IGF-I retards proper development of acinar structures formed by bovine mammary epithelial cells via sustained activation of Akt kinase

2013 ◽  
Vol 45 (3) ◽  
pp. 111-121 ◽  
Author(s):  
M. Gajewska ◽  
K. Zielniok ◽  
B. Debski ◽  
T. Motyl
2009 ◽  
Vol 88 (2) ◽  
pp. 117-130 ◽  
Author(s):  
Agnieszka Sobolewska ◽  
Malgorzata Gajewska ◽  
Joanna Zarzyńska ◽  
Barbara Gajkowska ◽  
Tomasz Motyl

1999 ◽  
Vol 79 (3) ◽  
pp. 277-283 ◽  
Author(s):  
F. Cheli ◽  
B. Zavizion ◽  
O. Todoulou ◽  
I. Politis

The objectives of this study were to examine 1) the effect of extracellular calcium on proliferation of bovine mammary epithelial cells, 2) whether extracellular calcium regulates the mitogenic effect of insulin-like growth factor (IGF-I) and epidermal growth factor (EGF) towards mammary epithelial cells, and 3) whether the effects of calcium on growth are mediated through changes in the plasminogen activating system. The BME-UV1 cells were used as a model system. Results showed that optimal proliferation of BME-UV1 cells grown in the presence of 10% dialyzed FBCS was achieved when the culture medium was supplemented with 1–2 mmol L−1 of extracellular Ca2+. IGF-I (P<0.01) but not EGF, increased proliferation of BME-UV1 cells. Furthermore, calcium does not regulate IGF-I and EGF responsiveness of BME-UV1 cells. Northern blot analysis was performed to examine the effect of extracellular calcium on expression of urokinase-type plasminogen activator (u-PA), PA inhibitor 1 (PAI-1) and u-PA receptor (u-PAR) genes by BME-UV1 cells in culture. Results showed that calcium increased expression of all above-mentioned genes after 24 h of exposure of cells to calcium, at a time that the effect of calcium on growth was not apparent. Calcium had no effect on u-PA and u-PAR expression after 48 and 72 h of exposure of cells to calcium, at a time that the effect of calcium on growth was predominant. Calcium caused a small increase of PAI-1 expression after 48 and 72 h but this small increase is apparently of limited biological value. Key words: Mammary epithelial cells, calcium, growth factors, plasminogen activating system


2001 ◽  
Vol 68 (2) ◽  
pp. 157-164 ◽  
Author(s):  
STIG PURUP ◽  
SØREN KROGH JENSEN ◽  
KRIS SEJRSEN

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.


Molecules ◽  
2021 ◽  
Vol 26 (4) ◽  
pp. 1183
Author(s):  
Mst Mamuna Sharmin ◽  
Md Aminul Islam ◽  
Itsuki Yamamoto ◽  
Shin Taniguchi ◽  
Shinichi Yonekura

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.


2019 ◽  
Vol 86 (2) ◽  
pp. 177-180
Author(s):  
Jacqueline P. Kurz ◽  
Mark P. Richards ◽  
Matthew Garcia ◽  
Zhongde Wang

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.


1996 ◽  
Vol 63 (4) ◽  
pp. 543-553 ◽  
Author(s):  
Boris Zavizion ◽  
Andrew J. Bramley ◽  
Ioannis Politis

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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