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      Differential Expression of Extracellular Matrix and Adhesion Molecule Genes in the Brain of Juvenile versus Adult Mice in Responses to Intracerebroventricular Administration of IL-1

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          Abstract

          Objective: Intracerebroventricular (ICV) injection of interleukin-1 (IL-1) stimulates the recruitment of leukocytes into the central nervous system at different time points in juvenile versus adult mice. Our results showed that leukocytes entered brain parenchyma at 8 and 16 h after injection in juvenile and adult mice, respectively. This study compares the differential gene expression patterns of extracellular matrix and adhesion molecules in the brain of juvenile and adult mice. Methods: We analyzed these gene expressions in mice brains by microarray and real-time PCR at 2 and 8 h after ICV IL-1. Results: After ICV IL-1, the following genes were significantly upregulated in both juvenile and adult mice: LAMβ1-1, MMP17, TGFβ, THBS3 and VCAM1 were upregulated at 2 h after injection; LAMβ1-1 and TGFβ were upregulated at 8 h. Additional changes were found in adult mice only: CNTN1, ECM1, ICAM1 and LAMα4 were upregulated at 2 h after injection; COL4α1, MMP3 and VCAM1 were upregulated at 8 h; TIMP4 was downregulated. Comparing juvenile and adult mice, real-time PCR analysis showed that there was more induction of TGFβ at 8 h and a stronger downregulation of TIMP4 at 2 h after injection in juvenile mice. Higher expression of MMP17 was found in juvenile mice, compared to adult mice, at both 2 and 8 h after injection. Conclusions: These data show distinct expression patterns of molecules related to the extracellular matrix and adhesion molecules in juvenile versus adult mice, and suggest that increased expression of MMP17 and TGFβ and decreased expression of TIMP4 may contribute to the accelerated recruitment of leukocytes into the central nervous system in juvenile animals.

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          Most cited references 28

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          The role of cytokines in cartilage matrix degeneration in osteoarthritis.

          Chondrocytes are the single cellular component of hyaline cartilage. Under physiologic conditions, they show steady-state equilibrium between anabolic and catabolic activities that maintains the structural and functional integrity of the cartilage extracellular matrix. Implicit in the loss of cartilage matrix that is associated with osteoarthritis is that there is a disturbance in the regulation of synthetic (anabolic) and resorptive (catabolic) activities of the resident chondrocytes that results in a net loss of cartilage matrix components and deterioration in the structural and functional properties of the cartilage. Multiple mechanisms likely are involved in the disturbance of chondrocyte remodeling activities in OA. They include the development of acquired or age-related alterations in chondrocyte function, the effects of excessive mechanical loading, and the presence of dysregulated cytokine activities. Cytokines are soluble or cell-surface molecules that play an essential role in mediating cell-cell interactions. It is possible to classify the cytokines that regulate cartilage remodeling as catabolic, acting on target cells to increase products that enhance matrix degradation; as anticatabolic, tending to inhibit or antagonize the activity of the catabolic cytokines; and as anabolic, acting on chondrocytes to increase synthetic activity. This review will focus on the role of proinflammatory cytokines and their roles in mediating the increased matrix degradation that characterizes the osteoarthritic cartilage lesion.
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            Norepinephrine up-regulates the expression of vascular endothelial growth factor, matrix metalloproteinase (MMP)-2, and MMP-9 in nasopharyngeal carcinoma tumor cells.

            Recent studies using ovarian cancer cells have shown that the catecholamine hormones norepinephrine (norepi) and epinephrine (epi) may influence cancer progression by modulating the expression of matrix metalloproteinases (MMP) and vascular endothelial growth factor (VEGF). The purpose of this study is to determine if the stress hormone norepi can influence the expression of MMP-2, MMP-9, and VEGF in nasopharyngeal carcinoma (NPC) tumors by using three NPC tumor cell lines. The NPC cell lines HONE-1, HNE-1, and CNE-1 were treated with norepi. The effects of norepi on MMP-2, MMP-9, and VEGF synthesis were measured by ELISA; functional MMP activity was measured by the invasive potential of the cells using a membrane invasion culture system whereas functional activity of VEGF was analyzed using a human umbilical vein endothelial cell tube formation assay. Norepi treatment increased MMP-2, MMP-9, and VEGF levels in culture supernatants of HONE-1 cells, which could be inhibited by the beta-blocker propranolol. Norepi induced the invasiveness of all NPC cell lines in a dose-dependent manner, which was blocked by CMT-3, an MMP inhibitor, and propranolol. Norepi stimulated the release of functional angiogenic VEGF by HONE-1 cells as well. Finally, HONE-1 cells were shown to express beta-adrenergic receptors as did seven of seven NPC biopsies examined. The data suggest that catecholamine hormones produced by the sympathetic-adrenal medullary axis may affect NPC tumor progression, in part, through modulation of key angiogenic cytokines.
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              TGF-beta-induced SMAD signaling and gene regulation: consequences for extracellular matrix remodeling and wound healing.

              Members of the transforming growth factor-beta (TGF-beta) superfamily are pleiotropic cytokines that have the ability to regulate numerous cell functions, including proliferation, differentiation, apoptosis, epithelial-mesenchymal transition, and production of extracellular matrix, allowing them to play an important role during embryonic development and for maintenance of tissue homeostasis. Three TGF-beta isoforms have been identified in mammals. They propagate their signal via a signal transduction network involving receptor serine/threonine kinases at the cell surface and their substrates, the SMAD proteins. Upon phosphorylation and oligomerization, the latter move into the nucleus to regulate transcription of target genes. This review will summarize recent advances in the understanding of the mechanisms underlying SMAD modulation of extracellular matrix gene expression in the context of wound healing and tissue fibrosis.
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                Author and article information

                Journal
                NIM
                Neuroimmunomodulation
                10.1159/issn.1021-7401
                Neuroimmunomodulation
                S. Karger AG
                1021-7401
                1423-0216
                2007
                August 2007
                15 August 2007
                : 14
                : 1
                : 46-56
                Affiliations
                Department of Oral Biology, Ohio State University, Columbus, Ohio, USA
                Article
                107288 Neuroimmunomodulation 2007;14:46–56
                10.1159/000107288
                17700040
                © 2007 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 4, Tables: 3, References: 45, Pages: 11
                Categories
                Original Paper

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