The role of WNT inhibitory factor I in adipose tissue development
Fat tissue is involved in many aspects of biology such as appetite regulation, vascular diseases, diabetes, hypertension, and obesity. It plays an important role in these processes through its endocrine factors and other secretory products. Thus, there is a need to understand better the mechanisms and molecules that control the formation of adipocytes and the expansion of adipose tissue. WNT signaling is one of several important factors that plays a crucial role in development, and may also be important for adipogenesis. The activity of WNT signaling is modulated by a plethora of extracellular modulators that mostly antagonize WNT signaling. The extracellular WNT antagonists consist of four conserved families: Wnt-inhibitory factor 1 (WIF1), secreted frizzled related protein (SFRP), Cerberus, and Dickkopf (Dkk). It has been found that WIF1 is upregulated in abdominal fat tissue in chickens during early development. Thus, we hypothesize that WIF1 plays a role in adipose tissue development by inhibiting WNT signaling, and thereby stimulating adipogenic gene expression. The objective of this research is to examine the in vitro regulation of adipogenesis by WIF1. Mouse WIF1 expression vector (pCMV6-ENTRY-WIF1) was prepared, and used to transfect the mouse pre-adipocyte cell line 3T3-L1.The mRNA levels for WIF1, PPARγ and C/EBPα were then examined with real time RT-qPCR. Results indicate that the transgene was expressed in the transfected cells within 30 hours after transfection, and the mRNA level of WNT target genes and CEBPα were affected. However, the mRNA level of PPARγ was not affected. In conclusion, exogenous WIF1 was expressed in 3T3-L1 cells, at least at the mRNA level. The exogenous WIF1 expression caused an elevation of CEBPα mRNA. Future studies should examine other genes, and more investigation should take place to better understand the mechanisms of adipogenesis.
"The role of WNT inhibitory factor I in adipose tissue development"
ETD Collection for Tennessee State University.