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PubMed2004

Connective tissue growth factor mediates high glucose effects on matrix degradation through tissue inhibitor of matrix metalloproteinase type 1: implications for diabetic nephropathy.

High glucose concentration inhibits matrix degradation and affects the activities of the enzymes responsible, the matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs). Connective tissue growth factor (CTGF) expression is increased in diabetic nephropathy and is a downstream mediator of TGF-beta actions. However, whether CTGF regulates matrix degradation and the mechanism of effect in diabetes has not been reported. Human mesangial cells were cultured in media containing 5 or 25 mM glucose and, in some experiments, with recombinant human (rh)CTGF (0-1000 ng/ml) and/or appropriate neutralizing antibodies. Matrix degradation was inhibited by rhCTGF in a dose-dependent manner, and the decrease in matrix degradation caused by high glucose and by TGF-beta was significantly attenuated by addition of CTGF-neutralizing antibody (by 40.2 and 69.1%, respectively). Similar to 25 mM glucose, addition of rhCTGF increased MMP-2, TIMP-1, and TIMP-3 mRNA by 2.5-, 2.1-, and 1.6-fold, respectively (P < 0.05) but had no effect on membrane-type (MT)1-MMP or TIMP-2. Addition of TIMP-1 antibody to conditioned medium abolished the decrease in degradation caused by rhCTGF and partially prevented (by 79%) the glucose-induced inhibition of matrix degradation. In vivo studies of glomeruli from diabetic and control rats showed that intensive insulin treatment prevented the increase in expression of CTGF and TIMP-1 and attenuated the decreased matrix degradation seen in diabetes. In summary, CTGF inhibits matrix degradation by increasing TIMP-1 expression, and by this action it contributes to the inhibition of matrix breakdown by high glucose, implying that CTGF has a role in the reduced matrix degradation observed in diabetic nephropathy.

Animals↗
PubMed1975

Connective tissue cells, cell proliferation and synthesis of extracellular matrix-a review.

The ubiquitous connective tissues contain a wide range of cells including fibroblasts, osteoblasts and chondroblasts. Recently it has been demonstrated that another principal cell of the connective tissue is the smooth muscle cell in several organ systems. These have been shown to be responsible for the synthesis of the connective tissue matrix components of the uterine myometrium and of the arterial system, including collagen, both elastic fibre proteins and glycosaminoglycan. Microtubule inhibitors such as colchicine and vinblastine, and iron chelators such as alpha,alpha -dipyridyl have been used to study their morphologic and chemical effects on collagen synthesis and secretion. Colchicine produces an increase in large Golgi-associated vacuoles, which sometimes contain material reminiscent of aggregates of collagen macromolecules. Vinblastine produces alterations in the endoplasmic reticulum cisternae similar to alterations seen in ascorbic acid deficiency, and alpha,alpha-dipyridyl increases the frequency of regions in cells, interpretable as potential sites of communication of rough endoplasmic reticulum cisternae with the cell surface. Ferritin conjugated anti-procallagen sera were used to localize procollagen in cells and demonstrated procollagen not only in the cisternae of rough endoplasmic reticulum but in all of the elements of the Golgi complex as well. The studies reported in this review have shown that in cell culture arterial smooth muscle will produce not only the microfibrillar protein of the elastic fibre but soluble and/or insoluble elastin as well. Recent studies on serum factors responsible for the proliferation of connective tissue cells have demonstrated that at least one of the principal factors responsible for fibroblast and/or smooth muscle cell proliferation in culture is derived from thrombocytes. Medium containing serum derived from cell-free plasma lacks most of this proliferative effect which can be reinstated when platelets are present during recalcification to form serum. This effect is due to the platelet release reaction as shown by combining supernatant factors derived from platelets exposed to purified thrombin to cell-free, plasma derived serum. Studies with macrophages have also suggested that phagocytic macrophages release factor(s) into a cell culture medium that may also participate in stimulating fibroblasts to proliferate in vitro. The means by which these factors stimulate fibroblast proliferation and connective tissue synthesis remains to be elucidated.

Animals↗
PubMed1998

Neuropathies associated with connective tissue disease.

Neuropathies are a common neurologic manifestation of diffuse connective tissue disease. Vasculitic neuropathy requires prompt diagnosis and treatment to improve its outcome. It is commonly multifocal but may be confluent and symmetrical. Vasculitic neuropathy needs to be distinguished from the more common syndromes of compression neuropathy, which may also be multifocal, and nonvasculitic distal axonal polyneuropathy. Sensory neuronopathy is a distinctive syndrome unique to Sjögren's syndrome among the connective tissue diseases. Trigeminal sensory neuropathy may be the presenting feature of systemic sclerosis or may develop during the course of other connective tissue diseases. This article reviews the clinical and diagnostic features of neuropathies associated with the common diffuse connective tissue diseases.

Connective Tissue Diseases↗
PubMed1985

Nevi of connective tissue. A reappraisal of their classification.

Nevi of connective tissue may be conveniently divided according to clinical and pathologic presentations into two types, namely, the adventitial and the reticular. Nevi of adventitial connective tissue are usually small and situated on the extremities. They are characterized by accumulations of fibroblasts and apposition of collagen around adnexa and vessels. Nevi of reticular connective tissue are usually situated on the trunk. They consist of faulty distributions and amounts of collagen bundles, elastic fibers, or proteoglycans.

Collagen↗
PubMed1986

Degradation of porcine dermal connective tissue by collagenase and hyaluronidase.

Selective destruction of connective tissue may be a useful therapeutic tool in conditions associated with abnormal deposition of scar tissue. We have investigated intradermal injections of clostridial collagenase and bovine testicular hyaluronidase alone and in combination in Yucatan miniature hairless pigs. Collagenase in combination with hyaluronidase was quite efficient at destroying the connective tissue matrix, although elastic tissue appeared to be completely spared. Collagenase alone at higher doses degraded collagen, but hyaluronidase had little effect on connective tissue architecture.

Animals↗
PubMed1997

Integrated connective tissue in bioabsorbable barrier material and periodontal regeneration.

The objective of this study was to evaluate the relationship between integrated connective tissue (ICT), that is, the presence of connective tissue into the membrane structure, and the clinical outcome of membrane-supported periodontal surgery. Twenty-six systemically healthy subjects affected by chronic adult periodontitis were enrolled in the study. One tooth site per patient, associated with an angular bony defect and an attachment loss of > 7 mm, was selected to be treated by means of a guided tissue regeneration procedure using a bioabsorbable membrane. Barrier material was surgically removed after 4 weeks for SEM analysis. For each treated site, the difference in clinical attachment loss, probing depth, and gingival recession between the baseline examination and follow-up 6 months after the second surgery was calculated. Gain of attachment was statistically (P < 0.001) greater in sites with no membrane exposure when compared to sites with exposed barrier material (5.5 +/- 1.0 vs. 4.0 +/- 0.6), while further gingival recession was greater (3.0 +/- 0.9 vs. 2.1 +/- 0.5) in sites with clinically exposed membranes. The results of SEM analysis revealed that when connective tissue structures were observed on membrane surfaces, no bacteria could be detected; conversely, areas heavily colonized by bacteria did not show the presence of connective tissue. Regression analysis indicated that integrated connective tissue on the external layer of the barrier material was positively correlated with the amount of attachment gain and negatively with the amount of gingival recession. Bacterial colonization of the membrane was negatively correlated with attachment gain and positively with gingival recession. It was concluded that connective tissue integration is an important biological phenomenon in preventing membrane exposure and bacterial plaque colonization and thus in enhancing the clinical outcome following guided tissue regeneration surgery.

Absorption↗
PubMed1984

Genetic and epigenetic control of connective tissues in the craniofacial structures.

The connective tissues of the craniofacial region can neither develop nor be maintained independently of their local environment. I have stressed such epigenetic control in the present brief review of the origin, differentiation, morphogenesis, and growth of selected craniofacial tissues. I began by discussing the origin of these tissues in the neural crest. The extensive migration of neural crest cells to form the craniofacial region of the embryo is epigenetically regulated by extracellular matrix products such as fibronectin, and by basal laminae of the epithelia along which some cells migrate. The trigger which initiates differentiation of these mesenchymal cells is provided by epithelia with which they come into contact either before, during, or after migration, as illustrated by the differentiation of both Meckel cartilage and mandibular dermal bones. Subsequent differentiation of secondary cartilage is also shown to be epigenetically initiated, in this case by the mechanical environment created by muscle action. Both secondary cartilages on avian dermal bones and the condylar cartilage of the mammalian dentary are discussed. The interplay between genetic and epigenetic factors in morphogenesis and growth of craniofacial connective tissues is then very briefly discussed.

Animals↗
PubMed1991

Blood tests in the diagnosis of connective tissue diseases.

Making the diagnosis of connective tissue disease can at times be extremely difficult. Obtaining a complete rheumatological and medical history, and performing a thorough physical examination are absolutely essential. This article has reviewed several of the laboratory parameters which can aid the clinician in the differential diagnosis of connective tissue diseases. Which tests should be ordered in any given individual patient should be determined by the clinical setting. Careful evaluation of the laboratory data, in the context of the patient's history and physical examination, should, in general, allow the clinician to make the proper rheumatological diagnosis.

Connective Tissue Diseases↗
PubMed2006

Genetic analysis of familial connective tissue alterations associated with cervical artery dissections suggests locus heterogeneity.

BACKGROUND AND PURPOSE: Cervical artery dissections (CAD) can be associated with connective tissue aberrations in skin biopsies. The analysis of healthy relatives of patients suggested that the connective tissue phenotype is familial with an autosomal dominant inheritance. METHODS: We performed genetic linkage studies in 3 families of patients with CAD. Connective tissue phenotypes for the patients and all family members were assessed by electron microscopic study of skin biopsies. A genome-wide linkage analysis of 1 family (1 patient with 8 healthy relatives) indicated 2 candidate loci. Three genes were subsequently studied by sequence analysis. Part of the genome was also studied by linkage analysis in 2 further families. RESULTS: The genome-wide scan in a single family suggested linkage between the hypothetical mutation causing the connective tissue phenotype and informative genetic markers on chromosome 15q24 (logarithm of the odds score: Z= +2.1). A second possible candidate locus (Z=+1.9) was found on chromosome 10q26. Sequence analysis of 3 candidate genes in the suggestive locus (chondroitin sulfate proteoglycan4 [CSPG4], lysyl oxidase-like1 [LOXL1] and fibroblast growth factor receptor2 [FGFR2]) did not lead to the identification of a mutation responsible for connective tissue alterations. In 2 additional smaller families the loci on chromosome 15q24 and 10q26 were excluded by linkage analysis. CONCLUSIONS: Linkage analysis of a large family with CAD-associated connective tissue alterations suggested the presence of a candidate locus on chromosome 15q2 or on chromosome 10q26. Sequence analysis did not lead to the identification of a mutated candidate gene in 1 of these loci. The study of 2 additional pedigrees indicated locus heterogeneity for the connective tissue phenotype of CAD patients.

Adult↗
PubMedDate not supplied

Serum levels of tissue inhibitor of metalloproteinases in patients with mixed connective tissue disease.

OBJECTIVE: To determine serum tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2 levels in patients with mixed connective tissue disease (MCTD) and investigate whether these levels were correlated with the clinical or serological features of this disease. METHODS: Serum TIMP-1 and TIMP-2 levels were measured with specific enzyme-linked immunosorbent assays. Serum samples from 26 patients with MCTD and 18 healthy individuals were examined. RESULTS; Serum levels of TIMP-1 were significantly higher in patients with MCTD than those in healthy individuals (mean +/- SD: 218.9 +/- 50.8 ng/ml versus 160.0 +/- 38.7 ng/ml, P < 0.0001). MCTD patients with elevated TIMP-1 had esophageal involvement at a significantly higher incidence than those without (77.8% versus 35.3%, p < 0.05). There was no difference in serum TIMP-2 levels between patients with MCTD and healthy controls (75.6 - 11.9 ng/ml versus 77.3 +/- 10.7 ng/ml). CONCLUSION: These results suggest that TIMP-1 is involved in the pathogenesis of MCTD, and that TIMP-1 may be a serological marker for the presence of esophageal involvement in these patients.

Adult↗
PubMed2002

Hard tissue formation on dentin surfaces applied with recombinant human bone morphogenetic protein-2 in the connective tissue of the palate.

The purpose of this study was to evaluate whether hard tissue might be formed on dentin surfaces applied with recombinant human bone morphogenetic protein-2 (rhBMP-2) in palatal connective tissue. Fifty-eight dentin blocks were prepared from rat roots, demineralized with 24% EDTA (pH 7.0), applied with 0, 50 and 100 microgram/ml rhBMP-2, and labeled as groups 0, 50 and 100. The dentin blocks were then transplanted into palatal connective tissue of rats, and specimens were prepared at two and four weeks after surgery for histologic and histomorphometric examinations. The results showed that the percentage of newly formed hard tissue in relation to the total dentin block surface length in groups 0, 50 and 100 was 0.0%, 2.8% and 4.4% at two weeks, and 0.0%, 1.6% and 12.8% at four weeks, respectively. New hard tissue formation in groups 50 and 100 was significantly promoted as compared to group 0 (p < 0.01). These findings thus indicate that rhBMP-2 application to dentin enhanced new hard tissue formation on dentin surfaces in the connective tissue of the palate.

Animals↗
PubMed1999

Connective tissue disease and silicosis.

BACKGROUND: To determine the prevalence of connective tissue disease in a cohort of individuals with silicosis, we reviewed the medical records and questionnaires from individuals reported from 1987 to 1995 to a state surveillance system for silicosis. Reporting of individuals with silicosis is required by state law. Cases were reported by hospitals, physicians, the state workers' compensation bureau, or from death certificates. Only individuals who met the criteria for silicosis developed by the National Institute for Occupational Safety and Health (NIOSH) were included in the analysis. RESULTS: A questionnaire was completed for all 583 cases. Medical records were available for 463. There were 24 people with rheumatoid arthritis, one with scleroderma, and one with systemic lupus erythematosus. All were men. The prevalence of rheumatoid arthritis was 5.2% (relative risk (RR) 2.73, 95% confidence limit (CL) 1.75-4.06). The prevalence of scleroderma was 0.2% (RR 15.65, 95% CL 0.21-87.03) and the prevalence of systemic lupus erythematosus was 0.2% (RR 11.37, 95% CL 0.15-63.23). This is an approximately 2.5-15-fold increased risk for these connective tissue diseases compared to estimated prevalences in the general population. Individuals with silicosis and connective tissue disease did not differ from individuals with silicosis but without connective tissue disease by race, age, type of industry where exposed to silica, history of tuberculosis, whether or not they had applied for workers' compensation, and whether or not they had progressive massive fibrosis on chest x-ray. CONCLUSION: Although the association between scleroderma and silicosis has been more widely reported in the literature, the prevalence of rheumatoid arthritis was greater than the prevalence of scleroderma or systemic lupus erythematosus among a cohort of individuals with silicosis.

Arthritis, Rheumatoid↗
PubMed2003

IgA and IgG tissue transglutaminase antibody prevalence and clinical significance in connective tissue diseases, inflammatory bowel disease, and primary biliary cirrhosis.

An association between celiac disease (CD) and other autoimmune diseases such as connective tissue diseases (CTD), inflammatory bowel diseases (IBD), and primary biliary cirrhosis (PBC) has been reported in several studies. However, a high rate of false positives in autoantibody testing was noted, especially when tissue transglutaminase (tTG) from guinea pig liver was used. Thus, the real prevalence of CD in CTD, IBD, and PBC is unclear. In a case-control study, 400 patients with CTD, 170 with IBD, 48 with PBC, and 120 healthy subjects were investigated for CD by the analysis of IgA and IgG tTG antibodies using the more specific human recombinant tTG immunoenzymatic assay. Patients and controls with positive findings were further tested for antiendomysial antibodies by indirect immunofluorescence and HLA typing, and those found positive by either of these tests underwent duodenal biopsy to confirm a possible diagnosis of CD. Twelve patients were positive for IgA or IgG tTG antibodies, showing an overall prevalence of 1.9%. Only 1 healthy subject (0.8%) had a low level positive reaction for IgA anti-tTG. Among the 12 patients and the healthy subject, only 2 (1 SLE and 1 ulcerative colitis patient) were subsequently confirmed to be affected with CD by positive EMA, HLA, and small bowel biopsy findings. The highest rate of false positives was found in PBC patients (10.4%). For these reasons, serological screening testing for CD is not recommended in CTD patients or in subjects affected with IBD or PBC, unless there is a relevant clinical suspicion of CD.

Adult↗
PubMedDate not supplied

[Cardiac manifestations of connective tissue diseases].

We have studied the cardiac manifestations of connective tissue diseases. In 213 files of patients with connective tissue disease of the Department of Medicina I, Hospital Santa Maria, during 21 years. Cardiac manifestations were observed in 63 (90%) SLE. Pericarditis was the most frequent manifestation and occurred in 33 patients (43%). The cardiac manifestations were observed in 40 (41%) RA. Pericarditis appeared in 11 patients, valvulopathy in 12 patients and coronaropathy in 11 patients. In 10 of PD diagnosed patients, ECG abnormalities were the only findings. Arrhythmias, conduction disturbances, cardiac failure and coronaropathy were the cardiac manifestations of PSS in 11 patients. Polyarteritis Nodosa patients had myocardial ischemia and another had a malignant hypertension diagnosis. We found pericardial effusion in one patient and angina in another one with MCTD diagnosis. We did'nt find any cardiac manifestation in AS. Cardiac manifestations are frequent in connective tissue diseases. The ECG, ECO and pathology show abnormal findings. Although there is not clinical cardiological expression of the disease we suggest the use of ECG. ECO Holter electrocardiography and isotopic myocardial perfusion scan technics in the clinical evaluation of such patients.

Adolescent↗
PubMed1995

Regulation of connective tissue synthesis in systemic sclerosis.

Excessive connective tissue deposition in the skin and other organs is the pathologic hallmark of systemic sclerosis (SSc), and fibrosis accounts for much of the chronic morbidity of this disease. Unregulated production of collagen in SSc skin fibroblasts has been demonstrated both in vivo and in vitro, and is considered to be a critical process in the development of fibrosis. In addition to collagen, other components of the extracellular matrix are also overexpressed in SSc fibroblasts, and may be important in the functional alterations of connective tissue. The transcriptional activity of several genes coding for matrix macromolecules is upregulated in SSc fibroblasts. The pleiotropic signaling molecule transforming growth factor-beta (TGF beta) is likely to be intimately involved in initiating and perhaps perpetuating the fibrotic response in SSc. TGF beta, a potent profibrotic cytokine, is highly expressed in endothelial cells, in fibroblasts near blood vessels, and in perivascular inflammatory cells in involved tissues in SSc. The apparent failure of SSc fibroblasts to down-regulate their collagen synthesis when cultured in a three-dimensional matrix suggest an additional mechanism for the maintenance of unregulated collagen production in these cells. Finally, subpopulations of fibroblasts with an activated biosynthetic phenotype may become dominant in SSc. Therefore, persistent elevation of extracellular matrix gene expression in SSc tissues may be the result of a series of events representing the interaction of genetic and hormonal factors. A precise delineation of the mechanisms of fibroblast activation is needed for understanding the pathogenesis of SSc, and for the rational design of therapeutic interventions aimed at interfering with the fibrotic process.

Collagen↗
PubMed1982

Some histological aspects of the structure of the connective tissue system and its relationships with the blood vessels in the human orbit.

The connective tissue septa in the human orbit are organized in a constant and characteristic fashion. In the collagen fibre meshwork of the septa, anteroposteriorly directed collagen fibre bundles are relatively rare. The number of smooth muscle cells present in a septum depends on the orbital level explored. In the apical region only few of these cells are found, at eye-ball level they are more numerous. No further regularity in distribution of smooth muscle cells in the septa is present. All connective tissue septa contain elastic fibres. Blood vessels and connective tissue form an integrated system. The venous walls merge with the fibrous structure of the septa; the arteries only make contact with the septa when they perforate them. In doing so, the arteries mainly run between the septal fibre bundles, only loosely connected to some of them. The microvascular system is predominantly confined to the adipose tissue compartments. The interrelationships of the vascular system and the connective tissue system are likely to be important factors in controlling and regulating orbital blood-flow. In addition, the well-defined morphological organization of the connective tissue in its interrelationships with the vascular system might serve a mechanical regulating function by both allowing and restricting certain eye-ball movements. For these functions, the physico-chemical properties of the connective tissue system and the microstructure of the vascular system are probably of considerable interest. Thus, the highly organized architecture of the connective tissue system in the human orbit together with its intricate interrelationships with the vascular system, might prove to be important for mechanical as well as metabolic purposes and so have consequences for interventions, diagnostic or surgical, in the orbit.

Blood Vessels↗
PubMed2006

Tensilin-like stiffening protein from Holothuria leucospilota does not induce the stiffest state of catch connective tissue.

The dermis of sea cucumbers is a catch connective tissue or mutable connective tissue that exhibits large changes in mechanical properties. A stiffening protein, tensilin, has been isolated from the sea cucumber Cucumaria frondosa. We purified a similar protein, H-tensilin, from Holothuria leucospilota, which belongs to a different family to C. frondosa. H-tensilin appeared as a single band with an apparent molecular mass of 34 kDa on SDS-PAGE. No sugar chain was detected. Tryptic fragments of the protein had homology to known tensilin. H-tensilin aggregated isolated collagen fibrils in vitro in a buffer containing 0.5 mol l(-1) NaCl with or without 10 mmol l(-1) Ca(2+). The activity of H-tensilin was quantitatively studied by dynamic mechanical tests on the isolated dermis. H-tensilin increased stiffness of the dermis in the soft state, induced by Ca(2+)-free artificial seawater, to a level comparable to that of the standard state, which was the state found in the dermis rested in artificial seawater with normal ionic condition. H-tensilin decreased the energy dissipation ratio of the soft dermis to a level comparable to that of the standard state. When H-tensilin was applied on the dermis in the standard state, it did not alter stiffness nor dissipation ratio. The subsequent application of artificial seawater in which the potassium concentration was raised to 100 mmol l(-1) increased stiffness by one order of magnitude. These findings suggest that H-tensilin is involved in the changes from the soft state to the standard state and that some stiffening factors other than tensilin are necessary for the changes from the standard to the stiff state.

Amino Acid Sequence↗