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Biomedical subjects

A Falus

Publications and source records attributed to A Falus.

At least 163 records · Page 9Linked to original sources
PubMed1990

Hormonal regulation of complement biosynthesis in human cell lines--II. Upregulation of the biosynthesis of complement components C3, factor B and C1 inhibitor by interleukin-6 and interleukin-1 in human hepatoma cell line.

The effect of interleukin (IL)-6 and IL-1 on the biosynthesis of complement components C3, factor B, C2, C4 and C1 inhibitor (C1 inh), as well as that of albumin, was studied in vitro in human hepatoma-derived cell line, HepG2. Measuring the amounts of secreted complement proteins we detected a significant upregulation of C3 by both hormones. The enhancement of the factor B and especially that of C1 inh production was predominant by IL-6. In our experimental system neither IL-1 nor IL-6 affected the biosynthesis of C2 and C4. Albumin secretion was significantly decreased only in the simultaneous presence of IL-1 and IL-6. Detection of the changes in the amounts of C3- and factor B-specific mRNA of HepG2 cells suggests a pretranslational regulation by these cytokines. The secretion of C3 and factor B was markedly potentiated when IL-1 and IL-6 were added together. However only the gene expression of factor B, but not of C3, was found to reveal synergism. IL-6 enhanced the in vitro production of C3 in mouse hepatocytes as well. This effect was greatly potentiated in the presence of histamine.

Carcinoma, Hepatocellular↗
PubMed1989

Effect of histamine on the T-cell colony formation of PHA-stimulated cells.

The effect of histamine on T-cell colony formation was studied in human peripheral blood mononuclear cells. Histamine inhibited dose-dependently (10(-4)-10(-6) M) the colony formation of PHA-stimulated T-cells. The inhibition was similar in normal controls and rheumatoid arthritis (RA) patients in spite of the fact that in RA the colony formation was significantly lower than in the normal controls. No increase of colony formation was observed at low concentrations (less than 10(-7) M). Impromidine was less effective than histamine, and pyridylethylamine (PEA) was inactive. Cimetidine counteracted the effect of histamine while chlorpheniramine did not. The results show that colony formation may be inhibited through H2-receptors. This action may be of importance in cellular interactions in tissues with high local histamine concentrations.

Colony-Forming Units Assay↗
PubMed1989

Spreading of streptomycin antibiotic resistance gene in Escherichia coli plasmids demonstrated by Southern blot analysis.

Plasmids from E. coli strains of 38 donors were transconjugated to common recipient SY663 Escherichia coli K12. The restriction patterns of the isolated plasmids were highly heterogenous. However, the streptomycin (Sm) resistance genes of the plasmids were identical or closely homologous in 29 of the 33 plasmids conferring Sm resistance. These data were based on Southern blot analysis, using the Sm resistance gene (encoding aminoglycoside phosphoryl transferase) as probe cut out from pBP1 plasmid. Our data suggest an extensive spreading of streptomycin resistance gene of this type.

Blotting, Southern↗
PubMed1989

Stimulation of histamine receptors of human monocytoid and hepatoma-derived cell lines and mouse hepatocytes modulates the production of the complement components C3, C4, factor B, and C2.

The influence of histamine (and the related agonists and antagonists) alone or in the presence of recombinant human interleukin 1 alpha (IL-1 alpha) and gamma interferon (IFN-gamma) was studied on the production of complement components C3, C2, factor B, and C4 in vitro with human monocytoid cell line U937, hepatoma-derived cell line HepG2, and mouse hepatocytes. Both U937 and HepG2 cells responded to histamine through H1 and H2 histamine receptors. The effect of histamine on the biosynthesis and gene expression of complement proteins was predominantly enhancing via the H1 histamine receptors and inhibitory through the H2 receptors. The actual predominance of the histamine receptor involved (and the outcome of the ligand interaction) seemed to be greatly affected by the simultaneous activation of the cells by IL-1 or IFN-gamma.

Animals↗
PubMed1989

Unequal expression of complement C4A and C4B genes in rheumatoid synovial cells, human monocytoid and hepatoma-derived cell lines.

C4A and C4B are closely related homologous complement proteins encoded in the class III region of major histocompatibility complex (MHC). The regulation of their expression is under genetic and hormonal control. In this study we investigated the synovial fluid plasma ratio of C4A and C4B of rheumatoid (RA) and osteoarthritis (OA) patients, and a predominance of the C4B gene expression by the synovial macrophages of RA patients was demonstrated. To clarify the tissue specificity of the expression of C4A and C4B genes, human monocytoid cell line U937 and hepatoma-derived HepG2 cells were studied. The gene expression of C4A and C4B were markedly different in these cells since a relative predominance of C4B mRNA in U937 cells and excess of that of C4A in HepG2 cells were detected. Recombinant interferon-gamma (IFN-gamma) up-regulated the expression of C4A gene in both cells, but had apparently no effect on the C4B gene. Our results demonstrate dissimilar expression patterns for the two human C4 genes, suggesting different tissue specific regulation of human C4A and C4B.

Anaphylatoxins↗
PubMed1989

Study on the origin of major histocompatibility complex (MHC) genes in recombinant mouse strains by detection of polymorphic variants of MHC class III gene, complement C4.

In recombinant mouse strains the elements of the major histocompatibility complex gene cluster are composed of those of the parental strains. The origin of elements except the S region was previously determined by immunological and biochemical typing methods. For determination of the origin of the S region and the possible location of the recombination event around the S region, Southern blot analysis was performed. By the detection of genetic polymorphic patterns of complement C4 gene in 2 of the 5 recombinant strains the recombination was localized down-stream of the C4 gene and before the D gene region.

Animals↗
PubMed1988

The use of molecular probes in the study of the action of histamine on macrophages.

The effect of histamine on the expression in vitro of C2, factor B and C3 genes in murine resident peritoneal macrophages was investigated. By measuring the levels of specific mRNA and the amount of the biosynthetically labelled gene products, we found that histamine decreases the biosynthesis of C2 and factor B. However, histamine had virtually no effect on the biosynthesis of C3 in the same cells. To clarify the mechanism of these effects, the H1 agonists (2-pyridylethylamine (PEA)and 2-methylhistamine), the H2-agonists (impromidine and 4-methyl-histamine), the H1-antagonist (chlorpheniramine) as well as the H2-antagonist (cimetidine) were also tested. We found that the inhibitory effect of histamine on C2 and factor B is produced only through H2 receptors. With the combination of histamine agonists and antagonists an inverse effect via H1- or H2-receptors was determined on the biosynthesis of C3. H1-receptor stimuli enhanced, and the stimulation of H2-receptors inhibited, C3 biosynthesis. All effects were pretranslational since the same results were obtained on mRNA and protein levels.

Animals↗
PubMed1988

Effect of histamine on the gene expression and secretion of complement components C2, factor B and C3 in murine macrophages--an opposite signal processing via H1 and H2 receptors.

The effect of histamine on the gene expression, biosynthesis and secretion of C2, factor B and C3 was studied in mouse resident and starch elicited peritoneal macrophages. Measuring the quantity of specific mRNAs and biosynthetically labelled proteins a down-regulation of the biosynthesis of C2, factor B and C3 via H2 receptor was found. On the contrary, histamine displayed no visible H1 receptor mediated influence on the biosynthesis of C2 and factor B. However, via H1 receptor a considerably up-regulation of C3 gene expression and biosynthesis was demonstrated. The data suggest a distinct signal processing mechanism acting on H1 and H2 receptors resulting in opposite effects on the transcriptions of C3 gene in macrophages.

Animals↗
PubMed1987

Induction and activation of tissue transglutaminase during programmed cell death.

During the involution of lead nitrate-induced hyperplasia in rat liver a significant increase of transglutaminase activity, enzyme concentration, transglutaminase messenger RNA and protein-bound epsilon-(gamma-glutamyl)lysine (product of transglutaminase action) coincided with programmed death (apoptosis) of hepatocytes. Immunohistochemical examination showed the appearance of transglutaminase in apoptotic hepatocytes. An increased transglutaminase level was also detected during glucocorticoid-induced apoptosis of rat thymocytes.

Animals↗
PubMed1987

The fifth component of complement (C5) in the mouse. Analysis of the molecular basis for deficiency.

C5-deficient mice differed from C5-sufficient mice both quantitatively and qualitatively in C5 protein, C5 mRNA, and the C5 gene. C5-deficient protein was present as decreased amounts of an unprocessed, single-chain precursor. C5-deficient mRNA was decreased in amount and present in two forms, the smaller of which was the same as the single form in normal cells. Nuclei from both normal and deficient cells contained the larger form of C5 mRNA, and C5-deficient DNA demonstrated differences from the normal pattern on Southern analysis for two restriction enzymes. These data suggest that the primary transcript of the C5-deficient gene is abnormal, retarding the processing of the C5 mRNA, and that the C5-deficient mRNA codes for an abnormal protein.

Animals↗
PubMed1987

Constitutive and IL 1-regulated murine complement gene expression is strain and tissue specific.

To study the molecular mechanisms accounting for strain- and tissue-specific variations in the production of complement proteins, complementary DNA probes were used to assess qualitative and quantitative differences in specific mRNA content of complement proteins C2, factor B, and C3 in extracts of tissues (liver, lung, spleen, kidney, and peritoneal macrophages) isolated from various mouse strains. Northern blot analysis of total hepatic RNA revealed differences in C2, factor B, and C3 mRNA levels in strains that share B10 background but differ in the H-2 region (e.g., H-2k, H-2u, H-2d, H-2f). In each instance, hepatic mRNA specific for the individual gene product corresponded in amount to the serum levels. By contrast, specific mRNA content of C2 and factor B in macrophages differed significantly from those observed in liver for each strain. Modulation of C2, factor B, and C3 expression was studied after in vivo administration of recombinant IL 1 or endotoxin to H-2k (B10.AKM) or H-2u (B10.PL) strain mice. As assessed by Northern blot analysis, neither endotoxin nor IL 1 affected liver C2-specific mRNA but increased specific C2 mRNA levels in kidney and lung. For both strains, IL 1 increased specific factor B mRNA in all tissues examined except for the H-2u strain liver factor B mRNA content, which was not affected by IL 1, whereas that of H-2k mice was increased. The lack of factor B modulation by IL 1 in the H-2u lines was specific to that gene and not a reflection of a generalized IL 1 unresponsiveness. Differences in tissue and strain specific constitutive and IL 1-regulated expression of the C3 gene were also observed in the H-2u and H-2k strains.

Animals↗
PubMed1987

DNA polymorphism of MHC III genes in inbred and wild mouse strains.

Genes encoding the second component (C2), factor B, and complement protein C4 and Slp (sex-limited protein) are members of the major histocompatibility complex class III gene cluster. In this report we describe isolation of a mouse C2 cDNA clone and its use together with factor B and C4 cDNA clones to examine the S region in a panel of 42 haplotypes in laboratory and wild mice representing 5 species and subspecies of Mus. Conservation of the C2 factor B gene duplex was evidenced by relatively limited polymorphism associated with speciation and nucleotide sequence homology between mouse and human C2 and factor B. The C4-Slp gene duplex, on the other hand, showed extensive polymorphism by DNA blot analysis. This polymorphism correlated poorly with the C2/factor B restriction fragment length polymorphism, suggesting independent evolution of these two segments of the S region. Taken together, these data will be of particular importance in studies of mouse strains with abnormal regulation of immune effector systems since the class III gene products are essential for activation of the complement cascade.

Amino Acid Sequence↗
PubMed1987

Effect of histamine on the gene expression and biosynthesis of complement components C2, factor B and C3 in mouse peritoneal macrophages.

The gene expression and biosynthesis of C2, factor B and C3 have been investigated in vitro in mouse resident peritoneal macrophages after incubation with histamine. C2- and factor B-specific mRNA and the amount of the immunoprecipitated C2 and factor B were decreased by 10(-4) M and 10(-8) M histamine. These effects can be abrogated by the H2 antagonist cimetidine and mimicked by the H2 agonists impromidine and 4-methylhistamine. Since the H1 antagonist chlorpheniramine and the H1 agonists PEA and 2-methylhistamine have little effect on C2 and are ineffective on factor B, a strong H2 receptor dependence of the inhibition of C2 and factor B gene expression and biosynthesis is suggested. Conversely, the C3 gene expression and biosynthesis can be influenced through both H1 and H2 receptors, e.g. elevated by histamine + cimetidine, PEA and 2-methylhistamine through H1 receptors, and inhibited by histamine + chlorpheniramine, impromidine and 4-methylhistamine through H2 receptors. The data obtained by quantification of C2, factor B and C3 mRNA concentration of peritoneal macrophages suggest that the regulation of biosynthesis of these complement components by histamine in mouse peritoneal macrophages is under pretranslational control.

Animals↗