Expression and regulation of transcript for the novel transmembrane protein Tmem182 in the adipocyte and muscle lineage.
BACKGROUND
White adipose tissue is not only an energy storage organ; it also functions as an endocrine organ. The coordination and integration of numerous gene expression events is required to establish and maintain the adipocyte phenotype.


RESULTS
We previously observed a 45-fold upregulation for a transcript encoding a novel predicted transmembrane protein, Tmem182, upon brown preadipocyte to adipocyte conversion. Here we use real-time PCR analysis to further characterize Tmem182 transcript expression in the adipocyte lineage. Analysis across a panel of 10 murine tissues revealed highest Tmem182 transcript expression in white adipose tissues (WAT), with 10-fold to 20-fold higher levels than in brown adipose tissue (BAT). Tmem182 transcript expression is ~3-fold upregulated in BAT of genetically obese (ob/ob) mice vs. wild type C57BL/6. Analysis of three in vitro models of white adipogenesis indicates markedly enriched expression of Tmem182 transcript in adipocytes vs. preadipocytes. Compared to 3T3-L1 preadipocytes, a 157-fold higher level of Tmem182 transcript is detected at 3 day post-induction of adipogenesis and an ~2500-fold higher level in mature 3T3-L1 adipocytes. TNFalpha treatment of 3T3-L1 adipocytes resulted in a ~90% decrease in Tmem182 transcript level. As skeletal muscle and heart were also found to express Tmem182 transcript, we assessed expression in C2C12 myogenesis and observed a ~770-fold upregulation upon conversion of myoblasts to myocytes.


CONCLUSIONS
WAT is the most prominent site of Tmem182 transcript expression and levels of transcript for Tmem182 are altered in adipose tissues of ob/ob mice and upon exposure of 3T3-L1 adipocytes to the proinflammatory cytokine TNFalpha. The dramatic upregulation of Tmem182 transcript during in vitro adipogenesis and myogenesis suggests Tmem182 may function in intracellular pathways important in these two cell types.
Wu
Yu
Y
Department of Biochemistry and Cancer Biology and Center for Diabetes and Endocrine Research, University of Toledo, Health Science Campus, Toledo, OH 43614, USA. yu.wu@utoledo.edu
Smas
Cynthia M
CM