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Biochem Biophys Res Commun. 2002 Nov 22;299(1):109-15.
Enhanced expression of the human chitinase 3-like 2 gene (YKL-39) but not chitinase 3-like 1 gene (YKL-40) in osteoarthritic cartilage.
Steck E, Breit S, Breusch SJ, Axt M, Richter W.
Department of Orthopaedic Surgery, University of Heidelberg, Schlierbacher Landstrasse 200a, 69118, Heidelberg, Germany.
The knowledge of molecular alterations in osteoarthritic cartilage is important to identify novel therapeutic targets or to develop new diagnostic tools. We aimed to characterize the molecular response to cartilage degeneration by identification of differentially expressed genes in human osteoarthritic versus normal cartilage. Gene fragments selectively amplified in osteoarthritic cartilage by cDNA representational difference analysis included YKL-39 and the oesophageal-cancer-related-gene-4 (ECRG4). YKL-39 expression was significantly upregulated in cartilage from patients with osteoarthritis (n=14) versus normal subjects (n=8) according to real-time PCR (19-fold, p=0.009) and cDNA array analysis (mean 15-fold, p<0.001) and correlated with collagen 2 up-regulation. In contrast, the homologous cousin molecule YKL-40 (chitinase 3-like 1), which is elevated in serum and synovial fluid of patients with arthritis, showed no significant regulation in OA cartilage. Enhanced levels of YKL-40 may, therefore, be derived from synovial cells while modulation of YKL-39 and collagen 2 expression reflected the cartilage metabolism in response to degradation.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12435396&dopt=Abstract
J Dermatol Sci. 2000 Nov;24(2):99-104.
Hypoxic conditions decrease the mRNA expression of proalpha1(I) and (III) collagens and increase matrix metalloproteinases-1 of dermal fibroblasts in three-dimensional cultures.
Yamanaka M, Ishikawa O.
Department of Dermatology, Gunma University School of Medicine, 3-39-22, Showa-machi, Maebashi, 371-8511, Gunma, Japan. myamanab.gunma-u.ac.jp
The effect of hypoxia on the expression of extracellular matrix-related genes by human dermal fibroblasts was investigated using a novel three-dimensional culture supplemented with L-ascorbic acid 2-phosphate. Experiments were performed by placing replicate dishes in either hypoxic (2%) or in normoxic (20%) condition for various periods of time ranging up to 72 h. The mRNA expression levels of proalpha1(I), proalpha1(III) collagens and MMP-1 were analyzed using Northern blotting. Hypoxia transiently increased proalpha1(I) and proalpha1(III) collagen gene expression at 24 h, but a prolonged exposure to hypoxia decreased them. A slight increase in MMP-1 mRNA was observed at 24 h and prolonged exposure for up 72 h resulted in significantly increased expression of MMP-1 gene. Our results suggest that enhanced degradation as well as decreased synthesis of collagens induced by hypoxia may account for the delayed wound healing associated with circulatory disturbances.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11064244&dopt=Abstract
Cardiovasc Pathol. 2000 Sep-Oct;9(5):281-6.
Matrix metalloproteinase expression in nonrheumatic aortic stenosis.
Edep ME, Shirani J, Wolf P, Brown DL.
Department of Medicine (Cardiovascular Medicine), Albert Einstein College of Medicine/Montefiore Medical Center, Bronx, NY 10461, USA.
BACKGROUND: Nonrheumatic aortic stenosis (NAS) is considered to be a degenerative process characterized by valve thickening, fibrocalcific masses, collagen disarray, and an inflammatory infiltrate. The matrix metalloproteinases (MMPs) are a family of zinc- and calcium-dependent enzymes produced by inflammatory cells that are capable of degrading collagen, elastin, and proteoglycans. This study sought to test the hypothesis that MMPs are involved in the pathogenesis of NAS. METHODS AND RESULTS: Aortic values were obtained from nine patients with NAS undergoing valve replacement and from four patients without NAS during autopsy. Microscopic analysis of NAS specimens revealed variable areas of calcium deposits, fibrosis, and an extensive cellular infiltrate consisting of macrophages, lymphocytes, and fibroblasts. Control aortic valves demonstrated normal architecture, a predominance of fibroblasts, occasional scattered macrophages, and no lymphocytes. Immunohistochemical staining with antibodies to MMP-1, -2, -3 and -9 revealed expression of each enzyme in macrophages, lymphocytes, and fibroblasts of all NAS patients. MMP-1, -2 and -3 were expressed by resident fibroblasts and macrophages in normal valves, but to a lesser degree. MMP-9 was not identified in normal valves. CONCLUSIONS: The current study confirms an inflammatory infiltrate composed of macrophages and lymphocytes in NAS. Additionally, the increased expression of MMP-1, -2, and -3, along with the unique expression of MMP-9 in NAS valve leaflets was documented. These findings are consistent with the hypothesis that NAS is associated with chronic inflammation and that the increased expression of MMPs may contribute to the pathogenesis of this disease process.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11064275&dopt=Abstract
Mol Microbiol. 2000 Oct;38(2):381-91.
The role of Mycobacterium avium complex fibronectin attachment protein in adherence to the human respiratory mucosa.
Middleton AM, Chadwick MV, Nicholson AG, Dewar A, Groger RK, Brown EJ, Wilson R.
Imperial College of Science, Technology and Medicine at the National Heart and Lung Institute and Royal Brompton Hospital, Manresa Road, London SW3 6LR, UK.
Mycobacterium avium complex (MAC) are opportunistic respiratory pathogens that infect non-immunocompromised patients with established lung disease, although they can also cause primary infections. The ability to bind fibronectin is conserved among many mycobacterial species. We have investigated the adherence of a sputum isolate of MAC to the mucosa of organ cultures constructed with human tissue and the contribution of M. avium fibronectin attachment protein (FAP) to the process. MAC adhered to fibrous, but not globular mucus, and to extracellular matrix (ECM) in areas of epithelial damage, but not to intact extruded cells and collagen fibres. Bacteria occasionally adhered to healthy unciliated epithelium and to cells that had degenerated exposing their contents, but never to ciliated cells. The results obtained with different respiratory tissues were similar. Two ATCC strains of MAC gave similar results. There was a significant reduction (P < 0.05) in the number of bacteria adhering to ECM after preincubation of bacteria with fibronectin and after preincubation of the tissue with M. avium FAP in a concentration-dependant manner. The number of bacteria adhering to fibrous mucus was unchanged. Immunogold labelling demonstrated fibronectin in ECM as well as in other areas of epithelial damage, but only ECM bound FAP. A Mycobacterium smegmatis strain had the same pattern of adherence to the mucosa as MAC. When the FAP gene was deleted, the strain demonstrated reduced adherence to ECM, and adherence was restored when the strain was transfected with an M. avium FAP expression construct. We conclude that MAC adheres to ECM in areas of epithelial damage via FAP and to mucus with a fibrous appearance via another adhesin. Epithelial damage exposing ECM and poor mucus clearance will predispose to MAC airway infection.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11069663&dopt=Abstract
Am J Respir Crit Care Med. 2000 Nov;162(5):1783-8.
Fibroproliferation occurs early in the acute respiratory distress syndrome and impacts on outcome.
Marshall RP, Bellingan G, Webb S, Puddicombe A, Goldsack N, McAnulty RJ, Laurent GJ.
Centre for Respiratory Research, Royal Free and University College London Medical School, Rayne Institute, London, United Kingdom. richard.marshalcl.ac.uk
The fibroproliferative phase of acute respiratory distress syndrome (ARDS) has traditionally been regarded as a late event but recent studies that suggest increased lung collagen turnover within 24 h of diagnosis challenge this view. We hypothesized that fibroproliferation is initiated early in ARDS, characterized by the presence of fibroblast growth factor activity in the lung and would relate to clinical outcome. Patients fulfilling American/European Consensus Committee criteria for ARDS and control patients ventilated for non-ARDS respiratory failure underwent bronchoalveolar lavage (BAL) and serum sampling within 24 h of diagnosis and again at 7 d. The ability of BAL fluid (BALF) to stimulate human lung fibroblast proliferation in vitro was examined in relation to concentrations of N-terminal peptide for type III procollagen (N-PCP-III) in BALF/serum and clinical indices. At 24 h, ARDS lavage fluid demonstrated potent mitogenic activity with a median value equivalent to 70% (range 31-164) of the response to serum, and was significantly higher than control lavage (32% of serum response, range 11-42; p < 0.05). At 24 h, serum N-PCP-III concentrations were elevated in the ARDS group compared with control patients (2.8 U/ml; range 0.6-14.8 versus 1.1 U/ml; range 0.4-3.7, p < 0.0001) as were BALF N-PCP-III concentrations (2.9 U/ml; range 0. 6-11.4 versus 0.46 U/ ml; range 0.00-1.63, p < 0.01). In addition, BALF N-PCP-III concentrations at 24 h were significantly elevated in nonsurvivors of ARDS compared with survivors (p < 0.05). At 7 d, the mitogenic activity remained elevated in the ARDS group compared with control (p < 0.05) and was also significantly higher in ARDS nonsurvivors compared with survivors (67%; range 45-120 versus 31%; range 16-64, p < 0.05). These data are consistent with the hypothesis that fibroproliferation is an early response to lung injury and an important therapeutic target.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11069813&dopt=Abstract
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