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Mol Med. 2000 Aug;6(8):705-19.
Suppression of type I collagen gene expression by prostaglandins in fibroblasts is mediated at the transcriptional level.
Riquet FB, Lai WF, Birkhead JR, Suen LF, Karsenty G, Goldring MB.
Rheumatology Division, Beth Israel Deaconess Medical Center, New England Baptist Bone & Joint Institute, Harvard Institutes of Medicine, Boston, Massachusetts, USA.
BACKGROUND: Tissues undergoing a chronic inflammatory process, such as the synovium in rheumatoid arthritis, are characterized by the infiltration of lymphocytes of different subsets and activation of monocyte/macrophages. Interleukin-1 (IL-1), a monocyte/ macrophage product that stimulates synovial fibroblasts to produce matrix metalloproteinases (MMPs), prostaglandins, and other cytokines, also has profound effects on the synthesis of extracellular matrix components such as type I collagen. In previous studies, we have shown that synovial fibroblasts and chondrocytes isolated from human joint tissues are particularly sensitive to prostaglandins, which modulate the effects of IL-1 on collagen gene expression in an autocrine manner. MATERIALS AND METHODS: BALBc/3T3 fibroblasts were treated with IL-1 and prostaglandins in the absence and presence of indomethacin to inhibit endogenous prostaglandin biosynthesis. Collagen synthesis was analyzed by SDS-PAGE as [3H]proline-labeled, secreted proteins, and prostaglandin production and cyclic adenosine 3',5'-cyclic monophosphate (camp) content were assayed. The expression of type I collagen gene (Col1a1) promoter-reporter gene constructs was examined in transient transfection experiments, and the binding of nuclear factors to the Col1a1 promoter region spanning -222 bp/+ 116 bp was analyzed by DNase I footprinting and electrophoretic mobility shift (EMSA) assays. RESULTS: IL-1 increased the synthesis of type I and type III collagens in BALBc/3T3 fibroblasts; greater increases were observed when IL-1-stimulated synthesis of PGE2 was blocked by indomethacin. Transient transfection experiments demonstrated dose-dependent inhibition of the-222 bp Col1a1 promoter by exogenously added prostaglandins with the order of potency of PGF2alpha > PGE2 > PGE1 DNase I footprinting showed increased protection, which extended from the region immediately upstream of the TATA box, owing to the binding of nuclear factors from PGE2- or PGE1-treated BALBc/3T3 cells. EMSA analysis showed zinc-dependent differences in the binding of nuclear factors from untreated and prostaglandin-treated cells to the -84 bp/-29 bp region of the Col1a1 promoter. CONCLUSIONS: These results show that the inhibition of Col1a1 expression by IL-1 in fibroblasts is mediated by prostaglandins at the transcriptional level and suggest that PGE-responsive factors may interact directly or indirectly with basal regulatory elements in the proximal promoter region of the Col1a1 gene.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11055589&dopt=Abstract
J Cell Physiol. 2000 Dec;185(3):432-9.
Differences in the mechanism for high- versus moderate-density fibroblast-populated collagen lattice contraction.
Ehrlich HP, Rittenberg T.
Section of Plastic and Reconstructive Surgery, Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA. pehrlicsu.edu
The free-floating fibroblast-populated collagen lattice (FPCL) model introduced by Bell contains 0.5 x 10(5) cell/ml and here is defined as a moderate-density FPCL (MD-FPCL). One modification of the model is to increase the cell density by a factor of 10, where 5 x 10(5) cells/ml defines a high-density FPCL (HD-FPCL). The initial detection of HD-FPCL contraction is 2 h, whereas MD-FPCL is later, 6 h. A contracted HD-FPCL has a doughnut-like appearance, due to the high density of cells accumulating at the periphery. A contracted MD-FPCL is a flattened disc. The compacted collagen of MD-FPCL lattice exhibits a strong birefringence pattern due to organized collagen fiber bundles. In contracted HD-FPCL, a minimal birefringence develops, indicating minimal organization of collagen fiber bundles. MD-FPCL contraction was reduced with less than 10% serum; the disruption of microtubules, uncoupling of gap junctions, inhibition of tyrosine kinases, and addition of a blocking antibody to alpha2beta1 collagen integrin. Making HD-FPCL with only 1% serum or including the inhibitory agents had only minimal affect on lattice contraction. On the other hand, platelet-derived growth factor stimulated HD-FPCL contraction but had no influence on MD-FPCL contraction. It is suggested that the mechanism for HD-FPCL contraction is limited to the process of cells spreading. HD-FPCL contraction is independent of collagen organization, microtubules, gap junctions, alpha2beta1 integrin, and tyrosine phosphorylation. MD-FPCL contraction involves collagen organization and is optimized by the involvement of microtubules, gap junctions, alpha2beta1 integrin, and tyrosine phosphorylation. When studying cell physiology in a collagen matrix, cell-density influences need to be considered. 2000 Wiley-Liss, Inc.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11056014&dopt=Abstract
Eur J Dermatol. 2000 Oct-Nov;10(7):513-6.
Preclinical diagnosis of pseudoxanthoma elasticum - methodological restrictions and ethical problems.
Hermes B, Grutzkau A, Hausser I, Kunze J, Henz BM.
Department of Dermatology, Krankenhaus Neukolln, Rudower Str. 48, D-12351 Berlin, Germany. hermenk-berlin.de
Pseudoxanthoma elasticum (PXE) is an inherited connective tissue disease. Only recently, mutations in the MRP6 gene on chromosome 16p13.1 have been identified in PXE families. Up to now, predictive testing has not been available. Since ultrastructural connective tissue alterations in overtly normal skin of predilection sites have supported preclinical diagnosis in children of affected individuals, we have screened the daughters of a PXE patient for these alterations. The patient's biopsy from lesional skin revealed elastin and collagen fibril abnormalities, but biopsies from the clinically inconspicuous daughters showed only ultrastructural alterations of collagen fibrils. These findings are inconclusive regarding the diagnosis of PXE in the daughters. Predictive or preclinical diagnosis of incurable, late-onset disorders creates complex social, ethical, and legal problems which call for special management strategies.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11056420&dopt=Abstract
Eur J Dermatol. 2000 Oct-Nov;10(7):522.
Upregulation of adhesion complex proteins and fibronectin by human keratinocytes treated with an aqueous extract from the leaves of Chromolaena odorata (Eupolin).
Phan TT, Allen J, Hughes MA, Cherry G, Wojnarowska F.
Department of Dermatology, The Churchill, The Oxford Radcliffe Hospital, Headington, OX3 7LS Oxford, UK.
The fresh leaves and extract of the plant Chromolaena odorata are a traditional herbal treatment in developing countries for burns, soft tissue wounds and skin infections. We have previously shown that the extract had an effect on the growth and proliferation of keratinocytes and fibroblasts in culture. This study has demonstrated that Eupolin extract increased expression of several components of the adhesion complex and fibronectin by human keratinocytes. Using indirect immunofluorescence we found increased expression (dose-dependent) of laminin 5, laminin 1, collagen IV, and fibronectin. The expression of the b1 and b4 integrins was upregulated by the extract at low concentrations (0.1 and 1 microg/ml), but the expression was decreased at higher doses of Eupolin (10 microg-150 microg/ml). A number of clinical studies carried out by Vietnamese and international medical investigators have demonstrated the efficacy of this extract on the wound healing process. In this study we have shown that Eupolin stimulated the expression of many proteins of the adhesion complex and fibronectin by human keratinocytes. The adhesion complex proteins are essential to stabilise epithelium and this effect could contribute to the clinical efficacy of Eupolin in healing.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11056422&dopt=Abstract
Eur J Dermatol. 2000 Oct-Nov;10(7):551-4.
Cerebriform plantar hyperplasia: ultrastructural study of two cases.
Winik BC, Boente MC, Asial RA.
Department of Electron microscopy, INSIBIO, CONICET, Universidad Nacional de Tucuman, Tucuman, Argentina. lamenont.edu.ar
In the present work we report the histopathological features of the cerebriform plantar hyperplasia observed in two patients with a mild form of the Proteus syndrome. Light microscopy revealed increased fibro-adipose tissue and adnexal structures in the dermis. Ultrastructurally, densely packed collagen fibrils variable in diameter and configuration, described as composite fibrils and unraveled fibrils, as well as a few fragmented elastic fibrils presenting an altered ratio between the elastin and the microfibrillar components were the major features observed. We consider that these histopathological findings will contribute to further delineate cerebriform plantar hyperplasia and also to establish clues for the early diagnosis of the Proteus syndrome.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11056430&dopt=Abstract
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