various metabolic pathways and their physiological and pathophysiological roles as revealed by the recently generated GM mouse models. Table 1 Predicted expression of human hydroxysteroid (17β) dehydrogenase (HSD17B) enzymes analysed by the data available
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Taija Saloniemi, Heli Jokela, Leena Strauss, Pirjo Pakarinen, and Matti Poutanen
Shiying Shao, Yun Gao, Bing Xie, Fei Xie, Sai Kiang Lim, and GuoDong Li
-producing cell lines from progenitor cells of early gastrulating mouse embryos ( Li et al . 2009 b ) and also from mouse ES cells ( Li et al . 2009 a ). Although these cell lines were derived from different precursors, they all displayed similar properties in
F Talamantes and R Ortiz
GH-binding protein (GHBP) in the mouse consists of a ligand-binding domain, which is identical to the extracellular portion of the GH receptor (GHR), and a hydrophilic C-terminal domain, in place of the transmembrane and intracellular domains of the GHR. The two proteins are encoded by separate mRNAs which are derived from a single gene by alternative splicing. Determination of the gestational profiles of GHR and GHBP mRNA expression in mouse liver and placenta shows that in the liver, the 1.4 kb mRNA corresponding to the mouse GHBP increases approximately 20-fold between non-pregnant and late pregnant mice, whereas the relative increase in the expression of the 4.2 kb mouse GHR was 8-fold. The rise in the steady-state levels of both mRNAs began on day 9 of gestation. Mouse GHBP mRNA levels continue to rise until day 15 of pregnancy, while GHR mRNA abundance reaches a plateau by day 13. By elucidating the temporal changes in GHR and GHBP mRNA abundance during pregnancy and lactation in multiple maternal tissues and by assessing the ontogeny of these mRNAs in fetal and early postnatal mouse liver, our studies have demonstrated that the alternative splicing of mouse GHR/GHBP mRNA precursor is regulated in a tissue-, developmental stage- and physiological state-specific manner. In vitro studies using hepatocytes in culture have begun to elucidate the hormonal factor(s) involved in the gestation control of the expression of GHR and GHBP. Treatment of hepatocytes with GH or estradiol (E2) alone did not have any effect on the cellular concentrations of GHBP and GHR. However, the combination of E2 and GH up-regulated the cellular concentrations of GHBP and GHR 2- to 3-fold. GHBP and GHR mRNA concentrations were also up-regulated 2- to 3-fold. ICI 182-780, a competitive inhibitor of E2 for the estrogen receptor (ER), at different concentrations inhibited the E2- and GH-induced stimulation of GHBP and GHR. Furthermore, ER concentrations increased 5- to 7-fold in hepatocytes treated with E2 and GH compared with those in untreated cells or cells treated with either E2 or GH alone. Our studies in the mouse suggest that GHBP is an important cell-surface receptor for GH in the liver. These studies postulate that an arginine-glycine-aspartic acid sequence found on mouse GHBP but absent in other species is responsible for the association of GHBP with the plasma membrane by binding to one or more integrins on the surface of liver cells.
Yuichiro Takeuchi, Keishi Yamauchi, Junko Nakamura, Satoshi Shigematsu, and Kiyoshi Hashizume
). Mesangial cells play important roles in the pathogenesis of glomerular diseases such as glomerular nephritis, glomerular sclerosis, and diabetic nephropathy. Previously, we confirmed that mouse cultured mesangial (MSG) cells express two subtypes of AngII
C S A Markides and J G Liehr
which chronic estrogen exposure induces malignant or benign tumors: hamster kidney ( Kirkman 1959 ), mouse uterus ( Newbold et al. 1990 , Newbold & Liehr 1999 ) or rat pituitary gland ( Bui & Weisz 1988 ). As mentioned above, specific 4-hydroxylation
Danielle Brown, Amiya P Sinha Hikim, Ekaterina L Kovacheva, and Indrani Sinha-Hikim
mouse model for investigating the molecular mechanisms by which T promotes muscle growth. The regeneration of skeletal muscle is largely dependent on a small population of self-renewing committed stem cells, the satellite cells ( Conboy & Rando 2002
L Bai, G Meredith, and B E Tuch
’s medium (KO DMEM), l -glutamine, β-mercaptoethanol, penicillin-streptomycin, fetal bovine serum (FBS), non-essential amino acids (NEAAs), B27 serum-free supplement, N 2 serum-free supplement, mouse basic fibroblast growth factor (bFGF), insulin
Ana B Ropero, Pablo Juan-Picó, Alex Rafacho, Esther Fuentes, F Javier Bermúdez-Silva, Enrique Roche, Ivan Quesada, Fernando Rodríguez de Fonseca, and Angel Nadal
Opticon Engine System (MJ Research) with the SYBR Green I detection format and using the QuantiTect SYBR Green PCR kit (Qiagen GmbH, Germany). Primers for PCR were designed based on NCBI database sequences of mouse Pparα (accession NM_011144.2) and
Yu-Chyu Chen, Madan L Nagpal, Douglas M Stocco, and Tu Lin
detected exclusively in the Sertoli cells ( Saunders et al. 1998 , Pelletier et al. 2000 ). Estradiol treatment suppressed progesterone synthesis ( Freeman 1985 ), but stimulated proliferation of mouse Leydig tumor cells ( Sato et al. 1987 , DuMond
J. M. Beardmore and R. C. Richards
A radioimmunoassay was used to measure the concentration of epidermal growth factor (EGF) in mouse milk throughout lactation.
The EGF content of mouse milk increased steadily from birth to a concentration of 427 μg/l at day 8 of lactation. These high levels were maintained until the approach of weaning, when values decreased from day 17 to 130 μg/l at day 22.
Milk samples chromatographed on a Biogel P10 column gave a major peak of immunoreactivity at the point at which pure standard EGF was eluted.
The origin of milk EGF is unknown, but the high concentrations of this peptide identified in mouse milk suggest that it must play a role in the neonate.
