Insulin acts via mitogen-activated protein kinase phosphorylation in rabbit blastocysts

Santos, Anne Navarrete; Tonack, Sarah; Kirstein, Michaela; Pantaleon, Marie; Kaye, Peter L.; Fischer, Bernd

doi:10.1530/rep.1.00204

Cited by 39 publications

(11 citation statements)

References 62 publications

(49 reference statements)

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“… H2AFZ : H2A histone family member Z [35]; GAPDH : glyceraldehyde-3-phosphate dehydrogenase [36]; SMARCA2 : SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 2; EMP1 : Epithelial membrane protein 1; CALC : calcitonin gene-related peptide variant 1; SCGB1A1 : secretoglobin family 1A member 1).…”

Section: Methodsmentioning

confidence: 99%

Transcriptome Profiling of Rabbit Parthenogenetic Blastocysts Developed under In Vivo Conditions

Naturil-Alfonso

Saenz-de-Juano²,

Peñaranda³

et al. 2012

PLoS ONE

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Parthenogenetic embryos are one attractive alternative as a source of embryonic stem cells, although many aspects related to the biology of parthenogenetic embryos and parthenogenetically derived cell lines still need to be elucidated. The present work was conducted to investigate the gene expression profile of rabbit parthenote embryos cultured under in vivo conditions using microarray analysis. Transcriptomic profiles indicate 2541 differentially expressed genes between parthenotes and normal in vivo fertilised blastocysts, of which 76 genes were upregulated and 16 genes downregulated in in vivo cultured parthenote blastocyst, using 3 fold-changes as a cut-off. While differentially upregulated expressed genes are related to transport and protein metabolic process, downregulated expressed genes are related to DNA and RNA binding. Using microarray data, 6 imprinted genes were identified as conserved among rabbits, humans and mice: GRB10, ATP10A, ZNF215, NDN, IMPACT and SFMBT2. We also found that 26 putative genes have at least one member of that gene family imprinted in other species. These data strengthen the view that a large fraction of genes is differentially expressed between parthenogenetic and normal embryos cultured under the same conditions and offer a new approach to the identification of imprinted genes in rabbit.

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Section: Methodsmentioning

confidence: 99%

Transcriptome Profiling of Rabbit Parthenogenetic Blastocysts Developed under In Vivo Conditions

Naturil-Alfonso

Saenz-de-Juano²,

Peñaranda³

et al. 2012

PLoS ONE

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“…In addition to indirect effects of EDCs on embryo development, exerted via changes in hormone profiles, direct embryotoxic effects are possible through actions of EDCs on hormone receptors (Agras et al ., 2007; Davey et al ., 2007). It has been shown that the hormone receptor expression in blastocysts differs between embryoblast and trophoblast, which represent different cell lineages, and this results in different developmental impacts (Navarrete Santos et al ., 2004a, 2004b and 2008). Along with steroid hormone receptors, many of the effects of EDCs on pre-implantation embryos, and on implantation, are mediated through the aryl hydrocarbon receptor (AhR) and peroxisome proliferator-activated receptor (PPAR) signalling pathways.…”

Section: Effects On Animal Physiologymentioning

confidence: 99%

Effects of environmental pollutants on the reproduction and welfare of ruminants

Rhind¹,

Evans²,

Bellingham³

et al. 2010

Animal

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Anthropogenic pollutants comprise a wide range of synthetic organic compounds and heavy metals, which are dispersed throughout the environment, usually at low concentrations. Exposure of ruminants, as for all other animals, is unavoidable and while the levels of exposure to most chemicals are usually too low to induce any physiological effects, combinations of pollutants can act additively or synergistically to perturb multiple physiological systems at all ages but particularly in the developing foetus. In sheep, organs affected by pollutant exposure include the ovary, testis, hypothalamus and pituitary gland and bone. Reported effects of exposure include changes in organ weight and gross structure, histology and gene and protein expression but these changes are not reflected in changes in reproductive performance under the conditions tested. These results illustrate the complexity of the effects of endocrine disrupting compounds on the reproductive axis, which make it difficult to extrapolate between, or even within, species. Effects of pollutant exposure on the thyroid gland, immune, cardiovascular and obesogenic systems have not been shown explicitly, in ruminants, but work on other species suggests that these systems can also be perturbed. It is concluded that exposure to a mixture of anthropogenic pollutants has significant effects on a wide variety of physiological systems, including the reproductive system. Although this physiological insult has not yet been shown to lead to a reduction in ruminant gross performance, there are already reports indicating that anthropogenic pollutant exposure can compromise several physiological systems and may pose a significant threat to both reproductive performance and welfare in the longer term. At present, many potential mechanisms of action for individual chemicals have been identified but knowledge of factors affecting the rate of tissue exposure and of the effects of combinations of chemicals on physiological systems is poor. Nevertheless, both are vital for the identification of risks to animal productivity and welfare.

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“…In diabetes, insulin has been shown to induce proliferation of vascular smooth muscle cells, suggesting that insulin might be involved in the progression of atherosclerosis [18]. Another study, performed on rabbit blastocysts, also showed that insulin functions as a growth‐inducing factor without affecting glucose transport [19]. Thus, insulin has the ability to function as a mitogen in a number of different cell types, and therefore could be directly involved in the complications associated with the diabetic condition.…”

Section: Discussionmentioning

confidence: 99%

Insulin‐induced proliferation of bladder cancer cells is mediated through activation of the epidermal growth factor system

2006

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The mechanism behind the growth‐promoting effect of insulin is a subject of debate. Employing RT4 bladder cancer cells, we examined the cross‐talk between insulin and the epidermal growth factor system. We found that insulin induced a time‐ and dose‐dependent (25–1000 nmol·L−1 insulin) increase in mRNA expression of three ligands from the epidermal growth factor system. Times for peak increase and fold increase after incubation with 250 nmol·L−1 insulin were as follows: heparin‐binding epidermal growth factor‐like growth factor, 0.5 h, 1.4‐fold, P < 0.05; epiregulin, 3 h, 14‐fold, P < 0.0001; and amphiregulin, 3 h, 12‐fold, P < 0.001. Induction of heparin‐binding epidermal growth factor‐like growth factor and amphiregulin was verified at the protein level. We demonstrate that incubation of RT4 bladder cancer cells for 24 h with 250 nmol·L−1 insulin increases proliferation by 43% (P < 0.0001) as compared to untreated cells. At the same time, phosphorylation and thereby activation of the epidermal growth factor receptor (HER1) was observed. Both phosphorylation and insulin‐induced proliferation were almost completely inhibited by the HER1 inhibitor Iressa (P < 0.0001). This shows that insulin leads to activation of HER1, and that HER1 plays an essential role in mediating the growth‐promoting effect of insulin. Iressa inhibited not only the activation of HER1 caused by insulin but also the insulin‐induced increase in the three ligands (heparin‐binding epidermal growth factor‐like growth factor, epiregulin and amphiregulin). As heparin‐binding epidermal growth factor‐like growth factor was induced before epiregulin and amphiregulin upon insulin stimulation, we speculated that the insulin‐induced heparin‐binding epidermal growth factor‐like growth factor initiated the activation of HER1, and that this in turn led to increased expression of epiregulin and amphiregulin and thereby to continued activation of HER1. Earlier reports have shown that insulin‐like growth factor receptor can activate HER1 via its ligand heparin‐binding epidermal growth factor‐like growth factor. In accord with this, we found that treatment of RT4 cells with recombinant heparin‐binding epidermal growth factor‐like growth factor mimicked the effect of insulin, with induction of mRNA for the three ligands. However, the insulin‐induced increase in mRNA expression of amphiregulin and epiregulin could not be prevented by the heparin‐binding epidermal growth factor‐like growth factor inhibitor CRM197, demonstrating that heparin‐binding epidermal growth factor‐like growth factor is not essential for the insulin‐induced increase in the expression of these ligands. In conclusion, we show that insulin‐induced growth in RT4 cells requires activated HER1. Furthermore, activation of HER1 is required for the insulin‐induced increase in expression of the HER1 ligands heparin‐binding epidermal growth factor‐like growth factor, amphiregulin and epiregulin.

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Insulin acts via mitogen-activated protein kinase phosphorylation in rabbit blastocysts

Cited by 39 publications

References 62 publications

Transcriptome Profiling of Rabbit Parthenogenetic Blastocysts Developed under In Vivo Conditions

Transcriptome Profiling of Rabbit Parthenogenetic Blastocysts Developed under In Vivo Conditions

Effects of environmental pollutants on the reproduction and welfare of ruminants

Insulin‐induced proliferation of bladder cancer cells is mediated through activation of the epidermal growth factor system

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