(1) Background: Excessive abdominal fat deposition in broilers not only causes feed waste but also leads to a series of metabolic diseases. It has gradually become a new breeding goal of the broiler industry to improve growth rates and to reduce abdominal fat rates. In a previous study, PROS1 was highly expressed in low-abdominal fat broilers, suggesting a potential role in broilers adipogenesis. However, the function of PROS1 in preadipocytes and its association with abdominal fat traits need to be characterized. (2) Methods: qRT-PCR and Western Blot were used to quantify gene expression at the RNA and protein levels; flow cytometry and EdU were carried out to detect cell proliferation; and a GLM analysis was used to determine the association between PROS1 SNPs and carcass traits. (3) Results: PROS1 was downregulated in high-abdominal fat chicken; PROS1 contributed preadipocyte proliferation but suppressed preadipocyte differentiation; and the SNPs in the PROS1 5′ flank were significantly associated with the abdominal fat weight rate. (4) Conclusions: Chicken PROS1 is able to suppress adipogenesis, and its polymorphisms are associated with the abdominal fat weight rate, which can be considered the molecular markers for chicken breeding, indicating that PROS1 is an effective potential gene in regulating abdominal fat deposition.

The immune cell inflammation response is closely related to the occurrence of disease, and much evidence has shown that circular RNAs (circRNAs) play vital roles in the occurrence of disease. However, the biological function and regulatory mechanisms of circRNAs in the immune cell inflammation response remain poorly understood. In this study, we constructed an inflammatory model using lipopolysaccharide (LPS)-stimulated chicken macrophage lines (also known as HD11) to verify the function and mechanism of the novel circDCLRE1C (ID: gga_circ_0001674), which was significantly upregulated in spleen tissues infected by coccidia and the macrophage cells exposed to LPS. The results showed that circDCLRE1C aggravated LPS-induced inflammation and apoptosis in HD11 cells. Systemically, circDCLRE1C acted as a sponge for miR-214b-3p binding sites thereby regulating the expression of STAT3. The overexpression of miR-214b-3p rescued the pro-inflammatory effect of circDCLRE1C in HD11 cells stimulated with LPS, and rescued the high expression of STAT3. In conclusion, our study showed that circDCLRE1C could aggravate LPS-induced inflammation and apoptosis through competitive adsorption of miR-214b-3p, thereby increasing the expression of STAT3.