bluuebunny/crossref_metadata_2025_split huggingface dataset:
Expression of granulocyte-colony stimulating factor and its receptor is regulated during the development of the human placenta
Authors: McCracken S , Layton J E , Shorter S C , Starkey P M , Barlow D H , Mardon H J 
Published: December 2004

Abstract
The development of the placenta is dependent upon the regulated proliferation, invasion and differentiation of trophoblast. Expression of cytokines at the feto-maternal interface suggests that these molecules may participate in placentation. The expression of granulocyte-colony stimulating factor (G-CSF) and G-CSF receptor (G-CSFR) during the development of the human placenta was studied by immunohistochemistry using an anti-G-CSF monoclonal antibody (mAb) and two novel anti-G-CSFR mAbs. G-CSF was present in the stroma of fetal chorionic villi and maternal decidual tissues throughout pregnancy. G-CSFR was detected at high levels in fetal first and third, but not second trimester placental tissues. Staining for G-CSFR was undetectable in maternal decidual tissue from all gestational stages. In first trimester tissues, staining for placental G-CSFR was strongest in differentiated syncytiotrophoblast and invasive, extravillous cytotrophoblast, and weak staining was evident in undifferentiated cytotrophoblast. Immunohistochemical data suggesting temporal regulation of G-CSFR were corroborated by Western blotting and amplification by reverse transcription and PCR of G-CSFR mRNA. These data suggested that expression of G-CSFR in the human placenta is regulated both temporally and spatially, and that placental G-CSF is involved in paracrine regulation, and indicate a role for G-CSF and G-CSFR in trophoblast growth or function during placentation.
Journal of Endocrinology (1996) 149, 249–258
Induction and involvement of endogenous IGF-I in pancreas regeneration after partial pancreatectomy in the dog
Authors: Hayakawa H , Kawarada Y , Mizumoto R , Hibasami H , Tanaka M , Nakashima K 
Published: December 2004

Abstract
To elucidate whether and how IGF-I is involved in the regeneration of the pancreas after partial pancreatectomy, IGF-I mRNA expression, IGF-I protein synthesis, ornithine decarboxylase (ODC) activity and DNA replication in the remnant pancreas were determined in the dog. After pancreatectomy, IGF-I mRNA expression was remarkably enhanced in the remnant pancreas, showing the maximal value at post-operative day (POD) 1. Subsequently, IGF-I synthesis in the tissue was significantly stimulated at POD 2, and its maximal concentration was observed at POD 3. Following IGF-I synthesis, ODC activity was induced and its maximal activity was also obtained at POD 3. Finally, DNA replication was induced in the remnant pancreas, and its maximal level was observed at POD 5. These responses in the remnant pancreatic tissue to partial pancreatectomy were greatly enhanced as the resection rate was increased up to 95%. Positive correlations were observed between IGF-I concentrations in the remnant pancreas and the activities of ODC and DNA synthesis in the tissue after 95% pancreatectomy. These results suggest that the gene expression of IGF-I is rapidly induced in the remnant pancreas after partial pancreatectomy, and subsequently synthesized endogenous IGF-I peptides may stimulate ODC and other cell growth-related activities in the tissue in paracrine and/or autocrine manners eventually to induce DNA replication and tissue regeneration.
Journal of Endocrinology (1996) 149, 259–267
Insulin-like growth factor-binding protein-6 produced by human PC-3 prostate cancer cells: isolation, characterization and its biological action
Authors: Srinivasan N , Edwall D , Linkhart T A , Baylink D J , Mohan S 
Published: December 2004

Abstract
The PC-3 human prostatic carcinoma cell line has been extensively used as a model for studies on the regulation of prostate tumor cell proliferation. Because of the importance of IGF-binding proteins (IGFBPs) in the control of IGF activities that regulate cell proliferation in normal and malignant cell types, we undertook studies to characterize the IGFBPs produced by PC-3 prostate tumor cells in culture. We previously found, using an IGF-I affinity column for purification and a polyethylene glycol (PEG) precipitation assay for IGFBP detection, that PC-3 cells in culture produced a single predominant IGFBP, IGFBP-4, which inhibits IGF activities. We now present evidence that PC-3 cells also produce IGFBP-6 in abundant quantity; in the previous study this was apparently not detected in the IGF-I-bound fraction with the PEG precipitation and Western ligand blot assays. In the current study, IGF-II affinity purification of IGFBPs produced by PC-3 cells, followed by C8 HPLC reverse-phase chromatography using a shallow acetonitrile gradient, produced two major protein peaks. N-terminal amino acid sequence of peak 1 was identical to that of IGFBP-6 while that of peak 2 was identical to that of IGFBP-4. Characterization of purified IGFBP-6 from PC-3 cells revealed properties which are distinct from other IGFBPs. PEG did not precipitate the complex of 125I-IGF-II/IGFBP-6 while it precipitated the complexes between 125I-IGF-II and other IGFBPs. Indeed, IGFBP-6 decreased the amount of 125I-IGF-II tracer in the PEG precipitate in a dose-dependent manner. Also, the binding of IGFBP-6 with 125I-IGF-II was poor in Western ligand blots compared with other IGFBPs. In studies on IGFBP-6 actions, IGFBP-6 completely inhibited IGF-II-induced [3H]thymidine incorporation in MC3T3-E1 mouse osteoblast cells while it had only minimal inhibitory effects on IGF-I-induced [3H]thymidine incorporation. This differential effect is associated with the fact that IGFBP-6 has greater affinity for IGF-II than IGF-I. The results of this study indicated that (1) Western ligand blotting is not sensitive for identification of IGFBP-6, (2) the unique behavior of IGFBP-6 in the PEG assay system necessitates the use of charcoal adsorption procedure for IGFBP-6 activity detection and (3) PC-3 cells should provide a useful model system for studying regulation of IGFBP-6 expression and the role of IGFBP-6 in modulating IGF actions.
Journal of Endocrinology (1996) 149, 297–303
Anti-idiotypic antibody as an oestrogen mimetic in vivo: stimulation of creatine kinase specific activity in rat animal models
Authors: Sömjen D , Amir-Zaltsman Y , Mor G , Gayer B , Lichter S , Barnard G , Kohen F 
Published: December 2004

Abstract
Previous studies indicated that the anti-idiotypic antibody (clone 1D5) significantly increased the specific activity of creatine kinase (CK) activity in the rat uterus, and in vitro in skeletal cells capable of responding to oestradiol (E2), suggesting that the antibody has oestrogenic-like activity. Moreover, the F(ab′)2 dimer of clone 1D5 acted like an antagonist and completely inhibited the increase in CK specific activity by either E2 or clone 1D5 in these skeletal cells. In the present study, we examined the in vivo effects of clone 1D5 and its proteolytic fragment, the F(ab′)2 dimer, E2 and dihydrotestosterone (DHT) on CK specific activity in the epiphyseal cartilage, diaphyseal bone, uterus, prostate, thymus and pituitary of immature or gonadectomized female and male rat animal models. In the intact immature animals, clone 1D5 caused an increase in CK in all organs of the female except in the pituitary. In the diaphyseal bone and prostate of male rats there was no stimulation by 1D5. The CK response in the uterus, epiphysis, and diaphysis of immature female rats was dose-dependent and was blocked by either the anti-oestrogen tamoxifen or the F(ab′)2 dimer of clone 1D5. E2, DHT, as well as clone 1D5, stimulated CK specific activity in both the diaphysis and epiphysis of ovariectomized female and castrated male rats, whereas sex specificity in the CK response was observed also in the uterus and the prostate of gonadectomized animals. Collectively, these results suggest that, as in cell culture, an intact antibody is necessary for the observed stimulation of CK specific activity and the F(ab′)2 dimer can act as an antagonist. Furthermore, the observed biological effects of clone 1D5 which are absolutely parallel to E2, imply that the anti-idiotypic antibody is able to penetrate the cell and reach the nuclear oestrogen receptor and transduces a signal to the nucleus, by as yet uncharacterized mechanisms.
Journal of Endocrinology (1996) 149, 305–312
Demonstration of in vivo metabolic effects of 3,5-di-iodothyronine
Authors: Cimmino M , Mion F , Goglia F , Minaire Y , Géloën A 
Published: December 2004

Abstract
The objective of the present study was to test in vivo the metabolic effects of 3,5-di-iodothyronine (3,5-T2) in unanesthetized and unrestrained male Sprague–Dawley rats. Amino acid and lipid metabolisms were investigated by breath tests using as tracers the 13C-carboxyl-labeled molecules of leucine, α-ketoisocaproic acid (KIC) and octanoic acid, in four different groups of rats: hypothyroid animals (receiving propylthiouracil (PTU) and iopanoic acid), hypothyroid animals treated with either a daily i.p. injection of 3,5-T2 (25 μg/100 g body weight), or triiodothyronine (T3) (1 μg/100 g body weight), and control euthyroid animals receiving equivalent volumes of the vehicle solutions. Energy expenditure was measured by continuous monitoring of O2 consumption and CO2 production in these different groups. Daily energy expenditure was decreased by 30% in PTU-treated rats. The chronic treatments with 3,5-T2 and T3 restored daily energy expenditure to the control level. 13CO2 recovered in breath following the i.v. injection of octanoic acid-[1-13C] was decreased in hypothyroid animals compared with control animals (P<0·05) and restored to control values by T3 and 3,5-T2 treatments. The 13CO2 recovered in breath after i.v. injection of leucine-[1-13C]was increased in PTU-treated compared with control animals (P<0·05). Chronic treatment with either 3,5-T2 or T3 restored 13CO2 to control values. Excretion of 13CO2 recovered in breath following the i.v. injection of KIC-[1-13C] was increased in PTU-treated compared with control animals. Chronic treatments with either 3,5-T2 or T3 did not restore KIC decarboxylation. These results suggest that 3,5-T2 exerts metabolic effects on energy expendi ture, on both lipid β-oxidation and leucine metabolism in hypothyroid rats. We conclude that 3,5-T2 is a metabolically active iodothyronine.
Journal of Endocrinology (1996) 149, 319–325
Pup contact induces the expression of long form prolactin receptor mRNA in the brain of female rats: effects of ovariectomy and hypophysectomy on receptor gene expression
Authors: Sugiyama T , Minoura H , Toyoda N , Sakaguchi K , Tanaka M , Sudo S , Nakashima K 
Published: December 2004

Abstract
Prolactin receptor (PRL-R) mRNA expression levels in the female rat brain (cerebrum) during pup contact stimulation were determined by the reverse transcription-PCR method. The high expression levels of long form PRL-R mRNA found in the brain of lactating rats were markedly reduced by removal of pups, and long form PRL-R mRNA levels were recovered by resumption of pup contact. Interestingly, pup contact stimuli of nulliparous virgin rats also markedly induced long form but not short form PRL-R mRNA expression in the brain in 1·3 days, together with the expression of maternal behaviour. In ovariectomized (OVX) or hypophysectomized (HYPOX) virgin rats, or in OVX plus HYPOX virgin rats, however, brain long form PRL-R mRNA was not significantly induced by pup contact stimuli for as long as 7 days, while maternal behaviour was fully expressed in these rats after 7 days of pup contact. The in situ hybridization experiments revealed that the long form PRL-R mRNA induced in virgin rats in contact with pups or in lactating rats was localized in the epithelial cells of the choroid plexus. No significant increase in mRNA was detected in other regions of the brain, such as the hypothalamus or cortex, in these maternal female rats. These results suggest that pup contact induces the expression of long form PRL-R mRNA in the choroid plexus of the brain in the presence of female sex steroid and pituitary hormones for the rapid expression of maternal behaviour. Our studies also suggested that maternal behaviour can be expressed in OVX or HYPOX rats after exposure to pups for 7 days without any significant increase in brain PRL-R mRNA expression.
Journal of Endocrinology (1996) 149, 335–340
Cortisol decreases IGF-I mRNA levels in human osteoblast-like cells
Authors: Swolin D , Brantsing C , Matejka G , Ohlsson C 
Published: December 2004

Abstract
Excess levels of glucocorticoids are known to cause osteoporosis. It is speculated that the effect of glucocorticoids could be mediated via regulation of IGF-I. The aims of the present study were to detect and quantify the expression of IGF-I and/or IGF-II mRNA transcripts in human osteoblast-like cells and to investigate whether glucocorticoids regulate the expression of IGF-I mRNA transcripts in human osteoblast-like cells.
Cultures of human osteoblast-like cells from trabecular bone were established. The IGF-IA and IGF-IB transcripts were detected in human osteoblast-like cells from seven out of nine patients while the IGF-II transcript was detected in human osteoblast-like cells from eight out of nine patients, as determined by RT-PCR assays. Human osteoblast-like cells, as well as human muscle tissue, expressed approximately 1/10 of the IGF-I mRNA levels found in liver, as determined by RNase protection solution hybridization assay. The IGF-I mRNA levels did not decrease with age in the human osteoblast-like cells and no difference was seen between males and females. However, cortisol (10−6 mol/l) decreased IGF-I mRNA levels.
In summary, the present study has shown that human osteoblast-like cells express IGF-I and IGF-II mRNA transcripts and that cortisol down-regulates the IGF-I mRNA levels, indicating that some of the inhibitory effect of glucocorticoids on bone formation in humans is mediated via a reduced autocrine/paracrine expression of IGF-I.
Journal of Endocrinology (1996) 149, 397–403
Hormonal regulation of IGF-binding protein-2 expression in proliferating C2C12 myoblasts
Authors: Ernst C W , White M E 
Published: December 2004

Abstract
No studies have investigated the hormonal regulation of IGF-binding protein-2 (IGFBP-2) secretion and mRNA expression in myoblasts. In this study, cells of the C2C12 mouse myoblast cell line were used to examine the effects of various agents on the hormonal regulation of IGFBP-2. Conditioned medium (CM) was collected and cells were harvested at 2, 4, 6, 15 and 24 h after exposure to treatment media containing porcine insulin (pINS) or recombinant human IGF-I (rhIGF-I), and at 6, 15 and 24 h after exposure to treatment media containing dexamethasone (DEX) or prostaglandin E2 (PGE2). Relative abundance of a single 1·8 kb IGFBP-2 mRNA transcript was determined by Northern analysis using total cellular RNA and a labeled cDNA specific for rat IGFBP-2. IGFBP-2 was detected in CM by probing Western blots with 125I-IGF-I (ligand blot analysis). We have previously shown by immunoblot analysis that the predominant 32 000 Mr protein on ligand blots is IGFBP-2. Treatment with 10−9 or 10−6 m pINS led to a rapid reduction (P<0·01) in relative IGFBP-2 mRNA abundance and protein secretion relative to controls. Treatment with 7 × 10−10 or 7 × 10−9 m (5 or 50 ng/ml) rhIGF-I increased IGFBP-2 mRNA abundance and protein secretion (P<0·01). Cultures treated with 10−8 m DEX exhibited significantly increased (P<0·001) IGFBP-2 mRNA and protein. IGFBP-2 secretion was not affected by 10−6 m PGE2 but mRNA levels were higher than controls at 24 h (P<0·01). These findings suggest that multiple factors, including growth factors and metabolic hormones, are involved in regulating IGFBP-2 expression in C2C12 myoblasts.
Journal of Endocrinology (1996) 149, 417–429
Changes in the binding characteristics of the μ, δ and κ subtypes of the opioid receptor in the hypothalamus of the normal cyclic ewe and in the ovariectomised ewe following treatment with ovarian steroids
Authors: Thom B , Canny B J , Cowley M , Wright P J , Clarke I J 
Published: December 2004

Abstract
The μ, δ and κ opioid receptor subtypes were measured across the oestrous cycle of the ewe and in ovariectomised (OVX) ewes treated with oestrogen and/or progesterone. We have used a subtype-specific opioid receptor binding assay, in which [3H]diprenorphine non-preferentially labelled each receptor subtype in the presence of blocking concentrations of site-specific opioid analogues. The density and affinity of each receptor subtype was measured in the preoptic area (POA) of the hypothalamus and the mediobasal hypothalamus (MBH). Normally cycling ewes were killed during the luteal phase of the oestrous cycle and at various times after an injection of a synthetic prostaglandin (cloprostenol) to synchronise the onset of the follicular phase. OVX ewes were either untreated as controls (n=4) or treated with oestrogen (n=4), progesterone (n=4) or oestrogen and progesterone combined (n=4). The total number of opioid receptors did not alter across the oestrous cycle or with steroid hormone treatment. In the POA, the mean (± s.e.m.) number of δ receptors was significantly (P<0·05) greater during the luteal phase than 24 h into the follicular phase (133 ± 45 vs 35 ± 8 fmol/mg protein). A significantly (P<0·05) greater number of δ receptors was also found in the OVX progesterone-treated ewes compared with the control animals (172 ± 9 vs 39 ± 4 fmol/mg protein). In the MBH, the number of δ receptors was significantly (P<0·01) greater in ewes killed 56 h after prostaglandin than luteal-phase ewes (184 ± 40 vs 51 ± 7 fmol/mg protein). The number of μ receptors in both the POA and the MBH was also significantly (P<0·05) higher in the 56-h group than in the 12-h group. A similar trend was also observed in the steroid-treated animals, although differences did not reach statistical significance. The δ:μ ratio in the POA was significantly (P<0·05) higher in the luteal-phase animals than any of the other groups killed after a cloprostenol injection that causes luteolysis. Similarly the ratio of δ receptor density to μ receptor density was greater (P<0·05) in the OVX progesterone-treated ewes than in the OVX control ewes. No differences were found in the κ receptor density across the cycle or with different steroid treatments. These data suggest that the relative proportions of the δ and μ subtypes of the opioid receptor in the hypothalamus change during the oestrous cycle. Regulation appears to be due to the feedback effects of ovarian steroids with progesterone altering the δ:μ ratio. In the MBH, there was a general increase in both δ and μ subtypes during the follicular phase of the oestrous cycle. This may explain, in part, how the responsiveness of the GnRH/LH axis to opioid peptides and antagonists changes across the cycle.
Journal of Endocrinology (1996) 149, 509–518
Nutritional regulation of gene expression of insulin-like growth factor-binding proteins and the acid-labile subunit in various tissues of rats
Authors: Takenaka A , Mori M , Yamada S , Ohgane J , Takahashi S-I , Noguchi T 
Published: December 2004

Abstract
The plasma concentration and liver mRNA content of IGF-I are regulated by the quantity and quality of dietary proteins. To determine whether the synthesis of IGF-binding proteins (BPs) is also affected by protein nutrition, we assessed plasma concentration, tissue mRNA content and liver transcription rate of each BP after rats were fed either a 12% casein or a protein-free diet for 1 week. Protein deprivation reduced the plasma concentration of IGFBP-3 and IGFBP-4 and increased that of IGFBP-1 and IGFBP-2. The mRNA content in tissues and liver transcription rates of IGFBP-3 and IGFBP-4 did not change in response to protein deprivation although their plasma concentrations decreased. The increased plasma IGFBP-1 and IGFBP-2 concentrations were explained by the increased mRNA content and transcription rate of their genes in the liver. Although IGFBP-1 mRNA was increased by protein deprivation not only in liver but also in kidney, IGFBP-2 mRNA was increased only in liver and did not increase in any other tissue examined. In addition, the liver mRNA content of the acid-labile subunit, which can form a ternary complex with IGFs and IGFBP-3, was not affected by protein deprivation. These results show that tissue-specific synthesis of each BP is regulated in a distinct way in response to protein deprivation.
Journal of Endocrinology (1996) 150, 33–41
The ovine pancreatic protein which binds insulin-like growth factor binding protein-3 is procarboxypeptidase A
Authors: Fowke P J , Hodgkinson S C 
Published: December 2004

Abstract
Insulin-like growth factor binding protein-3 (IGFBP-3) is known to modulate the actions of insulin-like growth factors (IGF)-I and -II at the level of the cell. Proposed mechanisms include association of IGFBP-3 with cell surface proteoglycan, with cell surface binding proteins, proteolysis and/or internalization of IGFBP-3. In previous studies we have characterized a protein of 40 kDa in extracts of ovine pancreas and muscle which binds IGFBP-3 on ligand blot analyses. This paper reports the identity of the pancreatic species as procarboxypeptidase A (peptidyl-l-amino acid hydrolase, E.C. 3.4.17.1; proCPA). Identity was established by amino terminal sequence analysis, binding studies with pure bovine carboxypeptidase A (CPA) and observations that the binding activity was present in pancreatic secretions consistent with the role of proCPA as a secretory zymogen. The binding activity was inhibited by unlabelled IGFBP-3 at high doses (10 μg/ml) and reduced but not abolished by preincubation of 125I-IGFBP-3 with excess IGF-I. Digestion of 125I-IGFBP-3 with mature CPA produced a 26 kDa product. Modification of IGFBP-3 by CPA or binding to proCPA may provide a mechanism for modulation of IGFBP activity and hence IGF action.
Journal of Endocrinology (1996) 150, 51–56