scholarly journals miR-15b negatively correlates with lipid metabolism in mammary epithelial cells

2018 ◽  
Vol 314 (1) ◽  
pp. C43-C52 ◽  
Author(s):  
Meiqiang Chu ◽  
Yong Zhao ◽  
Shuai Yu ◽  
Yanan Hao ◽  
Pengfei Zhang ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Epithelial Cells ◽  
Steroid Hormones ◽  
Lipid Content ◽  
Mammary Epithelial Cells ◽  
Lipid Production ◽  
Fatty Acid Synthetase ◽  
Lipid Synthesis ◽  
Mammary Epithelial ◽  
Lipid Formation

Mammary epithelial cells are regulated by steroid hormones, growth factors, and even microRNAs. miR-15b has been found to regulate lipid metabolism in adipocytes; however, its effects on lipid metabolism in mammary epithelial cells, the cells of lipid synthesis and secretion, are as yet unknown. The main purpose of this investigation was to explore the effect of miR-15b on lipid metabolism in mammary epithelial cells, along with the underlying mechanisms. miR-15b was overexpressed or inhibited by miRNA mimics or inhibitors; subsequently, lipid formation in mammary epithelial cells, and proteins related to lipid metabolism, were investigated. Through overexpression or inhibition of miR-15b expression, the current investigation found that miR-15b downregulates lipid metabolism in mammary epithelial cells and is expressed differentially at various stages of mouse and goat mammary gland development. Inhibition of miR-15b expression increased lipid content in mammary epithelial cells through elevation of the lipid synthesis enzyme fatty acid synthetase (FASN), and overexpression of miR-15b reduced lipid content in mammary epithelial cells with decreasing levels of FASN. Moreover, the steroid hormones estradiol and progesterone decreased miR-15b expression with a subsequent increase in lipid formation in mammary epithelial cells. The expression of miR-15b was lower during lactation and negatively correlated with lipid synthesis proteins, which suggests that it may be involved in lipid synthesis and milk production. miR-15b might be a useful target for altering lipid production and milk yield.

scholarly journals Circadian Gene PER2 Silencing Downregulates PPARG and SREBF1 and Suppresses Lipid Synthesis in Bovine Mammary Epithelial Cells

Biology ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1226
Author(s):  
Yujia Jing ◽  
Yifei Chen ◽  
Shan Wang ◽  
Jialiang Ouyang ◽  
Liangyu Hu ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Epithelial Cells ◽  
Circadian Clock ◽  
Lipid Droplets ◽  
Mammary Epithelial Cells ◽  
Lipid Synthesis ◽  
Mammary Epithelial ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Bovine Mammary Epithelial Cells

PER2, a circadian clock gene, is associated with mammary gland development and lipid synthesis in rodents, partly via regulating peroxisome proliferator-activated receptor gamma (PPARG). Whether such a type of molecular link existed in bovines was unclear. We hypothesized that PER2 was associated with lipid metabolism and regulated cell cycles and apoptosis in bovine mammary epithelial cells (BMECs). To test this hypothesis, BMECs isolated from three mid-lactation (average 110 d postpartum) cows were used. The transient transfection of small interfering RNA (siRNA) was used to inhibit PER2 transcription in primary BMECs. The silencing of PER2 led to lower concentrations of cellular lipid droplets and triacylglycerol along with the downregulation of lipogenic-related genes such as ACACA, FASN, LPIN1, and SCD, suggesting an overall inhibition of lipogenesis and desaturation. The downregulation of PPARG and SREBF1 in response to PER2 silencing underscored the importance of circadian clock signaling and the transcriptional regulation of lipogenesis. Although the proliferation of BMECs was not influenced by PER2 silencing, the number of cells in the G2/GM phase was upregulated. PER2 silencing did not affect cell apoptosis. Overall, the data provided evidence that PER2 participated in the coordination of mammary lipid metabolism and was potentially a component of the control of lipid droplets and TAG synthesis in ruminant mammary cells. The present data suggested that such an effect could occur through direct effects on transcriptional regulators.

scholarly journals LPS-induced reduction of triglyceride synthesis and secretion in dairy cow mammary epithelial cells via decreased SREBP1 expression and activity

2018 ◽  
Vol 85 (4) ◽  
pp. 439-444 ◽  
Author(s):  
Jianfa Wang ◽  
Xu Zhang ◽  
Xianjing He ◽  
Bin Yang ◽  
Hai Wang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Dairy Cow ◽  
Milk Fat ◽  
Mammary Epithelial Cells ◽  
Fatty Acid Synthetase ◽  
Mammary Epithelial ◽  
Acetyl Coa Carboxylase ◽  
Milk Fat Depression ◽  
Fat Synthesis ◽  
Lps Treatment

Sterol regulatory element binding protein 1 (SREBP1) has a central regulatory effect on milk fat synthesis. Lipopolysaccharides (LPS) can induce mastitis and cause milk fat depression in cows. SREBP1 is also known to be associated with inflammatory regulation. Thus, in the current study, we hypothesized that LPS-induced milk fat depression in dairy cow mammary epithelial cells (DCMECs) operates via decreased SREBP1 expression and activity. To examine the hypothesis, DCMECs were isolated and purified from dairy cow mammary tissue and treated with LPS (10 µg/ml). LPS treatment of DCMECs suppressed lipid-metabolism-related transcription factor SREBP1 mRNA expression, nuclear translocation and protein expression, leading to reduced triglyceride content. The transcription levels of acetyl-CoA carboxylase-1 and fatty acid synthetase were significantly down-regulated in DCMECs after LPS treatment, suggesting that acetyl-CoA carboxylase-1 and fatty acid synthetase involved in de novo milk fat synthesis was regulated by SREBP1. In summary, these results suggest that LPS induces milk fat depression in dairy cow mammary epithelial cells via decreased expression of SREBP1 in a time-dependent manner.

scholarly journals Expression of BRCA1 gene in ewe mammary epithelial cells during pregnancy: regulation by growth hormone and steroid hormones

2001 ◽  
pp. 763-770 ◽  
Author(s):  
K Laud ◽  
L Hornez ◽  
I Gourdou ◽  
L Belair ◽  
A Arnold ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Mammary Gland ◽  
Epithelial Cells ◽  
Mrna Expression ◽  
Steroid Hormones ◽  
Mammary Epithelial Cells ◽  
Brca1 Gene ◽  
Mammary Epithelial ◽  
Short Period ◽  
Brca1 Mrna

OBJECTIVE: Steroid hormones (estradiol and progesterone) in association with prolactin and growth hormone are involved in lobulo alveolar development of the mammary gland during pregnancy. We hypothesized that the BRCA1 gene may be induced by these different hormones. METHODS AND RESULTS: In this study, we have demonstrated by Northern blot and in situ hybridization, that the expression of ovine (o) BRCA1 mRNA in mammary epithelial cells increased dramatically during a short period in the second half of pregnancy (days 70 to 112) and decreased at the end of pregnancy. The increase in oBRCA1 mRNA expression is concomitant with rapid lobulo alveolar growth. Using an in vivo protocol to artificially induce mammary gland development, we demonstrated by the real-time RT-PCR method that growth hormone in association with estrogen, progesterone and hydrocortisone induces an increase of BRCA1 mRNA expression in the ewe mammary gland. Moreover, we showed that estradiol and progesterone induce oBRCA1 expression in primary cultures of ewe mammary gland. CONCLUSIONS: These results suggest that BRCA1 is a potential regulator of the effects of steroid hormones and growth hormone in the induction of mammary epithelial cell proliferation.

MicroRNA-221 may be involved in lipid metabolism in mammary epithelial cells

2018 ◽  
Vol 97 ◽  
pp. 118-127 ◽  
Author(s):  
Meiqiang Chu ◽  
Yong Zhao ◽  
Shuai Yu ◽  
Yanan Hao ◽  
Pengfei Zhang ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial

MicroRNA-141 participates in milk lipid metabolism by targeting SIRT1 in bovine mammary epithelial cells

2020 ◽  
Vol 60 (16) ◽  
pp. 1877
Author(s):  
Yujia Sun ◽  
Hailei Xia ◽  
Xubin Lu ◽  
Chong Xu ◽  
Mingxun Li ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Epithelial Cells ◽  
Dairy Cows ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Luciferase Assay ◽  
Milk Lipid ◽  
Potential Candidate ◽  
Bovine Mammary Epithelial Cells ◽  
Sirt1 Gene

Context The regulation of milk lipids is important for the evaluation of dairy cows’ performance. Lipids are produced and secreted by mammary gland under the regulation of steroid hormones, growth factors and microRNAs (miRNAs). MicroRNAs have been verified to be involved in numerous biological processes. Previous studies have shown that miR-141 is expressed at higher levels in dairy cows at peak lactation than in those at early lactation. However, the roles of miR-141 in bovine mammary epithelial cells (BMECs) and the mechanisms how it affects lipid metabolism are as yet unknown. Aims The aims of this study were to clarify (i) the molecular mechanisms of miR-141 in milk lipid metabolism, and (ii) how miR-141 affects milk lipid metabolism in BMECs. Methods Triglycerides were observed in BMECs using triglyceride analysis after overexpression or inhibition of miR-141; selected potential candidate genes that are targeted by miR-141 using TargetScan. The regulatory relationship among miR-141, SIRT1 gene and lipid metabolism-related genes (SREBF1, FASN and PPARγ) by using the dual luciferase assay, quantitative real-time PCR and western blotting. Key results Through overexpression or inhibition of miR-141 expression, we found that miR-141 promoted lipid metabolism in BMECs and an increase in triglycerides was observed in these cells. Further, miR-141 targets the 3′UTR of SIRT1 mRNA, and negative regulates the expression of SIRT1 gene in BMECs. Also, the expression levels of SREBF1, FASN and PPARγ, which are related to milk lipid metabolism, were also altered after overexpression miR-141. Conclusions Our results have revealed that miR-141 could promote milk lipid metabolism in BMECs by means of negative regulates SIRT1 gene and positive effects lipid metabolism-related genes (SREBF1, FASN and PPARγ) in BMECs. Implications Our research indicates that miR-141 could be considered a marker in cattle breeding to obtain high quality dairy products. It would be useful to study the function of miRNAs in milk lipid metabolism and synthesis. In the long term these findings might be helpful in developing practical means to improve the quality of ruminant milk.

scholarly journals β-Hydroxybutyrate Facilitates Fatty Acids Synthesis Mediated by Sterol Regulatory Element-Binding Protein1 in Bovine Mammary Epithelial Cells

2015 ◽  
Vol 37 (6) ◽  
pp. 2115-2124 ◽  
Author(s):  
Min Zhang ◽  
Shiqi Zhang ◽  
Qi Hui ◽  
Lin Lei ◽  
Xiliang Du ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Epithelial Cells ◽  
Fatty Acid Synthase ◽  
Mammary Epithelial Cells ◽  
Regulatory Element ◽  
Lipid Synthesis ◽  
Mammary Epithelial ◽  
Control Group ◽  
Bovine Mammary Epithelial Cells ◽  
Sterol Regulatory Element

Background/Aims: In dairy cows, β-hydroxybutyrate (BHBA) is utilized as precursors of de novo synthesized fatty acids in mammary gland. Ketotic cows are characterized by excessive negative energy balance (NEB), which can further increase the blood BHBA concentration. Sterol regulatory element-binding protein1 (SREBP1) and cell death-inducing DNA fragmentation factor-alpha-like effector α (Cidea) play crucial roles in lipid synthesis. Therefore, we hypothesized that BHBA could stimulate SREBP1/Cidea pathway to increase milk fat synthesis in bovine mammary epithelial cells. Methods: Bovine mammary epithelial cells were treated with different concentrations of BHBA and transfected with adenovirus to silence SREBP1 expression. The effects of BHBA on the lipid synthesis in bovine mammary epithelial cells were investigated. Results: The results showed that BHBA could significantly increase the expression of SREBP1, fatty acid synthase (FAS), acetyl-CoA carboxylase α (ACC-α), Cidea and diacylglycerol transferase-1 (DGAT-1), as well as the triglycerides (TG) content in bovine mammary epithelial cells. BHBA treatment also increased the transfer of mature SREBP1 to nucleus compared with control group. However, SREBP1 silencing could significantly down-regulate the overexpression of FAS, ACC-α, Cidea and DGAT-1, as well as TG content induced by BHBA. Conclusion: The present data indicate that BHBA can significantly increase TG secretion mediated by SREBP1 in bovine mammary epithelial cells.

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