Todorčević et al. BMC Genomics 2010, 11:39 http://www.biomedcentral.com/1471-2164/11/39 R E S E A R C H A R T I C L E Open Access Gene expression profiles in Atlantic salmon adipose-derived stromo-vascular fraction during differentiation into adipocytes Marijana Todorčević1,2*†, Stanko Škugor1,2†, Aleksei Krasnov1, Bente Ruyter1 Abstract Background: Excessive fat deposition is one of the largest problems faced by salmon aquaculture industries, leading to production losses due to high volume of adipose tissue offal. In addition, increased lipid accumulation may impose considerable stress on adipocytes leading to adipocyte activation and production and secretion of inflammatory mediators, as observed in mammals. Results: Microarray and qPCR analyses were performed to follow transcriptome changes during adipogenesis in the primary culture of adipose stromo-vascular fraction (aSVF) of Atlantic salmon. Cellular heterogeneity decreased by confluence as evidenced by the down-regulation of markers of osteo/chondrogenic, myogenic, immune and vasculature lineages. Transgelin (TAGLN), a marker of the multipotent pericyte, was prominently expressed around confluence while adipogenic PPARg was up-regulated already in subconfluent cells. Proliferative activity and subsequent cell cycle arrest were reflected in the fluctuations of pro- and anti-mitotic regulators. Marked regulation of genes involved in lipid and glucose metabolism and pathways producing NADPH and glycerol-3-phosphate (G3P) was seen during the terminal differentiation, also characterised by diverse stress responses. Activation of the glutathione and thioredoxin antioxidant systems and changes in the iron metabolism suggested the need for protection against oxidative stress. Signs of endoplasmic reticulum (ER) stress and unfolded protein response (UPR) occured in parallel with the increased lipid droplet (LD) formation and production of secretory proteins (adipsin, visfatin). The UPR markers XBP1 and ATF6 were induced together with genes involved in ubiquitin-proteasome and lysosomal proteolysis. Concurrently, translation was suppressed as evidenced by the down-regulation of genes encoding elongation factors and components of the ribosomal machinery. Notably, expression changes of a panel of genes that belong to different immune pathways were seen throughout adipogenesis. The induction of AP1 (Jun, Fos), which is a master regulator of stress responses, culminated by the end of adipogenesis, concurrent with the maximal observed lipid deposition. Conclusions: Our data point to an intimate relationship between metabolic regulation and immune responses in white adipocytes of a cold-blooded vertebrate. Stress imposed on adipocytes by LD formation and expansion is prominently reflected in the ER compartment and the activated UPR response could have an important role at visceral obesity in fish. Background Feeds used in modern Atlantic salmon aquaculture con- tain large amounts of lipids, which provide rapid growth, reduce environmental load from farms, but increase visceral fat deposition [1]. Very little is, * Correspondence: marijana.todorcevic@nofima.no † Contributed equally 1Nofima, Norwegian Institute of Food, Fisheries and Aquaculture Research, P. O. Box 5010, Ås NO-1430, Norway however, known about the factors regulating develop- ment and functions of adipose tissue in fish, and whether increased fat deposition may lead to health pro- blems. Previously regarded principally as energy storage, white adipose tissue (WAT) in mammals is now recog- nized as a highly active endocrine tissue producing numerous secretory proteins, including adipokines, a suite of small signalling proteins specifically produced in WAT [2,3]. Under normal conditions, adipocytes are © 2010 Todorčević et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.