scholarly journals Studies of the regulation of the mouse carboxyl ester lipase gene in mammary gland

1998 ◽  
Vol 336 (3) ◽  
pp. 577-585 ◽  
Author(s):  
Marie KANNIUS-JANSON ◽  
Ulf LIDBERG ◽  
Kåre HULTÉN ◽  
Amel GRITLI-LINDE ◽  
Gunnar BJURSELL ◽  
...  

The lactating mammary gland and pancreas of mouse constitute the main tissues for synthesis and secretion of a bile-salt-stimulated lipase called carboxyl ester lipase (CEL). In this paper we have analysed the endogenous CEL gene expression in mammary gland. It is shown that the gene is expressed at day 14 of pregnancy, which is synchronous with that of the whey acidic protein (WAP) gene. Even though the CEL and WAP genes are induced at the same time during mammary gland differentiation, their regulation is different with respect to dependence on lactogenic hormones. The high induction of the WAP gene expression due to the activation of signal transducer and activator of transcription (STAT)5 by prolactin has not been observed for the CEL gene, even though it has been demonstrated that both STAT5 isoforms interact with one of the γ-interferon activation sequence sites in the promoter of the CEL gene. Hence we have demonstrated that the prolactin/STAT5 signal is not involved in a general and significant activation of ‘milk genes ’. Instead of a direct effect of the lactogenic hormones, the up-regulation of the CEL gene is correlated with an increase in the number of differentiated epithelial cells. Furthermore, promoter studies using the mammary-gland-derived cell line, HC11, show that a major positive element in the CEL gene promoter interacts with a member(s) of the CCAAT-binding transcription factor/nuclear factor 1 family, binding to a palindromic site. Binding of this factor(s) is important for the tissue-specific activation of the CEL gene in the mammary gland, because no activation by this factor(s) was seen in cells of pancreatic origin.

2008 ◽  
Vol 20 (4) ◽  
pp. 460 ◽  
Author(s):  
Rachael O'Dowd ◽  
Mary E. Wlodek ◽  
Kevin R. Nicholas

Adequate mammary development and coordinated actions of lactogenic hormones are essential for the initiation of lactation. Pregnancies compromised by uteroplacental insufficiency impair mammary development and lactation, further slowing postnatal growth. It is not known whether the initiation of lactation or galactopoesis is compromised. Uteroplacental insufficiency induced in rats by bilateral uterine vessel ligation (Restricted) or sham surgery (Control) on Day 18 of gestation preceded collection of mammary tissue on Day 20 of pregnancy. Mammary explants were cultured with combinations of insulin, cortisol and prolactin and analysed for α-lactalbumin and β-casein gene expression. Mammary tissue from late pregnant Restricted rats had elevated α-lactalbumin, but not β-casein, mRNA, which is consistent with premature lactogenesis resulting from an early decline in peripheral maternal progesterone. Explants from Restricted rats were more responsive to hormone stimulation after 3 days in culture, indicating that compromised galactopoesis, not lactogenesis, most likely leads to the reduced growth of suckled pups.


2005 ◽  
Vol 72 (S1) ◽  
pp. 34-43 ◽  
Author(s):  
Tina Lenasi ◽  
Nadja Kokalj-Vokac ◽  
Mojca Narat ◽  
Antonella Baldi ◽  
Peter Dovc

Casein genes are expressed in a tissue-specific and highly coordinated manner. The main goals of casein gene promoter studies are to unravel cis- and trans-acting factors involved in the complex signalling pathway controlling milk production, and to explore the possibility of using these promoters for tissue-specific production of heterologous proteins in the mammary gland. Here we present a comparative study of the equine β-casein and κ-casein gene proximal promoters. In order to confirm the assumption that in the horse, as in other mammalian species, casein genes are organized in a cluster located on a single chromosome, we performed in situ hybridization of pro-metaphase chromosomes with two BAC clones containing different equine casein genes. Sequence analysis of the β-casein and κ-casein gene proximal promoters revealed binding sites for activators (STAT5, GRE, NF1, MAF) and repressors (YY1, PMF), characteristic for casein genes. The alignments of casein gene promoters revealed the highest sequence identity in the proximal promoter region between the equine and human β-casein gene promoters. We directly compared the activity of equine β-casein and κ-casein gene promoters in vitro using bovine mammary gland cell line BME-UV1. In this system, the κ-casein gene proximal promoter activated the reporter gene expression more efficiently than the β-casein gene promoter of approximately the same length. The 810 bp of β-casein promoter activated the reporter gene expression more efficiently than the long fragment (1920 bp) and the 1206 bp fragment of the same promoter, which included also 396 bp of 5′ UTR.


animal ◽  
2008 ◽  
Vol 2 (4) ◽  
pp. 566-573 ◽  
Author(s):  
S. Ollier ◽  
S. Chauvet ◽  
P. Martin ◽  
Y. Chilliard ◽  
C. Leroux

Genomics ◽  
1995 ◽  
Vol 29 (1) ◽  
pp. 115-122 ◽  
Author(s):  
A-S. Lidmer ◽  
M. Kannius ◽  
L. Lundberg ◽  
G. Bjursell ◽  
J. Nilsson

2005 ◽  
Vol 33 (6) ◽  
pp. 1397-1398
Author(s):  
R. Zaragozá ◽  
E.R. García-Trevijano ◽  
V.J. Miralles ◽  
M. Mata ◽  
C. García ◽  
...  

GSH delivery to the lactating mammary gland is essential for the maintenance of lactation as its decrease leads to apoptosis and involution of the mammary gland. In fact, it has already been demonstrated that some of the changes in gene expression found in the lactating mammary gland after forced weaning are reproduced in rats treated with buthionine sulphoximine to deplete GSH levels. An oligonucleotide microarray experiment would give us a better knowledge of the mRNA expression patterns during lactation and after weaning and the possible functions of GSH in the modulation of these events.


2003 ◽  
Vol 373 (3) ◽  
pp. 825-834 ◽  
Author(s):  
Rosa ZARAGOZÁ ◽  
Concha GARCÍA ◽  
A. Diana RUS ◽  
Federico V. PALLARDÓ ◽  
Teresa BARBER ◽  
...  

In the lactating mammary gland, weaning produces mitochondrial cytochrome c release and nuclear DNA fragmentation, as determined by gel electrophoresis. This is followed by a significant decrease in lactation. Weaning for 2 h produces an early induction of the tumour suppressor/transcription factor p53, whereas the oncoprotein c-Jun and c-Jun N-terminal kinase are elevated after 24 h of weaning when compared with controls. The expression of p21cip1 and p27kip1, cyclin-dependent kinase inhibitors, was significantly higher in weaned rats when compared with control lactating rats. All the changes mentioned above also happen in the lactating mammary gland when propargylglycine, an inhibitor of the liver trans-sulphuration pathway, is administered. This effect is partially reversed by N-acetylcysteine administration. The administration of buthionine sulphoximine, an irreversible inhibitor of γ-glutamylcysteine synthetase, to lactating rats produces a decrease in GSH levels and changes in protein concentrations and gene transcripts similar to those in rats with impaired trans-sulphuration pathway. These data suggest that the inter-tissue flux of GSH is an important mechanism of l-cysteine delivery to the lactating mammary gland and emphasize the importance of this physiological event in maintaining the gene expression required to sustain lactation.


1973 ◽  
Vol 73 (4) ◽  
pp. 700-712 ◽  
Author(s):  
J. D. Bruce ◽  
X. Cofre ◽  
V. D. Ramirez

ABSTRACT On the day following delivery (day 1 of lactation) one abdominal mammary gland was implanted with oestrogen and the contralateral gland received an empty needle. At 2, 5 or 10 days of lactation the rats were anaesthetized with pentobarbital and the nipples of both abdominal glands were cannulated and their pressures recorded by means of transducers coupled to an amplifier and recording system. The normal mammary glands of 5-day lactating rats responded to very low doses of oxytocin (Syntocinon®, Sandoz) (5× 10−8 mU) with a rhythmic elevation in pressure. However, saline infusion also evoked a small rise in intra-mammary pressure. Earlier (2 days) and later (10 days) in lactation the responses were smaller. Oestrogen decreases significantly the milk ejection response to oxytocin, and the effect was maximal at day 10 of lactation. Histological observations confirmed the diminished reaction of the gland to oxytocin, since the milk was retained in the alveoli of rats bearing a mammary-oestrogen implant. A paradoxical rise in pressure was detected in normal as well as in oestrogen-implanted glands when the lowest dose of oxytocin was injected in lactating rats which had previously received a high dose of oxytocin (50 mU or 500 mU). These results reinforce the hypothesis that oestrogen alters the milk ejection response to oxytocin and that the mechanism is probably related to changes in the contractility of the myoepithelial cells.


1960 ◽  
Vol XXXIV (IV) ◽  
pp. 543-557 ◽  
Author(s):  
B. Berde ◽  
A. Cerletti

ABSTRACT A study was made of the influence of pharmacological amounts of synthetic oxytocin (»Syntocinon«) on the lactating mammary gland of the rabbit. The drug was given by intravenous infusion, by intramuscular injection and by intranasal administration. Two different types of reaction were noted: a tonic reaction, i. e. a lasting increase in pressure in the mammary gland without significant fluctuations, or a rhythmic reaction, i. e. a series of increases in pressure at more or less regular intervals. In order to elicit reactions approximately identical in intensity and character with those produced by intravenous infusion, it was necessary to give approximately 1.5 to 8.0 times as much by intramuscular injection and approximately 10 to 100 times as much by intranasal administration. Intravenous administration of adrenaline transiently suppressed a long-lasting reaction to oxytocin.


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