Open Access

14-3‑3γ regulates cell viability and milk fat synthesis in lipopolysaccharide-induced dairy cow mammary epithelial cells

  • Authors:
    • Lixin Liu
    • Li Zhang
    • Ye Lin
    • Yanjie Bian
    • Xuejun Gao
    • Bo Qu
    • Qingzhang Li
  • View Affiliations

  • Published online on: January 28, 2016     https://doi.org/10.3892/etm.2016.3029
  • Pages: 1279-1287
  • Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Our previous study demonstrated that 14-3-3γ overexpression was able to inhibit the production of lipopolysaccharide (LPS)-induced cytokines in dairy cow mammary epithelial cells (DCMECs) by inhibiting the activation of nuclear factor‑κB (NF‑κB) signaling pathways. However, the association between 14‑3‑3γ overexpression and milk fat synthesis in LPS‑induced DCMECs remains unclear. Therefore, the present study investigated the effect of 14‑3‑3γ on cell viability and milk fat synthesis in LPS‑induced DCMECs. The results of the MTT assay and lactate dehydrogenase activity assay demonstrated that 14‑3‑3γ overexpression was able to attenuate LPS‑induced cytotoxicity in DCMECs, and increase the viability of the cells. In addition, the results of reverse transcription‑quantitative polymerase chain reaction suggested that mRNA expression levels of genes associated with milk fat synthesis, including sterol regulatory element binding protein (SREBP1), peroxisome proliferator‑activated receptor‑γ (PPARG), cluster of differentiation 36, acetyl‑coA carboxylase (ACC), fatty acid synthase (FAS) and fatty acid binding protein‑3, were significantly upregulated in cells overexpressing the 14‑3‑3γ protein. In addition, as compared with the LPS‑treated group, the activities of FAS and ACC were significantly increased. Furthermore, western blotting demonstrated that 14‑3‑3γ overexpression enhanced the protein expression levels of phosphorylated SREBP1 and PPARG. These results suggested that high levels of 14‑3‑3γ protein were able to attenuate LPS‑induced cell damage and promote milk fat synthesis in LPS‑induced DCMECs by increasing the cell viability and upregulating the expression levels of transcription factors associated with milk fat synthesis.
View Figures
View References

Related Articles

Journal Cover

April-2016
Volume 11 Issue 4

Print ISSN: 1792-0981
Online ISSN:1792-1015

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Liu L, Zhang L, Lin Y, Bian Y, Gao X, Qu B and Li Q: 14-3‑3γ regulates cell viability and milk fat synthesis in lipopolysaccharide-induced dairy cow mammary epithelial cells. Exp Ther Med 11: 1279-1287, 2016.
APA
Liu, L., Zhang, L., Lin, Y., Bian, Y., Gao, X., Qu, B., & Li, Q. (2016). 14-3‑3γ regulates cell viability and milk fat synthesis in lipopolysaccharide-induced dairy cow mammary epithelial cells. Experimental and Therapeutic Medicine, 11, 1279-1287. https://doi.org/10.3892/etm.2016.3029
MLA
Liu, L., Zhang, L., Lin, Y., Bian, Y., Gao, X., Qu, B., Li, Q."14-3‑3γ regulates cell viability and milk fat synthesis in lipopolysaccharide-induced dairy cow mammary epithelial cells". Experimental and Therapeutic Medicine 11.4 (2016): 1279-1287.
Chicago
Liu, L., Zhang, L., Lin, Y., Bian, Y., Gao, X., Qu, B., Li, Q."14-3‑3γ regulates cell viability and milk fat synthesis in lipopolysaccharide-induced dairy cow mammary epithelial cells". Experimental and Therapeutic Medicine 11, no. 4 (2016): 1279-1287. https://doi.org/10.3892/etm.2016.3029