoracic femoral chordotonal organ (mtFCO) with its insertion at the femoro-tibial joint are described. The apodeme complex is shown to consist of a distal cuticular rod that is replaced proximally by dorsal and ventral ligaments. The dorsal ligament is a direct continuation of the distal rod but proximally it is replaced by ligamentous cells. The ventral ligament has no cuticular core and consists of ligamentous cells throughout its length. The ligaments are composed of bundles of connective tissue cells that are each enclosed in an extracellular matrix containing acid-fuchsin-staining fibrils. Internally the cells are packed with microtubules. During extension and flexion of the joint, the two ligaments move differentially. During passive extension of the tibia, the ventral ligament remains taut but the dorsal one buckles to form a slack loop. Direct observation of living preparations shows that the loop is first detectable during extension of the tibia at joint angles greater than about 51°. During flexion, the loop gradually tightens and disappears. It has completely disappeared at joint angles of less than about 36°. Changes in loop shape were demonstrable using preparations in which the tibia was moved sinusoidally ±10° about a mean femoro-tibial angle of 90° and photographs were taken using phase-locked illumination. Other details of the apodeme complex are described and the significance of the findings is discussed in relation to mtFCO function.

Abstract 311: Osteogenic Transcription Factor Runx2 Represses Connective Tissue Growth Factor Gene Expression And TGFβ Signaling In Vascular Smooth Muscle Cells

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Toru Tanaka ◽  
Takehisa Shimizu ◽  
Norimichi Koitabashi ◽  
Hiroki Matsui ◽  
Hiroshi Doi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Extracellular Matrix ◽  
Transcription Factor ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Connective Tissue ◽  
Vascular Smooth Muscle Cells ◽  
Tissue Growth ◽  
Matrix Synthesis ◽  
Tgfβ Signaling

[Objective] Runx2, a key transcription factor in osteoblast differentiation, is expressed in calcified atherosclerotic plaques. We have recently shown that Runx2 represses vascular smooth muscle cells (VSMCs) differentiation and promotes their osteogenic differentiation. Connective tissue growth factor (CTGF) has been implicated in the progression to vulnerable plaque by inducing mononuclear cell chemotaxis and VSMCs apoptosis despite of its potent stimulatory effect on connective tissue cell the proliferation and extracellular matrix synthesis. To assess the role of Runx2 in the process of plaque development, we investigated the molecular mechanism of the CTGF gene expression by Runx2 in VSMCs. [Methods and Results] RT-PCR analyses showed that adenovirally overexpressed Runx2 significantly repressed the basal expression of the CTGF gene in human aortic SMCs (HASMCs). Consistent with this, knockdown of the Runx2 expression in HASMCs by small interfering RNA (siRNA) increased CTGF mRNA levels. Luciferase assays showed that Runx2 reduced the transcriptional activity of the CTGF promoter. Transfection of a series of 5′-deletion constructs revealed that Runx2 inhibited CTGF expression through the sequence element located at 5′ untranslated region of CTGF mRNA. We next examined the effects of Runx2 on the TGFβ-induced CTGF expression. Runx2 overexpression significantly repressed CTGF expression in HASMCs stimulated with TGFβ, and knockdown of Runx2 by siRNA enhanced the induction of CTGF expression in response to TGFβ. Runx2 repressed TGFβ-induced CTGF promoter activity through the sequence including Smad binding element (SBE). Overexpression of Runx2 significantly reduced TGFβ- and Smad3-mediated luciferase activity of Smad-dependent promoter which contains four copies of SBE. Biotinylated DNA pulldown assay using SBE of CTGF promoter showed that Runx2 formed a complex with Smad3 and Smad4. [Conclusion] Runx2 repressed basal and TGFβ-induced CTGF gene expression in VSMCs. Thus, in addition to the potential for inducing vascular calcification, Runx2 may affect plaque stability by modulating extracellular matrix synthesis through inhibiting CTGF gene expression and TGFβ signaling.

scholarly journals MicroRNA in localized scleroderma: a review of literature

2019 ◽  
Vol 312 (5) ◽  
pp. 317-324 ◽  
Author(s):  
Katarzyna Wolska-Gawron ◽  
Joanna Bartosińska ◽  
Dorota Krasowska
Keyword(s):  
Extracellular Matrix ◽  
Connective Tissue ◽  
Noncoding Rna ◽  
Extracellular Matrix Proteins ◽  
Tissue Growth ◽  
Matrix Proteins ◽  
Mitogen Activated Protein Kinase ◽  
Localized Scleroderma ◽  
Mesenchymal Transition ◽  
Adjacent Structures

Abstract Localized scleroderma (LoSc) is rare connective tissue disease that manifests with inflammation and fibrosis of the skin. Depending on the LoSc subtype, adjacent structures such as subcutaneous tissue, fascia, muscles, bones may be affected. The hallmark of fibrosis is tissue remodelling with excess deposition of extracellular matrix proteins (ECM), principally collagens. MicroRNAs (miRNAs) are small, noncoding RNA molecules that consist of 19–24 nucleotides and act as negative regulators of gene expression at the posttranscriptional level. Based on the current articles, approximately 40 microRNAs have been linked to fibrosis in different organs and diseases. The majority of these molecules promote or inhibit fibrosis by targeting connective tissue growth factor (CTGF), extracellular matrix proteins, TGF-β pathway and MAPK (mitogen-activated protein kinase) pathway. Further, particular microRNAs regulate fibrogenesis by altering epithelial-to-mesenchymal transition (EMT) or activating proliferation of myofibroblasts. MiRNAs are relatively stable, detectable in tissues and body fluids (serum, plasma) which suggest that they may serve as beneficial biomarkers to monitor the course of the disease and response to treatment. Herein, we report the present state of knowledge on microRNA expression in localized scleroderma.

scholarly journals Targeted Deletion of the SPARC Gene Accelerates Disc Degeneration in the Aging Mouse

2005 ◽  
Vol 53 (9) ◽  
pp. 1131-1138 ◽  
Author(s):  
Helen E. Gruber ◽  
E. Helene Sage ◽  
H. James Norton ◽  
Sarah Funk ◽  
Jane Ingram ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Connective Tissue ◽  
Matricellular Protein ◽  
Secreted Protein ◽  
Wild Type ◽  
Variable Size ◽  
Targeted Deletion ◽  
Ultrastructural Studies ◽  
Aging Mouse ◽  
Lower Lumbar

SPARC (secreted protein, acidic, and rich in cysteine) is a matricellular protein that is present in the intervertebral disc; in man, levels of SPARC decrease with aging and degeneration. In this study, we asked whether targeted deletion of SPARC in the mouse influenced disc morphology. SPARC-null and wild-type (WT) mice were studied at 0.3–21 months of age. Radiologic examination of spines from 2-month-old SPARC-null mice revealed wedging, endplate calcification, and sclerosis, features absent in age-matched WT spines. Discs from 3-month-old SPARC-null mice had a greater number of annulus cells than those of WT animals (1884.6 ± 397.9 [mean ± SD] vs 1500.2 ± 188.2, p=0.031). By 19 months discs from SPARC-null mice contained fewer cells than WT counterparts (1383.6 ± 363.3 vs 1466.8 ± 148.0, p=0.033). Histology of midsagittal spines showed herniations of lower lumbar discs of SPARC-null mice ages 14–19 months; in contrast, no herniations were seen in WT age-matched animals. Ultrastructural studies showed uniform collagen fibril diameters in the WT annulus, whereas in SPARC-null disc fibrils were of variable size with irregular margins. Consistent with the connective tissue deficits observed in other tissues of SPARC-null mice, our findings support a fundamental role for SPARC in the production, assembly, or maintenance of the disc extracellular matrix.

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