Phytoestrogens Weaken the Blood–Milk Barrier in Lactating Mammary Epithelial Cells by Affecting Tight Junctions and Cell Viability

2017 ◽  
Vol 65 (50) ◽  
pp. 11118-11124 ◽  
Author(s):  
Yusaku Tsugami ◽  
Kota Matsunaga ◽  
Takahiro Suzuki ◽  
Takanori Nishimura ◽  
Ken Kobayashi
Keyword(s):  
Epithelial Cells ◽  
Cell Viability ◽  
Tight Junctions ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial

scholarly journals Caffeic Acid Prevented LPS-Induced Injury of Primary Bovine Mammary Epithelial Cells through Inhibiting NF-κB and MAPK Activation

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Mingjiang Liu ◽  
Guoqing Fang ◽  
Shaojie Yin ◽  
Xin Zhao ◽  
Chi Zhang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cell Viability ◽  
Signaling Pathways ◽  
Caffeic Acid ◽  
Proinflammatory Cytokines ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Signal Pathways ◽  
Dependent Manner ◽  
Bovine Mammary Epithelial Cells

In our previous study, lipopolysaccharide (LPS) significantly reduced the cell viability of primary bovine mammary epithelial cells (bMEC) leading to cell apoptosis, which were prevented by caffeic acid (CA) through inhibiting NF-κB activation and reducing proinflammatory cytokine expression. While the underlying mechanism remains unclear, here, we determined that LPS induced the extensive microstructural damage of bMEC, especially the mitochondria and endoplasmic reticulum. Then, the obvious reduction of mitochondrial membrane potential and expression changes of apoptosis-associated proteins (Bcl-2, Bax, and casepase-3) indicated that apoptosis signaling through the mitochondria should be responsible for the cell viability decrease. Next, the high-throughput cDNA sequencing (RNA-Seq) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were employed to verify that the MAPK and JAK-STAT signaling pathways also were the principal targets of LPS. Following, the critical proteins (ERK, JNK, p38, and c-jun) of the MAPK signaling pathways were activated, and the release of proinflammatory cytokines (TNF-α, IL-1β, IL-6, and IL-8) regulated by NF-κB and MAPKs was significantly increased, which can promote a cascade of inflammation that induces cell injury and apoptosis. Meanwhile, CA significantly inhibited the activation of MAPKs and the release of proinflammatory cytokines in a dose-dependent manner, which were similar to its effects on the NF-κB activation that we previously published. So we concluded that CA regulates the proteins located in the upstream of multiple cell signal pathways which can reduce the LPS-induced activation of NF-κB and MAPKs, thus weakening the inflammatory response and maintaining cell structure and function, which accordingly inhibit apoptosis.

scholarly journals Dipeptide (Methionyl-Methionine) Transport and Its Effect on β-Casein Synthesis in Bovine Mammary Epithelial Cells

2018 ◽  
Vol 49 (2) ◽  
pp. 479-488 ◽  
Author(s):  
Caihong Wang ◽  
Fengqi Zhao ◽  
Jianxin Liu ◽  
Hongyun Liu
Keyword(s):  
Epithelial Cells ◽  
Cell Viability ◽  
Transport Properties ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Janus Kinase ◽  
Initiation Factor ◽  
Peptide Transporter ◽  
Small Interference Rna ◽  
Bovine Mammary Epithelial Cells

Background/Aims: The aim of this study was to investigate the transport properties and utilization of methionyl-methionine dipeptide (Met-Met) in β-casein (β-CN) synthesis in bovine mammary epithelial cells (BMECs). Methods: The transport properties were studied for the effects of time, pH, concentration, temperature and inhibitors using Met-Met-FITC in BMECs. BMECs were treated with different concentrations of Met-Met (0, 20, 40, 80, 120 and 160 µg/ml). In several experiments, the cells were treated with Janus kinase 2 (JAK2) inhibitor (tyrphostin AG-490, 50 µM) and mammalian target of rapamycin (mTOR) inhibitor (rapamycin, 100 ng/ml). Results: The uptake of Met-Met-FITC by BMECs was rapid during the first fifteen minutes and became saturated after 15 minutes. The transport of Met-Met-FITC in BMECs exhibited a Michaelis constant of 52.4 µM and maximum transport velocity of 14.8 pmol/min/mg protein. The uptake of Met-Met-FITC in BMECs was pH-dependent, peaked at pH 6.5 and was significantly inhibited by other peptides, including Met-Lys, Lys-Lys, Gly-Met, Gly-Leu and Met-Leu. Knocking down the peptide transporter 2 (PepT2) with small interference RNA markedly decreased Met-Met-FITC uptake. Met-Met concentration-dependently increased the PepT2 expression and β-CN synthesis in BMECs with an optimal concentration of 80 µg/ml. At 80 µg/ml, Met-Met also enhanced the cell viability and cyclin D1 expression and promoted cell cycle transition from G1 phase to S phase. In addition, 80 µg/ml Met-Met increased the mRNA abundance of JAK2 and signal transducer and activator of transcription 5 (STAT5) and enhanced the phosphorylation of JAK2, STAT5, mTOR, p70 ribosomal S6 kinase 1 and eukaryotic initiation factor 4E binding protein 1. The inhibition of JAK2 and mTOR significantly decreased Met-Met-induced increase in cell viability and β-CN synthesis in BMECs. Conclusion: Our data elucidated the properties of peptide transporter and its effect on β-CN synthesis in BMECs. Met-Met, taken up by PepT2, enhances cell proliferation and promotes β-CN synthesis by activating JAK2-STAT5 and mTOR signaling pathways in BMECs.

scholarly journals Effects of Chinese Propolis in Protecting Bovine Mammary Epithelial Cells against Mastitis Pathogens-Induced Cell Damage

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Kai Wang ◽  
Xiao-Lu Jin ◽  
Xiao-Ge Shen ◽  
Li-Ping Sun ◽  
Li-Ming Wu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cell Viability ◽  
Inflammatory Responses ◽  
Mammary Epithelial Cells ◽  
Cell Damage ◽  
Mammary Epithelial ◽  
Active Components ◽  
Antioxidant Genes ◽  
Bovine Mammary Epithelial Cells ◽  
Chinese Propolis

Chinese propolis (CP), an important hive product, can alleviate inflammatory responses. However, little is known regarding the potential of propolis treatment for mastitis control. To investigate the anti-inflammatory effects of CP on bovine mammary epithelial cells (MAC-T), we used a range of pathogens to induce cellular inflammatory damage. Cell viability was determined and expressions of inflammatory/antioxidant genes were measured. Using a cell-based reporter assay system, we evaluated CP and its primary constituents on the NF-κB and Nrf2-ARE transcription activation. MAC-T cells treated with bacterial endotoxin (lipopolysaccharide, LPS), heat-inactivatedEscherichia coli,andStaphylococcus aureusexhibited significant decreases in cell viability while TNF-αand lipoteichoic acid (LTA) did not. Pretreatment with CP prevented losses in cell viability associated with the addition of killed bacteria or bacterial endotoxins. There were also corresponding decreases in expressions of proinflammatory IL-6 and TNF-αmRNA. Compared with the mastitis challenged cells, enhanced expressions of antioxidant genes HO-1, Txnrd-1, and GCLM were observed in CP-treated cells. CP and its polyphenolic active components (primarily caffeic acid phenethyl ester and quercetin) had strong inhibitive effects against NF-κB activation and increased the transcriptional activity of Nrf2-ARE. These findings suggest that propolis may be valuable in the control of bovine mastitis.

Effect of Echinacea augustifolia extract on cell viability and differentiation in mammary epithelial cells

Phytomedicine ◽  
2008 ◽  
Vol 15 (8) ◽  
pp. 555-562 ◽  
Author(s):  
L. Starvaggi Cucuzza ◽  
M. Motta ◽  
P. Accornero ◽  
M. Baratta
Keyword(s):  
Epithelial Cells ◽  
Cell Viability ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial

scholarly journals Effects of Selenomethionine on Cell Viability, Selenoprotein Expression and Antioxidant Function in Porcine Mammary Epithelial Cells

2021 ◽  
Vol 8 ◽  
Author(s):  
Jun Chen ◽  
Yinzhi Zhang ◽  
Yantao Lv ◽  
Min Tian ◽  
Jinming You ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Epithelial Cells ◽  
Glutathione Peroxidase ◽  
Cell Viability ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Antioxidant Enzyme Activities ◽  
Lactation Performance ◽  
Antioxidant Function

This study investigated the effects of selenomethionine (Se-Met) on the cell viability, selenoprotein expression, and antioxidant function of porcine mammary epithelial cells (pMECs) to reveal the underlying molecular mechanism of Se-Met on the lactation performance and antioxidant capacity of sows in vitro. The pMECs were used as an in vitro model and were treated with various concentrations of Se-Met (0, 0.5, 1, 2, and 4 μM). Cells were analyzed for cell viability, selenoprotein transcriptome, selenoprotein expression, and antioxidant enzyme activities. The results showed that, with increasing Se-Met concentrations, cell viability first increased and then decreased at 24, 48, or 72 h posttreatment with maximum values at 0.5-μM Se-Met. As the Se-Met concentrations increased, the mRNA expression of 17 selenoproteins first upregulated and then downregulated, with maximum values at 0.5-μM Se-Met. The 17 selenoproteins included SEPHS2, SELENOP, GPX1, GPX2, GPX3, GPX6, TXNRD1, SELENOK, SELENOW, DIO1, DIO2, DIO3, SELENOF, SELENOS, SELENOH, SELENOI, and SELENOT. Additionally, the protein expression levels of SEPHS2, SELENOP, GPX1, and TXNRD1 and the activities of glutathione peroxidase and thioredoxin were highest at 0.5-μM Se-Met. In conclusion, 0.5-μM Se-Met promotes cell viability partially by improving selenoprotein expression and antioxidant function in pMECs, which provides evidence for the potential ability of Se-Met to improve mammary gland health in sows.

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