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      Heat Shock Protein 47: A Novel Biomarker of Phenotypically Altered Collagen-Producing Cells

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          Abstract

          Heat shock protein 47 (HSP47) is a collagen-specific molecular chaperone that helps the molecular maturation of various types of collagens. A close association between increased expression of HSP47 and the excessive accumulation of collagens is found in various human and experimental fibrotic diseases. Increased levels of HSP47 in fibrotic diseases are thought to assist in the increased assembly of procollagen, and thereby contribute to the excessive deposition of collagens in fibrotic areas. Currently, there is not a good universal histological marker to identify collagen-producing cells. Identifying phenotypically altered collagen-producing cells is essential for the development of cell-based therapies to reduce the progression of fibrotic diseases. Since HSP47 has a single substrate, which is collagen, the HSP47 cellular expression provides a novel universal biomarker to identify phenotypically altered collagen-producing cells during wound healing and fibrosis. In this brief article, we explained why HSP47 could be used as a universal marker for identifying phenotypically altered collagen-producing cells.

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          A new puffing pattern induced by temperature shock and DNP in drosophila

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            Pulmonary fibrosis: pathogenesis, etiology and regulation

            Pulmonary fibrosis and architectural remodeling of tissues can severely disrupt lung function, often with fatal consequences. The etiology of pulmonary fibrotic diseases is varied, with an array of triggers including allergens, chemicals, radiation and environmental particles. However, the cause of one of the most common pulmonary fibrotic conditions, idiopathic pulmonary fibrosis (IPF), is still unclear. This review examines common mechanisms of pulmonary wound-healing responses following lung injury, and highlights the pathogenesis of some of the most widespread pulmonary fibrotic diseases. A three phase model of wound repair is reviewed that includes; (1) injury; (2) inflammation; and (3) repair. In most pulmonary fibrotic conditions dysregulation at one or more of these phases has been reported. Chronic inflammation can lead to an imbalance in the production of chemokines, cytokines, growth factors, and disrupt cellular recruitment. These changes coupled with excessive pro-fibrotic IL-13 and/or TGFβ1 production can turn a well-controlled healing response into a pathogenic fibrotic response. Endogenous regulatory mechanisms are discussed including novel areas of therapeutic intervention. Restoring homeostasis to these dysregulated healing responses, or simply neutralizing the key pro-fibrotic mediators may prevent or slow the progression of pulmonary fibrosis.
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              Molecular chaperone functions of heat-shock proteins.

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                Author and article information

                Journal
                Acta Histochem Cytochem
                AHC
                Acta Histochemica et Cytochemica
                Japan Society of Histochemistry and Cytochemistry (Tokyo, Japan )
                0044-5991
                1347-5800
                28 April 2011
                21 April 2011
                : 44
                : 2
                : 35-41
                Affiliations
                [1 ]Department of Pathology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan
                [2 ]Department of Restorative Dentistry and Biomaterials Sciences, Harvard School of Dental Medicine, Boston, MA, USA
                [3 ]Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, Boston, MA, USA
                Author notes
                Correspondence to: M. Shawkat Razzaque, MD, PhD, Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, Room: 304, 188 Longwood Avenue, Boston, MA 02115, USA. E-mail: mrazzaque@ 123456hms.harvard.edu ; razzaque@ 123456med.nagasaki-u.ac.jp
                Article
                AHC11001
                10.1267/ahc.11001
                3096080
                21614164
                2def9a2e-6679-4dee-8769-b6a705985599
                © 2011 The Japan Society of Histochemistry and Cytochemistry

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 29 December 2010
                : 18 February 2011
                Categories
                Review

                Clinical chemistry
                biomarker,collagen,hsp47,fibrosis
                Clinical chemistry
                biomarker, collagen, hsp47, fibrosis

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