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Collagen Type (collagen + type)

Distribution by Scientific Domains
Medical Sciences75%

Terms modified by Collagen Type

  • collagen type i
  • collagen type ii
    		•
  • collagen type iii
  • collagen type iv
    		•

    Selected Abstracts

    Collagen type,I signaling reduces the expression and the function of human receptor activator of nuclear factor -,B ligand (RANKL) in T,lymphocytes

    EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 12 2005
    Steve Gendron
    Abstract The mechanisms by which ,1 integrins modulate T,cell functions are still poorly defined. We have previously reported that signaling via the collagen type,I (Coll,I) receptor, ,2,1 integrin, inhibited FasL expression and protected Jurkat T,cells from activation-induced cell death (AICD). In this study, we examined whether Coll,I signaling in T,cells also modulates the expression of the human receptor activator of nuclear factor-,B ligand (RANKL), a recently identified TNF family member which has important functions in osteoclastogenesis, cell survival and apoptosis. Our results show that in both Jurkat T,cells and human primary T,cells, Coll,I signaling significantly reduces activation-induced RANKL expression by 50,60%. We also found that RANKL is not involved in AICD but participates in doxorubicin-induced apoptosis of leukemia T,cell lines including Jurkat, CEM and HSB-2. In this respect, Coll,I protected leukemia T,cell lines from doxorubicin-induced apoptosis by inhibiting doxorubicin-induced RANKL expression. Together, our results suggest that by limiting the production of RANKL, Coll,I signaling may contribute to the resistance of leukemia T,cells to chemotherapy. Our study also emphasizes the importance Coll,I signaling may have in the control of RANKL-associated T,cell functions. [source]

    Epithelioid cell histiocytoma , histogenetic and kinetics analysis of dermal microvascular unit dendritic cell subpopulations

    JOURNAL OF CUTANEOUS PATHOLOGY, Issue 7 2003
    Jeffrey S. Silverman
    Background:, Epithelioid cell histiocytoma (ECH), also known as epithelioid fibrous histiocytoma, is a peculiar dermal tumor, which can mimic melanocytic, vascular, epithelial, or other histiocytic lesions. Thought to arise from dermal dendrocytes, most ECH contain approximately 50% FXIIIa+ histiocytic dendrocytes, but not all lesional cells express FXIIIa. A putative fibroblastic component has not been characterized. Methods:, We analyzed the differentiation and cell kinetics of dermal microvascular unit cells in 12 previously reported ECH using antibodies to FXIIIa, CD68 (KP1), CD34, CD117, CD31, smooth muscle actin, collagen type 1 aminopropeptide, and MIB-1, using single and double immunostains. Results:, In ECH, many variably sized CD34/CD31+ tumor vessels with actin+ myopericytes were surrounded by epithelioid-to-dendritic cells of three types. About 5,80% were dendritic histiocytes that expressed FXIIIa but not CD31 or KP1. Fibroblasts, in some cases showing mild nuclear pleomorphism, were usually collagen type 1+, but CD34 and actin, in 11/12 cases. One ,early' ECH had 40% CD34+ epithelioid cells, admixed with 50% FXIIIa+ histiocytes. Most ECH had about 2,20% KP1+, CD117+ mast cells. Mast cell numbers increased with FXIIIa+ histiocyte numbers and the intensity of FXIIIa expression. MIB-1/FXIIIa double-labeling showed only rare cycling histiocytes, with numerous cycling fibroblasts and endothelial cells. Conclusions:, Our findings support the impression that ECH is a vascular fibrous histiocytoma. The constituent cells appear to arise from the activation of resident microvascular CD34+ dermal fibroblasts and the accumulation of FXIIIa+ dendritic stromal assembly histiocytes. The CD34+ cells appear to differentiate toward collagenous fibrocytes in association with histiocytes and mast cells in forming collagenous stroma and vessels. ECH is a tumor composed of all requisite cell types consistent with the origin from the dermal microvascular unit. [source]

    Quantification of expression levels of cellular differentiation markers does not support a general shift in the cellular phenotype of osteoarthritic chondrocytes

    JOURNAL OF ORTHOPAEDIC RESEARCH, Issue 1 2003
    Pia Margarethe Gebhard
    Abstract Many studies have shown increased anabolic activity in osteoarthritic cartilage and have suggested changes in the cellular phenotypes of articular chondrocytes. Most of these studies relied on non-quantitative technologies, which did not allow the estimation of the relative importance of the different differentiation phenomena. In the present study, we developed and used quantitative PCR assays for collagen types I, II(total), IIA, III, and X as marker genes indicating cellular synthetic activity (collagen type II) as well as differentiation pattern of chondrocytes (collagen types I, IIA, III, and X) and quantified these genes in normal, early degenerative, and late stage osteoarthritic cartilage in parallel. At first sight, our results confirmed previously published data showing hardly any expression of collagen genes in normal and significantly enhanced expression in osteoarthritic cartilage. This included collagen types II, III, and IIA, but also collagen types I(,1) and X. However, if one considers the ratios of the various markers of chondrocytic differentiation in comparison to collagen type II, the main synthetic product of differentiated chondrocytes, no shift in the cellular phenotype was detectable. In fact, expression ratios remained constant or were even decreased in osteoarthritic cartilage. Our results confirm that normal adult human articular chondrocytes display hardly any expression activity of the collagen types investigated, whereas osteoarthritic chondrocytes show very increased synthetic activity. The largely unchanged ratios of collagen subtypes investigated indicate that no general shift in the cellular phenotype does occur in osteoarthritic cartilage as suggested by previous investigations. © 2002 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved. [source]