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Pregnancy is characterized by increased erythropoiesis within maternal and fetal compartments. The placenta has been shown to produce factors that stimulate erythropoiesis but convincing evidence for placental production of erythropoietin (EPO) is still lacking. Prolactin-like protein E (PLP-E) was recently found to stimulate expression of the adult beta major globin gene in mouse erythroleukemia cells. Here we demonstrate that PLP-E transiently expressed in COS-7 cells stimulates proliferation and erythroid differentiation of murine and human erythroid progenitor cell lines. Electrophoretic mobility shift assays were used to show the activation of STAT5 by PLP-E in the human erythroid cell line TF1. Furthermore, we compared the effects of PLP-E on murine myeloid FDCP1 cells which do not express EPO receptors (EPORs) with effects on cells genetically engineered to express functional EPORs. We provide evidence that PLP-E-dependent proliferation and STAT5 activation is independent of the expression of the EPOR. Taken together, these data suggest that PLP-E acts on specific receptors of erythroid-committed murine and human cells by the activation of intracellular signaling pathways promoting cell growth and differentiation.
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GH inhibits primary rat preadipocyte differentiation and expression of late genes required for terminal differentiation. Here we show that GH-mediated inhibition of fatty acid-binding protein aP2 gene expression correlates with the activation of the Janus kinase-2/signal transducer and activator of transcription (STAT)-5 signalling pathway. Within minutes of treatment, GH induced the tyrosine phosphorylation, nuclear localization and DNA binding of STAT5. Importantly, there was no evidence that STAT5 acted via an interaction with peroxisome proliferator-activated receptor gamma. To further understand the mechanism of STAT5 action, we reconstituted the inhibition of aP2 in a non-adipogenic cell line. Using this system, we showed that the ability of GH to inhibit a 520 bp aP2 reporter was largely dependent upon the presence of either STAT5A or STAT5B. Mutant analysis confirmed that the tyrosine phosphorylation of STAT5 was essential for this signalling. However, STAT5's C-terminal transactivation domain was fully dispensable for this inhibition. Taken together, these data confirm a key regulatory role of STAT5 in adipose tIssue and point to STAT5 as the repressing modulator of GH-mediated inhibition in primary preadipocytes.
Department of Anatomy and Developmental Biology, Murdoch Childrens Research Institute, Department of Paediatrics, Monash University, Building 73, Clayton, Victoria 3800, Australia
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Department of Anatomy and Developmental Biology, Murdoch Childrens Research Institute, Department of Paediatrics, Monash University, Building 73, Clayton, Victoria 3800, Australia
Department of Anatomy and Developmental Biology, Murdoch Childrens Research Institute, Department of Paediatrics, Monash University, Building 73, Clayton, Victoria 3800, Australia
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Department of Anatomy and Developmental Biology, Murdoch Childrens Research Institute, Department of Paediatrics, Monash University, Building 73, Clayton, Victoria 3800, Australia
Department of Anatomy and Developmental Biology, Murdoch Childrens Research Institute, Department of Paediatrics, Monash University, Building 73, Clayton, Victoria 3800, Australia
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place of donor-derived pancreatic tissue. Of particular interest are pluripotent stem cells, immortal stable cell lines that can be differentiated into any cell type found in the body, including insulin-producing β-cells. This review briefly discusses
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Expansion of adipose tissue in the orbits is a key feature of Graves' ophthalmopathy. Recent evidence shows that orbital fibroblasts are committed to differentiate into adipocytes under appropriate stimuli. Rosiglitazone, an agonist of the nuclear hormone receptor, peroxisome proliferator-activated receptor gamma (PPARgamma) is able to induce both differentiation of orbital fibroblasts into mature adipocytes and expression of the TSH receptor (TSHr) gene. Several studies have suggested an important role of the high mobility group AT-hook 2 (HMGA2) gene in adipocytic cell growth and development. To investigate further the association between adipogenesis-related genes and orbital fibroblasts, we treated fibroblasts from Graves' ophthalmopathy (FGOs) and from normal orbital tissues with fenofibrate, a specific agonist for PPARalpha. We then evaluated the expression of the PPARalpha, PPARgamma2, HMGA2, leptin and TSHr genes before and after 24 h of fenofibrate treatment, using semiquantitative and real-time PCR. For up to 96 h after exposure to fenofibrate, FGOs differentiated into adipocytes. PPARalpha and PPARgamma2 were expressed more in FGOs than in normal cultures, whereas TSHr mRNA was detected only in FGOs. Expression of HMGA2 mRNA and protein was significantly increased in FGOs from 6 to 24 h after fenofibrate, confirming its role in the early phase of adipocyte differentiation. Treatment with fenofibrate for 24 h significantly increased the expression of leptin and TSHr genes. Moreover, TSH treatment significantly increased the accumulation of cAMP, demonstrating that FGOs express functional TSHr. The high level of expression of PPARalpha other than PPARgamma2 transcripts and the stimulating effect of fenofibrate on adipogenesis and on HMGA2, leptin and TSHr genes also indicate that the PPARalpha pathway plays an important part in the adipocyte differentiation of FGOs. These findings suggest that novel drugs to antagonize PPARalpha, other than the PPARgamma signalling system, may also need to be considered in the treatment or prevention of Graves' ophthalmopathy.
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FOXL2 has been studied extensively in mammals ( Crisponi et al. 2001 , Cocquet et al. 2002 ) and non-mammalian vertebrates ( Loffler et al. 2003 ). FOXL2 ovarian expression in mammals starts before the morphological differentiation of the
Shanghai Key Laboratory for Bone and Joint Diseases, Department of Orthopedics, Shanghai Institute of Orthopaedics and Traumatology, Shanghai Ruijin Hospital, Shanghai Jiaotong University School of Medicine, No.197, The Second Ruijin Road, Luwan District, Shanghai 200025, People's Republic of China
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Shanghai Key Laboratory for Bone and Joint Diseases, Department of Orthopedics, Shanghai Institute of Orthopaedics and Traumatology, Shanghai Ruijin Hospital, Shanghai Jiaotong University School of Medicine, No.197, The Second Ruijin Road, Luwan District, Shanghai 200025, People's Republic of China
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. 2013 ). Results of previous studies have indicated that the induction of osteoblast apoptosis and the inhibition of osteoblast proliferation and differentiation eventually lead to a reduction in bone formation ( Weinstein et al . 1998 , Pereira et al
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BeiJing School, Beijing, China
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HangZhou XueJun High School, Hangzhou, China
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exocrine pancreas, demonstrating that its effect is specific to the endocrine pancreas. Figure 3 Failure of non-β endocrine cell differentiation in the rfx6 knockout fish. (A and B) In situ hybridization showed that the expression levels of
Institut National de la Santé et de la Recherche Médicale (INSERM) Unité 982, INSERM Unité 625, Department of Endocrinology, Unité d'Endocrinologie, Laboratory of Biochemical Neuroendocrinology, Laboratory of Neuronal and Neuroendocrine Differentiation and Communication, Rouen University, Institute for Research and Innovation in Biomedicine (IRIB), 76821 Mont-Saint-Aignan, France
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( Pagani et al . 1992 ), SgII mRNA levels correlate with the differentiation status of tumoral cells (benign vs malignant), suggesting that measurement of the SgII transcript is a potential predictor of malignancy. Western blot analysis indicated that
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Retinoic acid (RA) and sodium butyrate (NaB) are regulators of cell growth and differentiation. We studied their effect on normal (SVC1) or v-Ki-ras-transformed (Ki-SVC1) rat seminal vesicle (SV) epithelial cell lines. The treatment of these cells with 10(-((7( M RA did not produce significant changes in the morphological and biochemical parameters analyzed. When RA was used in combination with 2 mM NaB, the treatment induced substantial morphological changes, apoptosis-independent growth arrest, up-regulation of tissue transglutaminase (tTGase), and down-regulation of beta and gamma RA receptor (RAR) mRNA expression. The same cells did not express RAR alpha either before or after NaB/RA treatment. A similar treatment did not change the amount of mRNA coding for the protein SV-IV (a typical differentiation marker of the SV epithelium) in normal or ras-transformed cells nor the level of v-Ki-ras mRNA in Ki-SVC1 cells. These findings suggest that a defective RA/RARs signaling pathway is probably the biochemical condition that underlies the unresponsiveness to RA of our in vitro culture system, and indirectly points to the possibility that the NaB/RA-induced effects were brought about by a cooperation at the transcription level between the histone deacetylase inhibitory activity of NaB and the ability of RA/RAR to modulate the expression of various genes involved in the control of cell growth and differentiation.
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The mouse mammary epithelial cell line HC11 upregulates the synthesis of beta-casein (a differentiation marker) following treatment with the lactogenic hormone mix dexamethasone, insulin and prolactin (DIP). We demonstrate that the basal levels of IGF-binding protein (IGFBP)-5 secreted by undifferentiated HC11 cells are upregulated 10-fold during DIP-induced cellular differentiation whereas the level of the other IGFBP species secreted by HC11 cells (IGFBP-2) is downregulated during this process. As previously reported, the combination of all three of these hormones is required for synthesis of the differentiation marker beta-casein, whereas basal IGFBP-5 secretion is evident in the absence of any hormonal treatment and, unlike beta-casein, secretion of this protein can be stimulated by binary combinations of the hormones (although maximal levels of IGFBP-5 are achieved in the presence of all three lactogenic hormones). Additionally, levels of IGFBP-5 can be increased by DIP treatment under conditions (non-competency of HC11 cultures or presence of epidermal growth factor) where DIP treatment does not increase synthesis of beta-casein. For IGFBP-2, dexamethasone is a potent inhibitor of secretion whilst prolactin stimulated the secretion of this binding protein into the medium. For the IGFBP axis in HC11 cells we conclude that, although the levels of IGFBP-5 and -2 are influenced by the state of cellular differentiation, the hormonal regulation of the levels of these IGFBP species can be dissociated from the regulation of beta-casein synthesis. In a further series of experiments we demonstrate that IGF-I is able to replace insulin in the DIP lactogenic hormone mix and by the use of a specific IGF-I receptor blocking antibody indicate that the action of IGF-I is mediated through the cell surface IGF-I receptor and not by cross-reaction of IGF-I ligand at the insulin receptor. We discuss our data in the context of the potential role of the IGF axis in the process of cell differentiation and illustrate the significance of our findings in the context of the physiology and life cycle of the mammary epithelial cell.
