Effects of hormones and growth factors on TGF-β1 expression in bovine mammary epithelial cells

Abstract

The decline of mammary epithelial cell (MEC) number during mammary gland involution in the cow is due to inhibition of proliferation and induction of apoptosis. Transforming growth factorbeta 1 (TGF-b1) belongs to a group of intramammary auto/paracrine inhibitors of bovine MEC growth and inducers of apoptosis. However, the mechanism responsible for the regulation of TGF-b1 expression in MEC is not known. The present study examined the effect of the hormones, growth hormone (GH), somatostatin (STS), 17-b oestradiol (E2), progesterone (P4), as well as the growth factors, insulin-like growth factor I (IGF-I) and epidermal growth factor (EGF), on TGF-b1 expression in the bovine MEC lines, BME-UV1 and MAC-T. The model of apoptosis in bovine mammary gland in vitro was applied by reduction of fetal bovine serum (FBS) (from 10 % to 2% or 0 . 5 % FBS) in the cell environment to show the relationship between TGF-b1 expression and apoptosis in bovine MEC. RT-PCR, Western blot and laser scanning cytometry (LSC) were used for analysis of TGF-b1 transcript and protein level as well as apoptosis and cell cycle in examined MEC. In this model of apoptosis, FBS deficiency (mimicking the naturally occurring decline in the access of bioactive compounds and nutrients at the end of lactation and dry period) was associated with increased TGF-b1 expression at the level of transcript and protein, induction of apoptosis and inhibition of cell cycle. Exogenous TGF-b1, IGF-I, EGF and GH inhibited FBSdeficiency-stimulated TGF-b1 expression. The suppressive effect of GH was reversed when cells were maintained longer in FBS-deficient medium. In general, STS, E2 and P4 increased TGF-b1 expression. However, this effect was dependent on hormone concentration and cell line. BME-UV1 cells were much more responsive to the peptides, GH, STS, IGF-I and EGF, whereas MAC-T cells were more responsive to the steroid sex hormones: E2 and P4.

The Genome Response to Artificial Selection: A Case Study in Dairy Cattle

“…In addition to GH1, other important molecules participating to the different GH signal transduction pathways [28] belonged to GN such as GRB2, PLCH2, PLCL2, PLCB4, PLCG1 and SRC or PIK3C2G and PLCZ1, these two latter displaying footprints of selection. GN also contained TGFB1 which is an intramammary auto/paracrine inhibitor of mammary epithelial cells growth and an inducer of apoptosis, which plays a critical role during mammary gland involution [29]. Note that in bovine mammary epithelial cells, GH is also able through its interaction with GHR to suppress expression of TGFB1.…”

Cancer associated fibroblasts stimulated by transforming growth factor beta1 (TGF-β1) increase invasion rate of tumor cells: a population study

“…Since it has been reported that FBS contains TGF-b and cells in culture secrete TGF-b [36,[48][49][50], the levels of latent and activated TGF-b were measured in basal media (BM) and CM. The concentration of TGF-b1 was below detectable levels in non-acidified samples of BM and CM collected from normal and CAF cultures treated with 0 ng/ml TGF-b1.…”

Apical electrolyte concentration modulates barrier function and tight junction protein localization in bovine mammary epithelium

“…The original description included the claim that these immortalized cells exhibited many characteristics of mammary epithelia, including a cobblestone appearance when grown on solid supports, cytokeratin production, and synthesis of ␣-lactalbumin and ␣ s1 -casein (41). It has since been reported that BME-UV cells respond to a variety of hormones and pharmacological agents with changes in cell signaling, cellular metabolism, proliferation, and apoptosis (6,12,39,40,42). It has also been shown that BME-UV cells grow on a permeable support system to form a confluent, polarized monolayer that is capable of regulated ion transport (29).…”