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Erschienen in: Inflammation 5/2013

01.10.2013

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

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

Erschienen in: Inflammation | Ausgabe 5/2013

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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.
Literatur
1.
Zurück zum Zitat 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.PubMedCrossRef 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.PubMedCrossRef
2.
Zurück zum Zitat Ye, J. 2009. Emerging role of adipose tissue hypoxia in obesity and insulin resistance. International Journal of Obesity 33: 54–66.PubMedCrossRef Ye, J. 2009. Emerging role of adipose tissue hypoxia in obesity and insulin resistance. International Journal of Obesity 33: 54–66.PubMedCrossRef
4.
Zurück zum Zitat 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.PubMedCrossRef 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.PubMedCrossRef
5.
Zurück zum Zitat 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.PubMedCrossRef 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.PubMedCrossRef
6.
Zurück zum Zitat 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.PubMedCrossRef 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.PubMedCrossRef
7.
Zurück zum Zitat 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.PubMedCrossRef 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.PubMedCrossRef
8.
Zurück zum Zitat 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.PubMedCrossRef 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.PubMedCrossRef
10.
Zurück zum Zitat 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.PubMedCrossRef 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.PubMedCrossRef
11.
Zurück zum Zitat 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 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
12.
Zurück zum Zitat 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. 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.
14.
Zurück zum Zitat 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.PubMedCrossRef 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.PubMedCrossRef
15.
Zurück zum Zitat 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.CrossRef 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.CrossRef
16.
Zurück zum Zitat 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.PubMedCrossRef 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.PubMedCrossRef
17.
Zurück zum Zitat 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.PubMedCrossRef 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.PubMedCrossRef
18.
Zurück zum Zitat 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.PubMedCrossRef 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.PubMedCrossRef
Metadaten
Titel
Hypoxia Increases Serum Amyloid A3 (SAA3) in Differentiated 3T3-L1 Adipocytes
verfasst von
Edson Mendes de Oliveira
Silvana Sandri
Franciele Hinterholz Knebel
Caroline Garcia Iglesias Contesini
Ana Campa
Fabíola Branco Filippin-Monteiro
Publikationsdatum
01.10.2013
Verlag
Springer US
Erschienen in
Inflammation / Ausgabe 5/2013
Print ISSN: 0360-3997
Elektronische ISSN: 1573-2576
DOI
https://doi.org/10.1007/s10753-013-9644-9

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