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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
Gene Review

TNF  -  tumor necrosis factor

Felis catus

 
 
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Disease relevance of TNF

  • Similar findings were observed with respect to 45Ca2+ uptake and MTT metabolism in TNF-alpha-pretreated cells that were subjected to prolonged hypoxia [1].
  • A temporal relationship between TNF-alpha production and FIV p26 expression was noted [2].
  • Immunoprecipitates representing expression of TNF-alpha and of FIV p26 were localized in common foci of lymph nodes of FIV-infected cats during this period of active viremia [2].
  • These results suggest that TNF-alpha may play a role in regulating hematopoiesis in cats and may be involved in the pathogenesis of erythroid aplasia in cats infected with feline leukemia virus [3].
  • TNF-alpha levels were low in normal muscle and did not increase with esophagitis [4].
 

High impact information on TNF

  • First, in situ hybridization studies, using highly specific biotinylated probes, demonstrated TNF alpha mRNA in cardiac myocytes from endotoxin-stimulated hearts; in contrast, TNF alpha mRNA was not expressed in myocytes from diluent-treated hearts [5].
  • When freshly isolated hearts were stimulated with endotoxin in vitro, de novo TNF alpha mRNA expression occurred within 30 min, and TNF alpha protein production was detected within 60-75 min; however, TNF alpha mRNA and protein production were not detected in diluent-treated hearts [5].
  • Immunohistochemical studies localized TNF alpha to endothelial cells, smooth muscle cells, and cardiac myocytes in the endotoxin-treated hearts, whereas TNF alpha immunostaining was absent in the diluent-treated hearts [5].
  • TNF alpha mRNA and protein biosynthesis were examined in the adult feline heart after stimulation with endotoxin [5].
  • Thus, this study shows for the first time that the adult mammalian myocardium synthesizes biologically active TNF alpha [5].
 

Biological context of TNF

  • Thus, these studies constitute the initial demonstration that the negative inotropic effects of TNF alpha are the direct result of alterations in intracellular calcium homeostasis in the adult cardiac myocyte [6].
  • TNF-alpha stimulation of adult feline cardiac myocytes provoked a rapid (<15 min) increase in the hydrolysis of [14C]sphingomyelin in cell-free extracts, as well as an increase in ceramide mass, consistent with cytokine-induced activation of the neutral sphingomyelinase pathway [7].
  • TNF-alpha induced apoptosis in a feline fibroblastic cell line (CRFK) infected with FIV but not in its uninfected control [8].
  • TNF-alpha-induced cell death in feline immunodeficiency virus-infected cells is mediated by the caspase cascade [8].
  • The effects of tumor necrosis factor-alpha (TNF-alpha) on feline bone marrow hematopoietic progenitors were evaluated by exposing bone marrow mononuclear cells from specific pathogen-free cats to different concentrations of TNF-alpha (ranging from 50 to 800 pg/ml) for 2 h before plating for clonal assays of colony-forming units [3].
 

Anatomical context of TNF

  • In comparison to SPF cats, FIP cats had significantly higher IL-1beta levels and lower TNF levels in mesenteric lymph nodes and lower M-CSF levels in the spleen [9].
  • Studies in both the ventricle and the isolated adult cardiac myocyte showed that TNF alpha exerted a concentration- and time-dependent negative inotropic effect that was fully reversible upon removal of this cytokine [6].
  • Further, treatment with a neutralizing anti-TNF alpha antibody prevented the negative inotropic effects of TNF alpha in isolated myocytes [6].
  • To define the mechanism(s) responsible for the negative inotropic effects of tumor necrosis factor-alpha (TNF alpha) in the adult heart, we examined the functional effects of TNF alpha in the intact left ventricle and the isolated adult cardiac myocyte [6].
  • Finally, the effects of TNF-alpha on adult cardiac myocytes were shown to be dependent on cell-substrate interaction, suggesting that the cell signaling pathways used by TNF-alpha are dependent on a preserved interaction between cell integrins and the extracellular matrix [10].
 

Associations of TNF with chemical compounds

  • The functional significance of the intramyocardial production of TNF alpha was determined by examining cell motion in isolated cardiac myocytes treated with superfusates from endotoxin- and diluent-stimulated hearts [5].
  • Further studies showed that increased levels of nitric oxide, de novo protein synthesis, and metabolites of the arachidonic acid pathway were unlikely to be responsible for the TNF alpha-induced abnormalities in contractile function [6].
  • BACKGROUND: Previous studies in isolated cardiac myocytes have shown that tumor necrosis factor (TNF)-alpha provokes increased expression of 27- and 70-kD stress proteins as well as manganese superoxide dismutase, suggesting that TNF-alpha might play a role in mediating stress responses in the heart [1].
  • METHODS AND RESULTS: To determine whether TNF-alpha stimulation would protect isolated cardiac myocytes against environmental stress, myocyte cultures were pretreated with TNF-alpha for 12 hours and then subjected to continuous hypoxic injury (O2 content, 3 to 5 ppm) for 12 hours, followed by reoxygenation [1].
  • Thus, these studies suggest that sphingosine mediates the immediate negative inotropic effects of TNF-alpha in isolated cardiac myocytes [7].
 

Regulatory relationships of TNF

  • IL-1beta and TNF-alpha mRNA was constitutively expressed whereas IL-6, IL-10 and IL-12 p40 mRNA was generally expressed at a lower level and was occasionally not detected [11].
 

Other interactions of TNF

  • The cellular response correlated with a marked upregulation in IL10 transcription and delayed increase in TNF-alpha upregulation in FIV-infected cats [12].
  • Bioassays are currently available for the measurement of feline IL2, IL6 and TNF alpha but not for other biologically important cytokines [13].
  • IL-1 beta, IL-6, IL-12, IL-18, TNF-alpha, macrophage inhibitory protein (MIP)-1 alpha, and RANTES showed no upregulation in the brains of control cats, moderate upregulation in neurological FIP cats, and very high upregulation in generalized FIP cats [14].
 

Analytical, diagnostic and therapeutic context of TNF

  • A brief period of hemodynamic pressure overloading ex vivo resulted in de novo TNF-alpha mRNA expression within 30 minutes and de novo TNF-alpha protein production within 60 minutes; neither TNF-alpha mRNA nor protein was detected in hearts perfused at normal perfusion pressures [15].
  • From a TNF-alpha-raised permeability level (about 50% above control) and from a histamine-raised permeability level (about 60% above control), both drugs induced small reductions in the capillary filtration coefficient [16].
  • TNF-alpha at 1 ng/ml, however, did not affect the response to ACh or to electrical stimulation but inhibited both at higher concentrations [4].
  • Electrophoretic mobility shift assay using an NF-kappaB motif oligonucleotide and promoter assay using an NF-kappaB luciferase reporter construct indicated that TNF-alpha treatment had induced activation of NF-kappaB in both FIV-infected and uninfected CRFK cells [8].
  • TNF-alpha and FIV RNA were measured using competitive reverse transcriptase polymerase chain reaction (PCR) assays and the number of proviral genomes was estimated by competitive PCR [17].

References

  1. Tumor necrosis factor-alpha confers resistance to hypoxic injury in the adult mammalian cardiac myocyte. Nakano, M., Knowlton, A.A., Dibbs, Z., Mann, D.L. Circulation (1998) [Pubmed]
  2. Relationship between tumor necrosis factor alpha and feline immunodeficiency virus expressions. Kraus, L.A., Bradley, W.G., Engelman, R.W., Brown, K.M., Good, R.A., Day, N.K. J. Virol. (1996) [Pubmed]
  3. Effects of tumor necrosis factor-alpha on normal feline hematopoietic progenitor cells. Khan, K.N., Kociba, G.J., Wellman, M.L., Reiter, J.A. Exp. Hematol. (1992) [Pubmed]
  4. Proinflammatory cytokines alter/reduce esophageal circular muscle contraction in experimental cat esophagitis. Cao, W., Cheng, L., Behar, J., Fiocchi, C., Biancani, P., Harnett, K.M. Am. J. Physiol. Gastrointest. Liver Physiol. (2004) [Pubmed]
  5. Tumor necrosis factor-alpha gene and protein expression in adult feline myocardium after endotoxin administration. Kapadia, S., Lee, J., Torre-Amione, G., Birdsall, H.H., Ma, T.S., Mann, D.L. J. Clin. Invest. (1995) [Pubmed]
  6. Cellular basis for the negative inotropic effects of tumor necrosis factor-alpha in the adult mammalian heart. Yokoyama, T., Vaca, L., Rossen, R.D., Durante, W., Hazarika, P., Mann, D.L. J. Clin. Invest. (1993) [Pubmed]
  7. Sphingosine mediates the immediate negative inotropic effects of tumor necrosis factor-alpha in the adult mammalian cardiac myocyte. Oral, H., Dorn, G.W., Mann, D.L. J. Biol. Chem. (1997) [Pubmed]
  8. TNF-alpha-induced cell death in feline immunodeficiency virus-infected cells is mediated by the caspase cascade. Mizuno, T., Goto, Y., Baba, K., Masuda, K., Ohno, K., Tsujimoto, H. Virology (2001) [Pubmed]
  9. Natural feline coronavirus infection: differences in cytokine patterns in association with the outcome of infection. Kipar, A., Meli, M.L., Failing, K., Euler, T., Gomes-Keller, M.A., Schwartz, D., Lutz, H., Reinacher, M. Vet. Immunol. Immunopathol. (2006) [Pubmed]
  10. Tumor necrosis factor-alpha provokes a hypertrophic growth response in adult cardiac myocytes. Yokoyama, T., Nakano, M., Bednarczyk, J.L., McIntyre, B.W., Entman, M., Mann, D.L. Circulation (1997) [Pubmed]
  11. Cytokine mRNA levels in isolated feline monocytes. Kipar, A., Leutenegger, C.M., Hetzel, U., Akens, M.K., Mislin, C.N., Reinacher, M., Lutz, H. Vet. Immunol. Immunopathol. (2001) [Pubmed]
  12. Effect of feline immunodeficiency virus on cytokine response to Listeria monocytogenes in vivo. Dean, G.A., Bernales, J.A., Pedersen, N.C. Vet. Immunol. Immunopathol. (1998) [Pubmed]
  13. A reverse transcription-polymerase chain reaction technique to detect feline cytokine genes. Rottman, J.B., Freeman, E.B., Tonkonogy, S., Tompkins, M.B. Vet. Immunol. Immunopathol. (1995) [Pubmed]
  14. Inflammation and changes in cytokine levels in neurological feline infectious peritonitis. Foley, J.E., Rand, C., Leutenegger, C. J. Feline Med. Surg. (2003) [Pubmed]
  15. Hemodynamic regulation of tumor necrosis factor-alpha gene and protein expression in adult feline myocardium. Kapadia, S.R., Oral, H., Lee, J., Nakano, M., Taffet, G.E., Mann, D.L. Circ. Res. (1997) [Pubmed]
  16. Low-dose prostacyclin is superior to terbutaline and aminophylline in reducing capillary permeability in cat skeletal muscle in vivo. Möller, A.D., Grände, P.O. Crit. Care Med. (1999) [Pubmed]
  17. Tumor necrosis factor-alpha and virus expression in the central nervous system of cats infected with feline immunodeficiency virus. Poli, A., Pistello, M., Carli, M.A., Abramo, F., Mancuso, G., Nicoletti, E., Bendinelli, M. J. Neurovirol. (1999) [Pubmed]
 
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