Endocrinology

Wang, D. Y.; Bulbrook, R. D.

doi:10.1007/978-1-4684-2301-3_11

Cited by 8 publications

(4 citation statements)

References 162 publications

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“…It is believed that estrogen can a ect mammary gland development growth by virtue of its ability to induce progesterone receptors (Haslam, 1988;Wang et al, 1990) and PRL receptors (Ormandy et al, 1992). The addition of progesterone and PRL resulted in extensive penetration of the mammary fat pad, along with dichotomous and subordinate branching as would be expected during normal pubertal development.…”

Section: Discussionmentioning

confidence: 99%

Prolactin gene-disruption arrests mammary gland development and retards T-antigen-induced tumor growth

et al. 2000

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Prolactin (PRL), interacting with other hormones from the pituitary, gonad, and placenta, activates speci®c signals that drive the appropriately timed morphological and functional development of the mammary gland. A mouse model of isolated PRL de®ciency (PRL 7/7 ) was created by gene disruption in an e ort to further understand the molecular basis of mammary gland development and breast cancer. Whereas primary ductal growth was normal in PRL 7/7 mice, ductal arborization was minimal (branches/mm 2 =1.5+0.5), and lobular budding was absent. Replacement therapy with PRL injections stimulated a modest degree of lobular budding and ductal arborization (3.75+0.9). Pituitary transplants to the kidney capsule of PRL 7/7 mice restored lobular budding and ductal arborization, to the full extent of that seen in control animals (20.3+5.5). Pregnancy, established by mating progesterone-treated PRL 7/7 females with PRL 7/7 males, led to complete morphological development of the mammary gland, appropriate to the gestational stage. PRL treatment stimulated tyrosine phosphorylation and DNA binding activity of Stat5a, but not Stat1 in PRL 7/7 or PRL +/7 females, and Stat5a, but not Stat1, was elevated by estradiol within 24 h. PRL-de®cient mice were crossed with mice expressing a dominant oncogene (polyoma middle-T antigen driven by the MMTV promoter, PyVT mice). Palpable (1 mm 3 ) tumors were detected an average of 9 days earlier in hormonally normal females (PRL +/7 :PyVT) compared with littermates that were PRL-de®cient (PRL 7/7 :PyVT). The growth rate of PyVT-induced tumors was 30% faster in PRL +/7 , than in PRL 7/7 females.

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Section: Discussionmentioning

confidence: 99%

Prolactin gene-disruption arrests mammary gland development and retards T-antigen-induced tumor growth

et al. 2000

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“…This conversion between Ang II and Ang IV takes place extracellularly but probably also intracellularly. A receptor-mediated internalization of Ang II has been demonstrated [35 -38] and apparently, the intracellular Ang II is then rapidly converted into predominantly Ang IV [35,39,40]. The release of Ang IV is probably independent of neuronal depolarization since K + was unable to increase the striatal Ang IV concentration to detectable levels.…”

Section: Neuronal Stimulation With K + and Perfusion With Ang IImentioning

confidence: 98%

Nano‐LC‐MS/MS for the monitoring of angiotensin IV in rat brain microdialysates: Limitations and possibilities

Lanckmans

Stragier

Sarre

et al. 2007

J of Separation Science

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To broaden our knowledge about the central role of the angiotensin IV (Ang IV) peptide, we aimed to monitor its extracellular concentration in the brain using in vivo microdialysis. Ang IV was measured in the dialysates using a previously developed nano-LC-MS/MS assay with an LOD of 50 pM. Using this assay, baseline levels of Ang IV in dialysates from different brain structures were undetectable. However, immediately after microdialysis probe insertion, Ang IV could be detected in a concentration that varied between 120 and 187 pM. Using the zero-net-flux method, the extracellular levels of Ang IV in the striatum were estimated at 46 pM. These data may indicate that Ang IV is mainly present intracellularly. In addition, Ang IV was clearly measurable after striatal perfusion of Ang II. On the other hand, our nano-LC-MS/MS method was successful for the detection of Met-enkephalin and neurotensin in dialysates from the rat. In conclusion, the nano-LC-MS/MS method coupled with microdialysis is well suited to monitor the biologically significant conversion between Ang II and Ang IV in vivo, but physiological extracellular levels of Ang IV appear too low to be detected.

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“…Ductal branching and alveolar development are stimulated by progesterone and synthesis of the progesterone receptor is induced by estrogen. Lactogenesis and milk secretion requires the synergistic action of prolactin and glucocorticoids (Wang et al, 1990;Senkiti and Banerjee, 1979;Santarelli et al, 1996). After lactation, the majority of the ME-cells are eliminated by apoptosis and replaced by the adipose cells (Tzeng et al, 1998) but the signals regulating the cell death program are still not well understood.…”

Section: Introductionmentioning

confidence: 99%

The SV40 small t-antigen prevents mammary gland differentiation and induces breast cancer formation in transgenic mice; truncated large T-antigen molecules harboring the intact p53 and pRb binding region do not have this effect

et al. 2001

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We report here for the ®rst time, that the SV40 small tantigen inhibits mammary gland dierentiation during mid-pregnancy and that about 10% of multiparous WAP-SVt transgenic animals develop breast tumors with latencies ranging from 10 ± 17 months. Cyclin D1 is deregulated and over expressed in the small t-antigen positive mammary gland epithelial cells (ME-cells) and in the breast tumor cells. SV40 small t-antigen immortalized ME-cells (t-ME-cells) exhibit a strong intranuclear cyclin D1 staining, also in the absence of external growth factors and the cells continue to divide for several days without serum. In addition, the expression rate of cyclin E and p21Waf1 but not of p53 is increased. Coimmunoprecipitation experiments revealed that p21Waf1 is mainly associated with the cyclin D/CDK4 but not with the cyclin E/CDK2 complex. WAP-SVT transgenic animals exhibit an almost regular mammary gland development until late pregnancy but the majority of the ME-cells are eliminated by apoptosis during the early lactation period. Tumor formation is delayed and less ecient than in T/tantigen positive animals. Sequestration of p53 and pRb by the N-terminal truncated T-antigen molecules (T1-antigen and T2-antigen) does not aect mammary gland dierentiation and the transgenic animals (WAP-SVBstBam) do not develop breast tumors. Oncogene (2001) 20, 2325 ± 2332.

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Endocrinology

Cited by 8 publications

References 162 publications

Prolactin gene-disruption arrests mammary gland development and retards T-antigen-induced tumor growth

Prolactin gene-disruption arrests mammary gland development and retards T-antigen-induced tumor growth

Nano‐LC‐MS/MS for the monitoring of angiotensin IV in rat brain microdialysates: Limitations and possibilities

The SV40 small t-antigen prevents mammary gland differentiation and induces breast cancer formation in transgenic mice; truncated large T-antigen molecules harboring the intact p53 and pRb binding region do not have this effect

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