Molecular network including eIF1AX, RPS7, and 14-3-3γ regulates protein translation and cell proliferation in bovine mammary epithelial cells

2014 ◽  
Vol 564 ◽  
pp. 142-155 ◽  
Author(s):  
Cuiping Yu ◽  
Chaochao Luo ◽  
Bo Qu ◽  
Nagam Khudhair ◽  
Xinyu Gu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Protein Translation ◽  
Mammary Epithelial ◽  
Molecular Network ◽  
Bovine Mammary Epithelial Cells

scholarly journals Investigation of the transport of aflatoxin M1 by the transporter ABCG2 in bovine mammary epithelial cells

2020 ◽  
Vol 76 (08) ◽  
pp. 6440-2020
Author(s):  
YANYING ZHANG ◽  
ZHANG NA ◽  
DAN CHEN ◽  
GUANG HUANG ◽  
HUI CAO
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Aflatoxin M1 ◽  
Efflux Transporter ◽  
Bovine Mammary Epithelial Cells ◽  
Milk And Dairy Products

Aflatoxin M1 (AFM1), a hydrogenated metabolite of aflatoxin B1 (AFB1), is one of the most common and threatening aflatoxins found in milk and dairy products. The ATP-binding cassette G2 efflux transporter (ABCG2) plays an important role in the mammary transport of drugs and toxins in animals, but whether ABCG2 could affect the transport of AFM1 in bovine mammary epithelial cells (BMECs) has not been clarified. Therefore, this study aimed to investigate the effects of AFM1 on tight junctions (TJs), lactation and cells proliferation in BMECs, and explored the regulatory role of ABCG2 in AFM1 transport in vitro in BMECs. The results showed that the integrity of the TJs of BMECs was not permanently compromised after exposure to AFM1. AFM1 exposure had no obvious effects on lactation or cell proliferation in BMECs. Gene function study revealed that ABCG2 was a positive regulator of AFM1 transport. These results demonstrate that it has little effect on TJs, lactation or cell proliferation in BMECs exposed to a small dose of AFM1, and ABCG2 is a critical regulator for AFM1 transport in BMECs.

scholarly journals Overexpression of lncRNA H19 changes basic characteristics and affects immune response of bovine mammary epithelial cells

PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e6715 ◽  
Author(s):  
Xuezhong Li ◽  
Hao Wang ◽  
Yanfen Zhang ◽  
Jinjing Zhang ◽  
Shaopei Qi ◽  
...  
Keyword(s):  
Immune Response ◽  
Cell Proliferation ◽  
T Cells ◽  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Mrna Level ◽  
Cell Types ◽  
Mammary Epithelial ◽  
Inflammatory Factors ◽  
Bovine Mammary Epithelial Cells

The function of long non-coding RNA H19 (H19) on cell proliferation has been observed in various cell types, and the increased expression of H19 was also found in the lipopolysaccharide (LPS)-induced inflammatory bovine mammary epithelial cells (MAC-T). However, the roles of H19 in the inflammatory response and physiological functions of bovine mammary epithelial cell are not clear. In the present study, we found that overexpression of H19 in MAC-T cells significantly promoted cell proliferation, increased the protein and mRNA level of β-casein, and enhanced the expression of tight junction (TJ)-related proteins while inhibited staphylococcus aureus adhesion to cells. In addition, results demonstrated that overexpression of H19 affected the LPS-induced immune response of MAC-T cells by promoting expressions of inflammatory factors, including TNF-α, IL-6, CXCL2 and CCL5, and activating the NF-κB signal pathway. Our findings indicate that H19 is likely to play an important role in maintaining normal functions and regulating immune response of bovine mammary epithelial cells.

Differential effects of retinoids on proliferation of bovine mammary epithelial cells in collagen gel culture

2001 ◽  
Vol 68 (2) ◽  
pp. 157-164 ◽  
Author(s):  
STIG PURUP ◽  
SØREN KROGH JENSEN ◽  
KRIS SEJRSEN
Keyword(s):  
Cell Proliferation ◽  
Retinoic Acid ◽  
Growth Factors ◽  
Growth Factor ◽  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Collagen Gel ◽  
Mammary Epithelial ◽  
Bovine Mammary Epithelial Cells ◽  
Igf I

The effects of increasing concentrations of retinol, retinal and retinoic acid on proliferation of bovine mammary epithelial cells were investigated in collagen gel cultures. All retinoids significantly inhibited proliferation of mammary epithelial cells. The relative inhibitory potency of the retinoids was: retinoic acid > retinal > retinol. Maximal inhibition at 10 μg/ml corresponded to a 75–95% inhibition of proliferation obtained in basal medium. Retinol, retinal and retinoic acid also inhibited proliferation of cells growth-stimulated with insulin-like growth factor-I (IGF-I). Retinoids in highest concentrations (10 μg/ml) inhibited 68–85% of proliferation of cells obtained in culture medium containing 25 ng IGF-I/ml. Retinol and retinoic acid also inhibited proliferation of cells growth-stimulated by insulin and other growth factors from the IGF growth factor family (des(1-3)IGF-I and IGF-II), as well as growth factors from the epidermal growth factor family (EGF and TGF-α), with retinoic acid being more effective than retinol. At a concentration of 100 ng/ml, retinol and retinoic acid inhibited respectively 24–38 and 44–52% of mammary cell proliferation stimulated by growth factors of the IGF family, and at 10000 ng/ml, 61–71% of cell proliferation was inhibited. The growth-stimulating effect of insulin, EGF and TGF-α was inhibited 42–64% by retinol and retinoic acid at 100 ng/ml, and 64–84% at 10000 ng/ml. The present results show that retinol, retinal and retinoic acid are potent inhibitors of bovine mammary epithelial cell proliferation. It is suggested that retinoids may have concentration-dependent roles in regulation of pubertal mammary growth and development, indicating that the milk yield potential of heifers may be affected by vitamin A status.

scholarly journals mTORC2 Regulates Lipogenic Gene Expression through PPARγ to Control Lipid Synthesis in Bovine Mammary Epithelial Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Zhixin Guo ◽  
Keyu Zhao ◽  
Xue Feng ◽  
Dandan Yan ◽  
Ruiyuan Yao ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Critical Role ◽  
Lipid Synthesis ◽  
Mammary Epithelial ◽  
Lipogenic Gene ◽  
Bovine Mammary Epithelial Cells ◽  
Lipogenic Gene Expression

The mechanistic target of rapamycin complex 2 (mTORC2) primarily functions as an effector of insulin/PI3K signaling to regulate cell proliferation and is associated with cell metabolism. However, the function of mTORC2 in lipid metabolism is not well understood. In the present study, mTORC2 was inactivated by the ATP-competitive mTOR inhibitor AZD8055 or shRNA targeting RICTOR in primary bovine mammary epithelial cells (pBMECs). MTT assay was performed to examine the effect of AZD8055 on cell proliferation. ELISA assay and GC-MS analysis were used to determine the content of lipid. The mRNA and protein expression levels were investigated by RT/real-time PCR and western blot analysis, respectively. We found that cell proliferation, mTORC2 activation, and lipid secretion were inhibited by AZD8055. RICTOR was knocked down and mTORC2 activation was specifically attenuated by the shRNA. Compared to control cells, the expression of the transcription factor gene PPARG and the lipogenic genes LPIN1, DGAT1, ACACA, and FASN was downregulated in RICTOR silencing cells. As a result, the content of intracellular triacylglycerol (TAG), palmitic acid (PA), docosahexaenoic acid (DHA), and other 16 types of fatty acid was decreased in the treated cells; the accumulation of TAG, PA, and DHA in cell culture medium was also reduced. Overall, mTORC2 plays a critical role in regulating lipogenic gene expression, lipid synthesis, and secretion in pBMECs, and this process probably is through PPARγ. This finding provides a model by which lipogenesis is regulated in pBMECs.

scholarly journals 5-ALA Attenuates the Palmitic Acid-Induced ER Stress and Apoptosis in Bovine Mammary Epithelial Cells

Molecules ◽  
2021 ◽  
Vol 26 (4) ◽  
pp. 1183
Author(s):  
Mst Mamuna Sharmin ◽  
Md Aminul Islam ◽  
Itsuki Yamamoto ◽  
Shin Taniguchi ◽  
Shinichi Yonekura
Keyword(s):  
T Cells ◽  
Epithelial Cells ◽  
Palmitic Acid ◽  
Er Stress ◽  
Aminolevulinic Acid ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Protective Effects ◽  
Bovine Mammary Epithelial Cells ◽  
Induced Apoptosis

The conservation of mammary gland physiology by maintaining the maximum number of mammary epithelial cells (MECs) is of the utmost importance for the optimum amount of milk production. In a state of negative energy balance, palmitic acid (PA) reduces the number of bovine MECs. However, there is no effective strategy against PA-induced apoptosis of MECs. In the present study, 5-aminolevulinic acid (5-ALA) was established as a remedial agent against PA-induced apoptosis of MAC-T cells (an established line of bovine MECs). In PA-treated cells, the apoptosis-related genes BCL2 and BAX were down- and upregulated, respectively. The elevated expression of major genes of the unfolded protein response (UPR), such as CHOP, a proapoptotic marker (C/EBP homologous protein), reduced the viability of PA-treated MAC-T cells. In contrast, 5-ALA pretreatment increased and decreased BCL2 and BAX expression, respectively. Moreover, cleaved caspase-3 protein expression was significantly reduced in the 5-ALA-pretreated group in comparison with the PA group. The downregulation of major UPR-related genes, including CHOP, extended the viability of MAC-T cells pretreated with 5-ALA and also reduced the enhanced intensity of the PA-induced expression of phospho-protein kinase R-like ER kinase. Moreover, the enhanced expression of HO-1 (antioxidant gene heme oxygenase) by 5-ALA reduced PA-induced oxidative stress (OxS). HO-1 is not only protective against OxS but also effective against ER stress. Collectively, these findings offer new insights into the protective effects of 5-ALA against PA-induced apoptosis of bovine MECs.

Exogenous phospholipase A2 affects inflammatory gene expression in primary bovine mammary epithelial cells

2019 ◽  
Vol 86 (2) ◽  
pp. 177-180
Author(s):  
Jacqueline P. Kurz ◽  
Mark P. Richards ◽  
Matthew Garcia ◽  
Zhongde Wang
Keyword(s):  
Epithelial Cells ◽  
Phospholipase A2 ◽  
Inflammatory Responses ◽  
Mammary Epithelial Cells ◽  
Constitutive Expression ◽  
Mammary Epithelial ◽  
Inflammatory Factors ◽  
Bovine Mammary Epithelial Cells ◽  
Lps Challenge

AbstractThis Research Communication addresses the hypothesis that exogenously administered phospholipase A2 (PLA2) affects the inflammatory responses of bovine mammary epithelial cells (bMEC) in vitro with the aim of providing preliminary justification of investigation into the uses of exogenously administered PLA2 to manage or treat bovine mastitis. Primary bMEC lines from 11 lactating Holstein dairy cows were established and the expression of 14 pro-inflammatory genes compared under unchallenged and lipopolysaccharide (LPS)-challenged conditions, with and without concurrent treatment with bovine pancreatic PLA2G1B, a secreted form of PLA2. No differences in the expression of these genes were noted between PLA2-treated and untreated bMEC under unchallenged conditions. Following LPS challenge, untreated bMEC exhibited significant downregulation of CXCL8, IL1B, CCL20, and CXCL1. In contrast, PLA2-treated bMEC exhibited significant downregulation of IL1B and CCL20 only. These findings indicate that exogenous PLA2 affects the expression of some pro-inflammatory factors in immune-stimulated bMEC, but does not influence the constitutive expression of these factors. Further investigation of the influence of exogenous PLA2 in the bovine mammary gland is justified.

Cell cycle regulation of mammary epithelial cell detachment byStaphylococcus aureus

1996 ◽  
Vol 63 (4) ◽  
pp. 543-553 ◽  
Author(s):  
Boris Zavizion ◽  
Andrew J. Bramley ◽  
Ioannis Politis
Keyword(s):  
Cell Cycle ◽  
Epithelial Cells ◽  
Culture Medium ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Cell Detachment ◽  
Staph Aureus ◽  
Bovine Mammary Epithelial Cells ◽  
Isogenic Mutants ◽  
Cycle Regulation

SummaryThe effect ofStaphylococcus aureuson detachment of bovine mammary epithelial cells in culture was examined. Mammary epithelial cells became detached from fresh monolayers following a 3 h incubation in the presence ofStaph. aureusM60. Two different procedures indicated that cell detachment coincided with the S-phase of the cell cycle. The roles of proteinases, toxins and Ca availability in inducing cell detachment were examined. Addition of the proteinase inhibitor phenyl-methylsulphonyl fluoride (1 mM) to the culture medium prevented cell detachment. Addition of a combination of purified staphylococcal proteinases XVI and XVII-B to the culture medium of mammary epithelial cells induced cell detachment in the absence ofStaph. aureus. Cell detachment may be caused by a staphylococcal proteinase. However, addition of Ca (10 mM) to the culture medium abolishedStaph. aureus-induced cell detachment, despite the fact that proteinase activity was still apparently present. Isogenic mutants ofStaph. aureusM60, expressing either ± or β toxins but not both, induced cell detachment, but to a lesser extent than the wild type. Thus, Ca and toxins play some role during cell detachment. Clones established from detached cells that were washed and replated showed the same susceptibility toStaph. aureus-induced cell detachment as the parental cells. This indicated that there is no subclone of mammary epithelial cells more sensitive to this effect.

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