[The cell cycle pathway regulates chicken abdominal fat deposition as revealed by transcriptome sequencing].

With the improvement of growth traits and feed conversion rate, the abdominal fat rate of Chinese local breeds of broilers has been increasing. Excessive abdominal fat deposition not only reduces the slaughter rate and disease resistance of broiler chickens, but also produces waste due to the difficulty of fat treatment. In order to study the regulatory genes and pathways involved in abdominal fat deposition of broilers, we used high-fat diets to feed the Xinghua Chicken, which is a Chinese local breed. Two weeks after feeding, we found that the abdominal fat weight and rate of broilers in the high-fat diet group increased significantly, and the diameter and area of abdominal fat cells also increased significantly. Transcriptome sequencing of abdominal fat and livers showed that the differentially expressed genes in the abdominal fat were mainly enriched in the cell cycle, peroxisome proliferator- activated receptor (PPAR) and extracellular matrix (ECM) receptor signaling pathways. The differentially expressed genes in livers were also significantly enriched in the cell cycle pathway, as well as in the steroid biosynthesis and PPAR signaling pathway. By analyzing the common differentially expressed genes in abdominal fat and liver tissues, we found that these genes were also enriched in cell cycle. Finally, we used the chicken LMH (chicken hepatoma cell) cell line and chicken ICP (immortalized chicken preadipocytes) cell line to do the in vitro validation assays. We used high-fat and common medium to culture the cells. The results showed that after 48 hours, the high-fat medium could significantly promote cell cycle and increase the number of cells in S phase. Additionally, qRT-PCR results showed that the high-fat medium could significantly promote the expression of genes related to cell cycle. In conclusion, we found that high-fat diets activate the cell cycle progression of chicken hepatocytes and preadipocytes, promote cell proliferation, and then increase abdominal fat deposition.

miRNA­15a­5p facilitates the bone marrow stem cell apoptosis of femoral head necrosis through the Wnt/ß­catenin/PPARγ signaling pathway.

Bone marrow stem cells (BMSCs) are a group cells that function as an underlying cell source for bone tissue regeneration. However, the molecular mechanisms of how BMSCs are induced into apoptosis remains unclear. In the present study, it was demonstrated that the molecular mechanisms of BMSCs were exerted via microRNA­15a­5p (miR­15a­5p) in femoral head necrosis (FHN). Briefly, miRNA­15a­5p expression was elevated in a rat model of FHN. Overexpression of miR­15a­5p promoted the apoptosis of BMSCs and reduced cell growth through the Wnt/ß­catenin/peroxisome proliferator­activated receptor γ (PPARγ) signaling pathway. Downregulation of miR­15a­5p reduced the apoptosis of BMSCs and promoted cell growth through the Wnt/ß­catenin/PPARγ signaling pathway. The activation of Wnt attenuated the effects of miR­15a­5p on the apoptosis of BMSCs via the ß­catenin/PPARγ signaling pathway. In conclusion, the present results indicated that miRNA­15a­5p was involved in the regulation of the apoptosis of BMSCs through regulating the Wnt/ß­catenin/PPARγ signaling pathway, which may serve an important role in the regulation of FHN.