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At least 199 records · Page 11Linked to original sources

PubMed2002

Connective tissue growth factor/IGF-binding protein-related protein-2 is a mediator in the induction of fibronectin by advanced glycosylation end-products in human dermal fibroblasts.

Expansion of extracellular matrix with fibrosis occurs in many tissues, including skin, as part of the end-organ complications in diabetes. Advanced glycosylation end-products (AGEs) have been implicated as a pathogenic factor in diabetic tissue fibrosis. Connective tissue growth factor (CTGF), also known as IGF-binding protein-related protein-2, induces extracellular matrix. We have recently shown that CTGF mRNA and protein are up-regulated by AGE treatment of cultured human dermal fibroblasts. The aim of this study was to determine whether CTGF is an autocrine mediator in the induction of fibronectin (FN) by AGE. Primary cultures of nonfetal human dermal fibroblasts in confluent monolayer were treated with synthesized soluble AGE BSA, 0-200 microg/ml. Analysis of mRNA, by quantitative real-time RT-PCR and conditioned media from treated cultures, showed that FN mRNA was increased by approximately 4-fold at 48 h, and FN protein levels by Western immunoblot and FN ELISA were doubled, compared with control. In the same system, added recombinant human CTGF (0-500 ng/ml) induced FN mRNA and protein levels dose dependently and in a rapid time course. To test whether AGE BSA acts through cell-derived CTGF to induce FN, a CTGF neutralizing antibody was shown to significantly attenuate, but not fully inhibit, the AGE induction of FN mRNA. A pan-specific PKC inhibitor, GF109203X, at 0.2 microM, inhibited the induction of FN mRNA by AGE BSA. Although the same inhibitor did not significantly affect the induction of CTGF mRNA by AGE, it blocked the induction of FN mRNA by recombinant human CTGF. In summary, the induction of FN by AGE is partly mediated by the AGE-induced up-regulation of cell-derived CTGF and is dependent on PKC activity. These results have potential implications for the expansion of extracellular matrix in diabetes mellitus by advanced glycosylation end products.

Blotting, Western↗

PubMed1985

Connective tissue scarring in experimental spinal cord lesions: significance of dural continuity and role of epidural tissues.

Neoformation of connective tissue occurring at the level of spinal cord injury is considered a factor in the failure of regeneration in the mammalian spinal cord. The purpose of the present research was to experimentally investigate the origin and characteristics of connective proliferation following spinal cord lesion produced by compression in the rat. The role of the dural sheath and that of the tissues surrounding the spinal cord were studied. In one group of animals (1), the dura mater was left intact; in a second group (2) a transverse incision of the dura was performed at the level of the spinal cord compressive lesion. In group (1) a few collagenous fibres were seen within the lesion but no connective septum was observed. In group (2) a transversely orientated septum of fibrous scar tissue was constantly found within the lesioned cord. Our experimental study shows that: 1. dural continuity prevents the formation of connective tissue scarring and limits fibrous reactions in the epidural space; 2. opening of the dural sheath is followed by a vigorous fibroblastic reaction in the epidural tissue which extends into the spinal cord to form a connective septum.

Animals↗

PubMed2000

Width of keratinized tissue after gingivoplasty of healed subepithelial connective tissue grafts.

BACKGROUND: The subepithelial connective tissue graft has markedly broadened clinicians' abilities to treat gingival recession. Frequently, however, bulky soft tissue contours are sequelae of this procedure, and post-healing gingivoplasty is often performed to improve esthetics of the grafted site. As a secondary benefit, it is believed that the zone of keratinized tissue is additionally increased after gingivoplasty. METHODS: To further investigate this clinical impression, 16 bilateral pairs of sites with recession in 6 consecutive patients (mean age = 38 +/- 9 years) were studied. At the time of initial grafting, one site in each pair was randomly assigned to receive either gingivoplasty 2 months later (GP+) or no further treatment (GP-). Clinical measurement of recession and keratinized tissue width was standardized using customized acrylic stents and Schiller iodine solution, which stains epithelia; values were recorded at baseline (day of graft) and at 2, 3, and 5 months after grafting. Mean clinical gingival widths over time between GP+ and GP- sites, as well as within GP+ sites, were analyzed by t test. RESULTS: At 5 months, both the GP+ and GP- sites demonstrated a mean root coverage of 87.4% and increased keratinized tissue width (1.2 mm) when compared to their respective baseline measures. No differences in recession depth and width of keratinized tissue were seen at 5 months between the GP+ and GP- groups. In addition, no differences in recession or gingival width were found between 2- and 5-month observations for either the GP+ or GP- groups. CONCLUSIONS: These data suggest that the observed clinical improvements are the outcome of the initial graft surgery and that the gingivoplasty procedure does not result in additional (or "rebound") increases in keratinized tissue width.

Adult↗

PubMed1991

Effect of Aeromonas proteases on the binding of Aeromonas hydrophila strains to connective tissue proteins.

125I-labelled connective tissue protein binding to cells of Aeromonas hydrophila, A. caviae, and A. sobria strains isolated from diseased fish, was correlated with the Aeromonas protease degradation of 125I-labelled collagen types I and IV, fibronectin and laminin, immobilized on tissue culture microtitre plates. An inverse relation between 125I-labelled connective tissue protein binding to cells of Aeromonas strains and proteolytic degradation of immobilized connective tissue proteins by Aeromonas proteases was established. Inhibition of the Aeromonas proteolytic activity by protease inhibitors enhances the 125I-labelled connective tissue protein binding to cells of Aeromonas hydrophila strains. Culture conditions were found to influence both expression of proteolytic activity and binding properties.

Aeromonas↗

PubMed2003

Increased carotid artery intima-media thickness as an indicator of the onset of atherosclerosis in patients with connective tissue systemic diseases.

BACKGROUND: Systemic connective tissue diseases have an autoimmunological background. Atherosclerosis is the main cause of ischaemic heart disease in patients with these disorders, particularly in young females. Atherosclerotic process begins in the intimal and medial layers of arterial wall. Early detection of these changes may have important clinical implications. AIM: To assess the intima-media thickness (IMT) in carotid arteries in patients with connective tissue disorders and to correlate IMT with the presence of antiphospholipid (aPL) antibodies. METHODS: The study group consisted of 74 patients (63 females, 11 males) with documented connective tissue disease and 75 (62 females, 13 males) control subjects without clinical symptoms suggesting atherosclerosis. The IMT values, measured using ultrasonography, and aPL (IgG and IgM) antibody titre were assessed in all subjects. RESULTS: Mean aPL IgG and IgM values were significantly higher in patients than in controls (9.22 GMP/ml vs 6.59 GMP/ml, p<0.01; and 18.59 MPL/ml vs 12.05 MPL/ml, p<0.01, respectively). Patients with connective tissue diseases had significantly higher IMT values than controls (0.82 mm vs 0.57 mm, p<0.01). The IMT values positively correlated with age, presence of aPL antibodies, hypercholesterolemia and duration of the disease. CONCLUSIONS: The presence of aPL antibodies and increased IMT may indicate atherosclerosis in young patients with connective tissue diseases, and identify those who need more intensive prophylactic treatment in order to decrease the risk of atherosclerosis-related complications and death.

Adult↗

PubMed2005

A technique for augmenting the palatal connective tissue donor site: clinical case report and histologic evaluation.

This case report describes a simple method for augmenting tissue at prospective palatal connective tissue donor sites. The patient was referred for treatment of facial marginal tissue recession on the maxillary left canine. Clinical examination indicated that the palatal mucosa was thin and did not provide an adequate volume of soft tissue for donor harvesting, precluding the use of a palatal connective tissue graft for treatment of the recession defect. Sterile lyophilized bovine collagen sponge was therefore surgically inserted between a full-thickness palatal flap and bone at the prospective donor site. Eight weeks postoperative, the augmented palatal donor area showed a significant clinical increase in thickness and volume and served as a connective tissue donor source in the treatment of the facial marginal tissue recession. Histologic analysis of the donor tissue demonstrated normal structure, fibrous connective tissue, and abundant collagen. Clinical examination 6 months following surgery showed complete root coverage, with tissue texture, volume, and color similar to those of the adjacent soft tissue. Healing of the donor site was uneventful. This case report demonstrates that sterile lyophilized collagen sponge material may be used to augment palatal donor connective tissue and can subsequently be used as a donor source for soft tissue grafting.

Adult↗

PubMed2006

Acute manifestations of autoimmune connective tissue diseases.

Autoimmune connective tissue diseases are common conditions that often present non-specifically. Clinicians in emergency departments and acute medical assessment units may face these patients. This article provides an overview for the non-specialist clinician on the acute manifestations that may occur in these patients.

Adult↗

PubMed2005

Pulmonary vascular manifestations of mixed connective tissue disease.

Mixed connective tissue disease (MCTD) refers to a disease process with combined clinical features characteristic of systemic lupus erythematous, scleroderma, and polymyositis-dermatomyositis. This article focuses on the pulmonary vasculature manifestations of MCTD. We briefly discuss associations between MCTD and interstitial lung disease, pleural disease, and alveolar hemorrhage.

Humans↗

PubMed1990

Immunological features of diffuse connective tissue diseases.

Diffuse connective tissue diseases (DCTD) represent an heterogeneous group of disorders characterized by systemic inflammatory reactions that are currently classified on clinical grounds. Their aetiopathogenesis is largely unknown and appears to be very complex, associating exogenous factors with an immunogenetic predisposition. In the last decade, studies on human leukocyte antigen (HLA)-disease associations and antinuclear antibodies have provided some useful clues for the diagnosis and clinical management of DCTD.

Animals↗

PubMed1994

[MCTD (mixed connective tissue disease)].

Mixed connective tissue disease (MCTD) was proposed by Sharp and others in 1972. MCTD is a unique disease in which the presence of nuclear RNP antibody is characteristic and the patient shows partial symptoms of SLE, PSS and or PM/DM. Among them, Raynaud's phenomenon and sausage like finger or swollen hand are the most common symptoms. Although patients with MCTD generally respond to small amount of corticosteroid and the prognosis is not so bad, some patients with MCTD especially those with pulmonary hypertension show high mortality.

Humans↗

PubMed1984

Pulmonary hemorrhage and acute renal failure in a patient with mixed connective tissue disease.

Mixed connective tissue disease (MCTD) is considered to have a benign clinical course. Recently, renal disease has been recognized as a frequent complication (20%). This report describes a patient with MCTD who developed pulmonary hemorrhage and acute renal failure. The renal biopsy, in addition to a long-standing membranous nephropathy, revealed a tubulointerstitial nephritis. Immunofluorescent and electron microscopy showed immune complex deposition along the tubular basement membrane. Life-threatening, immune complex-mediated events can occur in the course of MCTD, manifested as pulmonary hemorrhage and tubulointerstitial nephritis.

Acute Kidney Injury↗

PubMedDate not supplied

Successful treatment of acute right cardiac failure due to pulmonary thromboembolism in mixed connective tissue disease.

Mixed connective tissue disease (MCTD) is characterized as a benign rheumatic disease with a favorable response to therapy. When pulmonary hypertension is a complication, however, it is often reported to be fatal. A 32-year-old female patient with MCTD who had developed rapidly progressive pulmonary hypertension and disseminated intravascular coagulopathy was admitted to our hospital and was successfully treated with corticosteroids and anticoagulants. The failure of microcirculation due to coagulopathy is considered to be one of the possible entities of pulmonary hypertension.

Adult↗

PubMedDate not supplied

Pulmonary hypertension in a child with mixed connective tissue disease.

Mixed connective tissue disease (MCTD) is characterized by high titers of antibody to ribonucleoprotein (RNP) in patients with features of several rheumatic diseases. We describe a child whose MCTD included arthritis, Raynaud's phenomenon, mucocutaneous ulcerations, sclerodermatous skin changes, restrictive lung disease, reduced carbon monoxide pulmonary diffusing capacity, abnormal esophogeal motility, and severe pulmonary hypertension. High antibody titers to ds-DNA and RNP were present. Clinical improvement followed therapy with prednisone and cyclophosphamide. Improvement in the degree of pulmonary hypertension was documented by repeat cardiac catheterization 8 months after the initiation of combination therapy.

Adolescent↗

PubMed1990

Orofacial manifestations of mixed connective tissue disease.

Mixed connective tissue disease (MCTD) is a multisystem disorder with overlapping features of systemic lupus erythematosus, scleroderma and polymyositis and is differentiated from them by a high titre of antibody to ribonucleoprotein. Orofacial manifestations of MCTD include trigeminal neuralgia-like pain, neuropathy, features suggestive of Sjögren's syndrome and lymphadenopathy. The recent experience of two patients presenting with trigeminal neuropathy as an early manifestation of this disease is described. One of these patients presented with 'lichenoid' oral mucosal lesions as a further early manifestation of MCTD. This appears to be the first case with this presenting feature to be described in the literature.

Adult↗

PubMed2005

Treatment of mixed connective tissue disease.

Mixed connective tissue disease (MCTD) is believed to be incurable and seems to have a variable prognosis. Some patients have a mild self-limited disease, whereas others develop major organ involvement that requires aggressive treatment. Because no controlled clinical trials have been performed to guide therapy in MCTD, treatment strategies must rely largely upon the conventional therapies that are used for similar problems in other rheumatic conditions (systemic lupus erythematosus, scleroderma, polymyositis). Given the heterogeneous clinical course of MCTD, therapy should be individualized to address the specific organ involved and the severity of underlying disease activity. Corticosteroids, antimalarials, methotrexate, cytotoxics (most often cyclophosphamide), and vasodilators have been used in the treatment of MCTD with varying degrees of success.

Cardiovascular Diseases↗

PubMed2000

Activation of protein kinase C inhibits the expression of connective tissue growth factor.

Connective tissue growth factor (CTGF) is a member of a protein family in which 38 cysteine residues are conserved. Although a wide variety of important biological functions have been ascribed to these proteins in recent years, the regulation of their gene expression for most members is virtually unknown. We studied the effects of protein kinase C (PKC) and tyrosine kinase on the expression of CTGF and observed that at the mRNA level CTGF expression is inhibited by the activation of PKC, but stimulated by the inhibition of PKC and tyrosine kinase. We further determined that the novel and the classical PKC isoforms are needed for the inhibition, but the atypical isoforms are not involved. Our data suggest that phosphorylation on serine/threonine and tyrosine by PKC and by tyrosine kinase are all inhibitory to the expression of CTGF.

Animals↗

PubMed1996

Long term follow-up of children with mixed connective tissue disease.

Mixed connective tissue disease (MCTD) is characterized by features of more than one of the rheumatic disorders with antinuclear antibodies in a speckled pattern and with antibodies to nuclear ribonucleoprotein (nRNP). MCTD is uncommon in children and long-term follow-up studies in children are infrequently reported. A retrospective review of clinical experience at five pediatric rheumatology centers provided 11 patients who met the following inclusion criteria: (1) Kasukawa's criteria for MCTD1; (2) presentation younger than 18th birthday; (3) greater than five years of follow-up; (4) completion of data collection form. The widely varying outcomes of these 11 children with MCTD on long-term follow-up may lend doubt that this is a unique and distinctive rheumatologic disorder.

Adolescent↗

PubMed2001

Hydrogen peroxide is a novel inducer of connective tissue growth factor.

Connective tissue growth factor (CTGF) has recently been described as a fibrogenic factor and is greatly induced by various extracellular stimuli, such as transforming growth factor-beta (TGF-beta), dexamethasone, and serotonin. CTGF induces collagen type I and fibronectin, and the deposition of such molecules leads to fibrotic disease in many tissues. Intracellular reactive oxygen species (ROS) are generated by extracellular stress conditions and are produced as by-products of cellular metabolism. Imbalanced cellular redox status is a potent pathogenic factor that leads to various degenerative diseases, including tissue fibrosis. Since CTGF is believed to play a crucial role in fibrotic disease formation in many tissues, we examined the role of ROS in CTGF gene expression in human lens epithelial cell line B3. The results showed that CTGF was induced by reactive oxygen species such as hydrogen peroxide and hydroxyl radicals. Next, we examined whether CTGF induction by ROS is via newly synthesized TGF-beta. The results showed that ROS directly induced CTGF mRNA not via the increased TGF-beta synthesis or activation. Next, we treated AG490, which is the well-known inhibitor of Janus kinase (JAK), with hydrogen peroxide. AG490 abrogated the CTGF induction by ROS in a dose-dependent manner. The results suggest that JAK-2/-3 seems to be involved in the enhanced CTGF mRNA expression by hydrogen peroxide. In this report, we present that hydrogen peroxide is a novel inducer of CTGF gene expression and that JAK-2/-3 activation seems to play a role in CTGF induction.

Amino Acid Sequence↗