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Publication : C1q/tumor necrosis factor-related protein 11 (CTRP11), a novel adipose stroma-derived regulator of adipogenesis.

First Author  Wei Z Year  2013
Journal  J Biol Chem Volume  288
Issue  15 Pages  10214-29
PubMed ID  23449976 Mgi Jnum  J:203503
Mgi Id  MGI:5527130 Doi  10.1074/jbc.M113.458711
Citation  Wei Z, et al. (2013) C1q/tumor necrosis factor-related protein 11 (CTRP11), a novel adipose stroma-derived regulator of adipogenesis. J Biol Chem 288(15):10214-29
abstractText  C1q/TNF-related proteins (CTRPs) are a family of secreted regulators of glucose and lipid metabolism. Here, we describe CTRP11, a novel and phylogenetically conserved member of the C1q family. Our studies revealed that white and brown adipose are major tissues that express CTRP11, and its expression is acutely regulated by changes in metabolic state. Within white adipose tissue, CTRP11 is primarily expressed by stromal vascular cells. As a secreted multimeric protein, CTRP11 forms disulfide-linked oligomers. Although the conserved N-terminal Cys-28 and Cys-32 are dispensable for the assembly of higher-order oligomeric structures, they are unexpectedly involved in modulating protein secretion. When co-expressed, CTRP11 forms heteromeric complexes with closely related CTRP10, CTRP13, and CRF (CTRP14) via the C-terminal globular domains, combinatorial associations that potentially generate functionally distinct complexes. Functional studies revealed a role for CTRP11 in regulating adipogenesis. Ectopic expression of CTRP11 or exposure to recombinant protein inhibited differentiation of 3T3-L1 adipocytes. The expression of peroxisome proliferator-activated receptor-gamma and CAAT/enhancer binding protein-alpha, which drive the adipogenic gene program, was markedly suppressed by CTRP11. Impaired adipogenesis was caused by a CTRP11-mediated decrease in p42/44-MAPK signaling and inhibition of mitotic clonal expansion, a process essential for adipocyte differentiation in culture. These results implicate CTRP11 as a novel secreted regulator of adipogenesis and highlight the potential paracrine cross-talk between adipocytes and cells of the stromal vascular compartment in maintaining adipose tissue homeostasis.
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