Ontogeny of the Insulin-like Growth Factor System (IGF-I, IGF-II, and IGF-1R) in Gilthead Seabream (Sparus aurata): Expression and Cellular Localization

Perrot, Valérie; Moiseeva, E.B.; Gozes, Yehoshua; Chan, Shu Jin; Ingleton, P. M.; Funkenstein, Bruria

doi:10.1006/gcen.1999.7337

Cited by 90 publications

(62 citation statements)

References 34 publications

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“…Immunohistological evidence from teleost larvae indicates that, early in development, epithelial cells are target cells for IGFs (22,26). In the present study on juvenile striped bass, an antibody raised against the COOH terminus of the human IGF-IR specifically stained large spherical cells at the base of the lamellae in the primary filament.…”

Section: Discussionmentioning

confidence: 43%

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IGF-I and branchial IGF receptor expression and localization during salinity acclimation in striped bass

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Luckenbach

Madsen³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Section: Discussionmentioning

confidence: 43%

“…In 35-day-old larvae of gilthead seabream, gill IGF-IR immunoreactivity was found to be strongest in epithelial cells localized at the base of the secondary lamellae (22). Collectively, these studies suggest an important role of IGF-I in the development of gill epithelia in teleosts.…”

mentioning

confidence: 66%

IGF-I and branchial IGF receptor expression and localization during salinity acclimation in striped bass

Tipsmark

Luckenbach

Madsen³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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“…No significant changes were found in serum levels of IGF-1 and IGF-2 under hypoxia in ovine fetus (15). Although immunoreactive IGF-1 and IGF-2 were detected in teleost embryonic tissues by immunohistochemistry (37,38), it is unclear whether hypoxia changes the levels of IGF peptides. A well characterized pathway of hypoxia-induced gene expression is the transcription factor HIF-1 and its close relatives HIF-2 and HIF-3 (39).…”

Section: Discussionmentioning

confidence: 98%

Insulin-like growth factor-binding protein-1 (IGFBP-1) mediates hypoxia-induced embryonic growth and developmental retardation

Kajimura

Aida

Duan

2005

Proc. Natl. Acad. Sci. U.S.A.

213

158

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Although reduced fetal growth in response to hypoxia has been appreciated for decades, we have a poor understanding of the effects of hypoxia on embryonic development and the underlying cellular and molecular mechanisms. Here we show that hypoxia treatment not only resulted in embryonic growth retardation but also caused significant delay in developmental zebrafish ͉ heart development ͉ craniofacial skeleton ͉ morphogenesis ͉ oxygen H ypoxic stress causes major metabolic changes in all organisms requiring oxygen. Hypoxic stress also influences fetal growth and development and the pathogenesis of several human diseases, including intrauterine growth restriction (IUGR) (1-3). Reduced birth weight is also observed at high altitudes (4). IUGR not only increases fetal and neonatal morbidity and mortality, but also increases the risk of having adult diseases, such as cardiovascular disease, type-2 diabetes, obesity, and hypertension (5).Recent evidence suggests that hypoxia may influence fetal growth through its connection to the insulin-like growth factor (IGF) signaling system. IGFs are well known fetal growth factors (6-9). Several groups have reported that the circulating level of IGF-binding protein (IGFBP)-1, a secreted protein that binds to IGF in extracellular environments, is elevated in IUGR fetuses (10-12) and that there is a striking inverse correlation between IGFBP-1 levels and fetal size (13). In addition, higher maternal serum IGFBP-1 levels are found at higher altitude (14). In vitro studies with cultured human cells and in vivo studies with mammalian animal models suggest that IGFBP-1 gene expression is elevated in hypoxic conditions (15)(16)(17) and that this up-regulation is mediated through the hypoxia-inducible factor (HIF)-1 pathway (16). Because IGFBP-1 binds IGFs with high affinity and inhibits IGF activities on cell growth in vitro (18,19) and because IGFBP-1-overexpressing transgenic mice had reduced birth weight (20-22), it was postulated that the elevated IGFBP-1 plays a major role in hypoxia-caused IUGR by binding fetal IGFs and inhibiting their growth-promoting activities (3,16,17). This appealing model, however, has not been directly tested in vivo, and a causative relationship between the elevated IGFBP-1 expression and IUGR has not been established. Moreover, the impact of hypoxia on early developmental processes, such as morphogenesis, is poorly understood, and the role of IGFBP-1, if any, in mediating the hypoxic effects on embryonic development is unknown.The zebrafish has now become an informative vertebrate model organism for the study of IGF signaling in early development (23). Zebrafish embryos develop externally, eliminating the complication of maternal compensation. Fast developing and transparent zebrafish embryos make it possible to manipulate environmental factors and observe the phenotypic changes in organ formation in real time. Furthermore, major components of the zebrafish IGFsignaling pathway, including IGF ligands, receptors, IGFBPs, and intracellular signal transdu...

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“…Igf1 transcripts have been detected in unfertilized gilthead sea bream eggs and its later expression appears to be tissue-and age-dependent, with skeletal muscle displaying high immunoreactivity (Perrot et al 1999). In Atlantic salmon, increased igf1 expression marks the transition from zero to fast growth and is followed by the increased expression of myosin genes including mlc2 (Bower et al 2008).…”

Section: Gene Expression and Muscle Developmentmentioning

confidence: 99%

Transient up- and down-regulation of expression of myosin light chain 2 and myostatin mRNA mark the changes from stratified hyperplasia to muscle fiber hypertrophy in larvae of gilthead sea bream (Sparus aurata L.)

et al. 2015

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Hyperplasia and hypertrophy are the two mechanisms by which muscle develops and grows. We study these two mechanisms, during the early development of white muscle in Sparus aurata, by means of histology and the expression of structural and regulatory genes. A clear stage of stratified hyperplasia was identified early in the development of gilthead sea bream but ceased by 35 dph when hypertrophy took over. Mosaic recruitment of new white fibers began as soon as 60 dph. The genes mlc2a and mlc2b were expressed at various levels during the main phases of hyperplasia and hypertrophy. The genes myog and mlc2a were significantly upregulated during the intensive stratified formation of new fibers and their expression was significantly correlated. Expression of mstn1 and igf1 increased at 35 dph, appeared to regulate the hyperplasia-to-hypertrophy transition, and may have stimulated the expression of mlc2a, mlc2b and col1a1 at the onset of mosaic hyperplasia. The up-regulation of mstn1 at transitional phases in muscle development indicates a dual regulatory role of myostatin in fish larval muscle growth.

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Ontogeny of the Insulin-like Growth Factor System (IGF-I, IGF-II, and IGF-1R) in Gilthead Seabream (Sparus aurata): Expression and Cellular Localization

Cited by 90 publications

References 34 publications

IGF-I and branchial IGF receptor expression and localization during salinity acclimation in striped bass

IGF-I and branchial IGF receptor expression and localization during salinity acclimation in striped bass

Insulin-like growth factor-binding protein-1 (IGFBP-1) mediates hypoxia-induced embryonic growth and developmental retardation

Transient up- and down-regulation of expression of myosin light chain 2 and myostatin mRNA mark the changes from stratified hyperplasia to muscle fiber hypertrophy in larvae of gilthead sea bream (Sparus aurata L.)

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