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  • 1
    Electronic Resource
    Electronic Resource
    C5 DEFICIENCY IN A/J MICE IS NOT ASSOCIATED WITH RESISTANCE TO THE DEVELOPMENT OF SECONDARY AMYLOIDOSIS (1992)
    Oxford, UK : Blackwell Publishing Ltd
    International journal of immunogenetics 19 (1992), S. 0 
    Details
    ISSN: 1744-313X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: The aim of the study was to determine whether C5 deficiency in the mouse is associated with resistance to the development of secondary amyloidosis. Chronic inflammation was induced in the F2 progeny, derived from matings between amyloid-susceptible and amyloid-resistance mice, by daily injections of azocasein for thirty days. Using a restriction fragment length polymorphism generated by digestion of genomic DNA with the restriction enzyme HindIII, C5 sufficient and deficient DNA can be clearly differentiated. Eight mice were found to be C5 sufficient, 32 were heterozygotes and 14 were found to be C5 deficient. Grading of the splenic amyloid load from negative to 4+ was performed after staining tissue squashes with Congo red and viewing them under a polarizing microscope. Seventeen mice were noted to have negative to trace, 18 had moderate (1+-2+) and 19 had heavy (3 H+-4+) amyloid deposition. There was no correlation between splenic amyloid load and C5 deficiency. Based on these results it is clear that C5 deficiency and resistance to secondary amyloidosis are not associated.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1744-313X.1992.tb00085.x
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  • 2
    Electronic Resource
    Electronic Resource
    Wallaby Serum Amyloid A Protein: cDNA Cloning, Sequence and Evolutionary Analysis (1996)
    Oxford, U.K. and Cambridge, USA : Blackwell Science Ltd
    Scandinavian journal of immunology 43 (1996), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: A serum amyloid A (SAA) clone was isolated from a Tammar wallaby cDNA library, the most distantly related mammalian species for which an SAA has been described to date. The clone predicts a premolecule of 127 amino acids with good homology to other mammalian SAAs, and consists of an 18 residue leader peptide and a mature protein of 109 amino acids. Evolutionary analysis at both the protein and nucleotide level indicate that the wallaby SAA clone clusters with the acute phase SAAs. However, as the SAA superfamily has undergone concerted evolution it is not possible to determine at this point which acute phase SAA it is most like. The grouping of wallaby SAA inside the acute phase SAA cluster demonstrates that at least some of the duplication events giving rise to multiple acute phase genes occured prior to the divergence of the eutherian and metatherian mammals.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-3083.1996.d01-34.x
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  • 3
    Electronic Resource
    Electronic Resource
    Human serum amyloid A (SAA): biosynthesis and postsynthetic processing of preSAA and structural variants defined by complementary DNA (1985)
    s.l. : American Chemical Society
    Biochemistry 24 (1985), S. 2931-2936 
    Details
    ISSN: 1520-4995
    Source: ACS Legacy Archives
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/bi00333a018
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  • 4
    Electronic Resource
    Electronic Resource
    In vitro Evaluation of an Enhanced Human Serum Amyloid A (SAA2) Promoter-Regulated Soluble TNF Receptor Fusion Protein for Anti-Inflammatory Gene Therapy (2001)
    Oxford, UK : Blackwell Science Ltd
    Scandinavian journal of immunology 53 (2001), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Tumour necrosis factor (TNF)-α contributes to the pathogenesis of many inflammatory diseases. Recombinant soluble TNF receptor fusion proteins (sTNFR:Ig) are potent TNF antagonists, both in vitro and in vivo. The concentration of serum amyloid A (SAA) increases by up to 1000-fold during inflammation, largely owing to cytokine-driven transcriptional upregulation. A reporter plasmid, comprising the proximal 0.7 kb of the human SAA2 promoter fused to a luciferase gene, was used in transient transfection experiments in human HepG2 hepatoma cells to assess the quantitative and qualitative TNF antagonist properties of a construct in which sTNFR:Ig synthesis is under the control of a chimera of the SAA2 promoter and a tat/HIV element. The SAA2-tat/HIV-sTNFR:Ig construct retained the fine-tuned cytokine responsiveness of the SAA2 promoter, while exhibiting the quantitatively enhanced level of protein expression conferred by the tat/HIV element. It produced a biologically significant TNF inhibition that was at least as strong as that achieved using a CMV promoter-driven sTNFR:Ig construct. There was a dose- and time-dependent relationship between the pro-inflammatory cytokine used, and the generation of TNF antagonist activity by SAA2-tat/HIV-sTNFR:Ig. Although sTNFR:Ig protein can be induced by either TNF-α or interleukin (IL)-1β, its antagonist activity is limited to the former cytokine. The SAA2-tat/HIV-sTNFR:Ig construct, and derivatives thereof, may therefore be ideally suited to gene therapy applications that require the local production of potent and specific immune modifiers only when there is active pathology. It may consequently be of particular use in the future treatment of diseases such as rheumatoid arthritis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-3083.2001.00919.x
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  • 5
    Electronic Resource
    Electronic Resource
    Structure of the Mouse Serum Amyloid A 5 (Saa5) Gene: Relationship to Other Members of the Serum Amyloid A Family (1997)
    Oxford, U.K. and Cambridge, USA : Blackwell Science Ltd
    Scandinavian journal of immunology 45 (1997), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The mouse and human genes which encode the serum amyloid A (SAA) proteins have been extensively characterized. In the present study, the authors report the sequencing of the constitutively expressed mouse Saa5 gene, including ≈2 kilobases of promoter sequence which extends into the sequence of the adjacent Saa4 pseudogene. The Saa5 gene was thus determined to have a 4 exon/3 intron structure, with a B2 repeat located ≈450 base pairs upstream, and a microsatellite contained within intron 2. Analyses of Saa5 intronic and promoter sequences, by comparison with representative members of the mouse Saa and human SAA families, provided evidence which strongly suggests that mouse Saa5 and the constitutively expressed human SAA4 gene are evolutionary and functional homologues. Furthermore, putative transcription motifs were identified within the Saa5 and SAA4 promoters which may account, in part, for the constitutive expression and unique induction profiles of these genes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-3083.1997.d01-385.x
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  • 6
    Electronic Resource
    Electronic Resource
    Regulation of the Human Acute Phase Serum Amyloid A Genes by Tumour Necrosis Factor-α, Interleukin-6 and Glucocorticoids in Hepatic and Epithelial Cell Lines (2004)
    Oxford, UK; Malden , USA : Blackwell Science Ltd
    Scandinavian journal of immunology 59 (2004), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The major acute-phase protein serum amyloid A, A-SAA, is upregulated by a variety of inflammatory stimuli, including cytokines and glucocorticoids (GCs). Elevated systemic concentrations of both A-SAA and tumour necrosis factor (TNF)-α are a feature of inflammatory diseases, such as rheumatoid arthritis and inflammatory bowel disease.Here, we examine the roles of TNF-α, interleukin-6 (IL-6) and GCs on the transcriptional regulation of the two human A-SAA genes (SAA1 and SAA2) and show that these stimuli have different effects on the SAA1 and SAA2 promoters in HepG2 hepatoma and KB epithelial cell lines. Both genes are induced modestly by TNF-α and IL-6 alone and synergistically by TNF-α plus IL-6. The TNF-driven induction of SAA1, but not that of SAA2, can be enhanced by GCs in both cell lines, whereas GCs alone can upregulate SAA1 only in epithelial cells. The upregulation of both genes by cytokines, and of SAA1 by GCs, is more rapid in epithelial cells than hepatoma cells.We established that the order in which either cell line was treated with TNF-α and IL-6 influenced A-SAA promoter transcriptional activation. Treatment with TNF-α followed by IL-6 resulted in a much greater induction of both A-SAA genes than treatment with IL-6 followed by TNF-α.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.0300-9475.2004.01369.x
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  • 7
    Electronic Resource
    Electronic Resource
    Efficient In Vitro Cleavage of Mouse Acute Phase Serum Amyloid A mRNA Mediated by a Synthetic Hammerhead Ribozyme (1997)
    Oxford, UK : Blackwell Science Ltd
    Scandinavian journal of immunology 46 (1997), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The authors designed a hammerhead ribozyme, mRibSAA2, to cleave the mRNA for mouse acute phase serum amyloid A 2 (A-SAA2), a major acute phase protein that is massively induced during inflammation and that is deposited as fibrils during secondary amyloidosis. Using computer based secondary structure analysis, a GUC triplet (nucleotides 408–410) on a predicted stem loop in A-SAA2 mRNA was chosen as the target site for mRibSAA2. The ribozyme was tested in vitro and gave efficient and specific magnesium-dependent cleavage of mouse A-SAA2 mRNA into the expected fragments of 197 and 425 bases. The authors also demonstrated that the ribozyme retains cleavage activity over several hours. The use of the mRibSAA2 ribozyme as a research tool and possible therapeutic agent in mouse models of amyloidosis is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-3083.1997.d01-97.x
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  • 8
    Electronic Resource
    Electronic Resource
    Expression and Regulation of Constitutive and Acute Phase Serum Amyloid A mRNAs in Hepatic and Non-Hepatic Cell Lines (1996)
    Oxford, U.K. and Cambridge, USA : Blackwell Science Ltd
    Scandinavian journal of immunology 44 (1996), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: ‘Acute phase’ and ‘constitutive’ SAA (A-SAA and C-SAA, respectively) mRNA levels were measured in hepatic and non-hepatic cell lines after treatment with monocyte conditioned medium (MoCM), with or without dexamethasone (Dex). A-SAA mRNAs were detected in MoCM-treated hepatoma cell lines (PLC/PRF/5, HuH7, HepG2, and Hep3B), a fibroblast cell line (MRC5), six epithelial cell lines (RT4/31, SW13, Hela Ohio, HCT-8, CaCo2, and KB), and an endothelial cell line ECV304. In KB cells, Dex alone caused a dramatic increase in A-SAA mRNA levels. C-SAA was detected in all hepatic and non-hepatic cell lines. Two differentially regulated size classes of C-SAA mRNA were detected in the hepatoma cell lines. A-SAA mRNA levels were measured in ECV304 cells treated with IL-1β, IL-6, TNFα and Dex, in various combinations, and revealed different profiles to those seen for hepatic cells. The extent of polyadenylation of A-SAA mRNA in ECV304 and KB cells differed whereas the polyadenylation of C-SAA mRNA remained constant. These data suggest that the parameters that determine the steady state mRNA levels and post-transcriptional regulation of A-SAA and C-SAA mRNAs are different and are cell type specific.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-3083.1996.d01-341.x
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  • 9
    Electronic Resource
    Electronic Resource
    Resistance to Secondary Amyloidosis in A/J Mice is Not Significantly Associated with Allelic Variants Linked to the Serum Amyloid A Gene Cluster (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 40 (1994), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We have tested the hypothesis that structural allelic variants of serum amyloid A confer relative resistance to secondary amyloidosis in the A/J mouse. F2 mice, previously generated from amyloid-resistant (A/J) and amyloid-susceptible (C57BL/6J) strains and categorized with respect to amyloid susceptibility, were genotyped by polymerase chain reaction (PCR) amplification of the polymorphic D7Nds5 microsatellite. This microsatellite is closely linked to the SAA gene cluster and can discriminate between D7Nds5 alleles of A/J and C57BL/6 J origin. The distribution of D7Nds5 genotypes in relation to splenic amyloid load did not deviate significantly from that expected of a random distribution, indicating that A/J amyloid resistance is not determined by variants at, or close to, D7Nds5. Therefore, structural alleles in the tightly-linked SAA gene cluster do not confer amyloid resistance in this mouse model.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1994.tb03473.x
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  • 10
    Electronic Resource
    Electronic Resource
    Effects of human recombinant growth hormone (rhGH) on inflammatory responses in patients undergoing abdominal aortic aneurysm repair (1998)
    Springer
    Intensive care medicine 24 (1998), S. 128-131 
    Details
    ISSN: 1432-1238
    Keywords: Key words Growth hormone ; Insulin-like growth factor-1 ; Acute phase proteins ; C-reactive protein ; Serum amyloid A ; Interleukin-6
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Background: Human recombinant growth hormone (rhGH) has been shown to increase skeletal muscle protein synthesis and improve nitrogen balance in critically ill patients and those undergoing surgery. rhGH effects on hepatic protein turnover in critically ill patients are less clearly understood. Objective: To examine rhGH effects on hepatic acute phase protein responses and inflammatory cytokine release in patients undergoing major surgery. Design: Prospective double blind randomised trial. Setting: Tertiary referral university teaching hospital. Patients: Patients undergoing elective abdominal aortic aneurysm repair. Intervention: Patients received rhGH (Genotropin, 0.3 IU/kg per day, n = 8) or placebo (n = 10) for 6 days prior to surgery. Results: Blood levels of growth hormone (GH) and insulin-like growth factor (IGF-1) were measured following rhGH treatment and C-reactive protein (CRP), serum amyloid A (SAA) and the cytokines interleukin-6 (IL-6) and the IL-1 receptor antagonist (IL-1ra) were measured for up to 24 h following surgery. Significant increases in plasma rhGH (0.84 ± 0.3, mean (sem) versus 52 ± 20 mU/l, p 〈 0.0008) and IGF-1 levels (119 ± 13 versus 644 ± 110 ng/ml, p 〈 0.0001) were seen prior to surgery following rhGH administration. No differences in acute phase protein or cytokine levels were seen following surgery in patients receiving rhGH. Conclusions: These results indicate that pre-operative administration of rhGH does not alter acute phase protein or inflammatory cytokine release in response to major surgery.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001340050533
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