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Hypoxia Increases Serum Amyloid A3 (SAA3) in Differentiated 3T3-L1 Adipocytes

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Abstract

Hypoxia has been implicated as a possible cause of adipose tissue inflammation. Furthermore, the acute phase protein serum amyloid A (SAA) has been associated with the modulation of the adipogenic process, and it is well-known that obese individuals have increased levels of SAA. The effect of hypoxia in the expression and production of SAA was examined in murine 3T3-L1 adipocytes. Hypoxia leads to a substantial increase in SAA3 mRNA and protein level, apparently in a time-dependent manner (threefold in 48 h), in fully differentiated 3T3-L1, followed by reestablishment of gene expression to basal levels after 24 h of reoxygenation. Hypoxia-induced SAA may be one of the key molecules to the development of the inflammatory response in adipose tissue.

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References

  1. Regazzetti, C., P. Peraldi, T. Gremeaux, R. Najem-Lendom, I. Ben-Sahra, M. Cormont, et al. 2009. Hypoxia decreases insulin signaling pathways in adipocytes. Diabetes 58: 95–103.

    Article  PubMed  CAS  Google Scholar 

  2. Ye, J. 2009. Emerging role of adipose tissue hypoxia in obesity and insulin resistance. International Journal of Obesity 33: 54–66.

    Article  PubMed  CAS  Google Scholar 

  3. Hotamisligil, G.S. 2006. Inflammation and metabolic disorders. Nature 444: 860–7.

    Article  PubMed  CAS  Google Scholar 

  4. Trayhurn, P., B. Wang, and I.S. Wood. 2008. Hypoxia in adipose tissue: a basis for the dysregulation of tissue function in obesity? British Journal of Nutrition 100: 227–235.

    Article  PubMed  CAS  Google Scholar 

  5. Poitou, C., N. Viguerie, R. Cancello, R. De Matteis, S. Cinti, V. Stich, et al. 2005. Serum amyloid A: production by human white adipocyte and regulation by obesity and nutrition. Diabetologia 48: 519–528.

    Article  PubMed  CAS  Google Scholar 

  6. Furlaneto, C.J., and A. Campa. 2000. A novel function of serum amyloid A: a potent stimulus for the release of tumor necrosis factor-alpha, interleukin-1 beta, and interleukin-8 by human blood neutrophil. Biochemical and Biophysical Research Communications 268: 405–408.

    Article  PubMed  CAS  Google Scholar 

  7. Sandri, S., D. Rodriguez, E. Gomes, H.P. Monteiro, M. Russo, and A. Campa. 2008. Is serum amyloid A an endogenous TLR4 agonist? Journal of Leukocyte Biology 83: 1174–1180.

    Article  PubMed  CAS  Google Scholar 

  8. Filippin-Monteiro, F.B., E.M. de Oliveira, S. Sandri, F.H. Knebel, R.C. Albuquerque, and A. Campa. 2012. Serum amyloid A is a growth factor for 3T3-L1 adipocytes, inhibits differentiation and promotes insulin resistance. International Journal of Obesity 36: 1032–9.

    Article  PubMed  CAS  Google Scholar 

  9. Faty, A., P. Ferre, and S. Commans. 2012. The acute phase protein serum amyloid A induces lipolysis and inflammation in human adipocytes through distinct pathways. Plos One 7(4): e34031. doi:10.1371/journal.pone.0034031.

    Article  PubMed  CAS  Google Scholar 

  10. Sommer, G., S. Weise, S. Kralisch, P.E. Scherer, U. Lossner, M. Bluher, et al. 2008. The adipokine SAA3 is induced by interleukin-1 beta in mouse adipocytes. Journal of Cellular Biochemistry 104: 2241–2247.

    Article  PubMed  CAS  Google Scholar 

  11. Ye, X.Y., Y.M. Xue, J.P. Sha, C.Z. Li, and Z.J. Zhen. 2009. Serum amyloid A attenuates cellular insulin sensitivity by increasing JNK activity in 3T3-L1 adipocytes. Journal of Endocrinological Investigation 32: 568–575.

    PubMed  CAS  Google Scholar 

  12. van Meerloo J, Kaspers GJL, Cloos J. Cell sensitivity assays: the MTT assay. In: Cree IA, ed. Cancer cell culture: methods and protocols. 731, 2011:237–245. Totowa: Humana.

  13. Reigstad, C.S., G.O. Lunden, J. Felin, and F. Backhed. 2009. Regulation of serum amyloid A3 (SAA3) in mouse colonic epithelium and adipose tissue by the intestinal microbiota. Plos One 4(6): e5842. doi:10.1371/journal.pone.0005842.

    Article  PubMed  Google Scholar 

  14. Sandri, S., E. Hatanaka, A.G. Franco, A.M.C. Pedrosa, H.P. Monteiro, and A. Campa. 2008. Serum amyloid A induces CCL20 secretion in mononuclear cells through MAPK (p38 and ERK1/2) signaling pathways. Immunology Letters 121: 22–26.

    Article  PubMed  CAS  Google Scholar 

  15. Connolly, M., A. Marrelli, M. Blades, J. McCormick, P. Maderna, C. Godson, et al. 2010. Acute serum amyloid A induces migration, angiogenesis, and inflammation in synovial cells in vitro and in a human rheumatoid arthritis/SCID mouse chimera model. Journal of Immunology 184: 6427–37.

    Article  CAS  Google Scholar 

  16. Han, C.Y., S. Subramanian, C.K. Chan, M. Omer, T. Chiba, T.N. Wight, et al. 2007. Adipocyte-derived serum amyloid A3 and hyaluronan play a role monocyte recruitment and adhesion. Diabetes 56: 2260–2273.

    Article  PubMed  CAS  Google Scholar 

  17. Hatanaka, E., P.T. Monteagudo, M.S.M. Marrocos, and A. Campa. 2007. Interaction between serum amyloid A and leukocytes—a possible role in the progression of vascular complications in diabetes. Immunology Letters 108: 160–166.

    Article  PubMed  CAS  Google Scholar 

  18. Wang, B., I.S. Wood, and P. Trayhurn. 2007. Dysregulation of the expression and secretion of inflammation-related adipokines by hypoxia in human adipocytes. Pflugers Archiv-European Journal of Physiology 455: 479–492.

    Article  PubMed  CAS  Google Scholar 

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Acknowledgments

We thank the Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP), the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES), and the Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) (Brazil) for their financial support.

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Authors and Affiliations

  1. Department of Clinical and Toxicological Analysis, Faculty of Pharmaceutical Sciences, University of São Paulo, Av. Prof. Lineu Prestes, 580, São Paulo, CEP 05508-900, Brazil

    Edson Mendes de Oliveira, Silvana Sandri, Franciele Hinterholz Knebel, Caroline Garcia Iglesias Contesini, Ana Campa & Fabíola Branco Filippin-Monteiro

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  1. Edson Mendes de Oliveira
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  2. Silvana Sandri
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  3. Franciele Hinterholz Knebel
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  4. Caroline Garcia Iglesias Contesini
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  5. Ana Campa
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  6. Fabíola Branco Filippin-Monteiro
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Correspondence to Edson Mendes de Oliveira.

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de Oliveira, E.M., Sandri, S., Knebel, F.H. et al. Hypoxia Increases Serum Amyloid A3 (SAA3) in Differentiated 3T3-L1 Adipocytes. Inflammation 36, 1107–1110 (2013). https://doi.org/10.1007/s10753-013-9644-9

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  • DOI: https://doi.org/10.1007/s10753-013-9644-9

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