Production, in Vitro Characterisation, in Vivo Clearance, and Tissue Localisation of Recombinant Barramundi (Lates calcarifer) Insulin-like Growth Factor II

2001 ◽  
Vol 123 (1) ◽  
pp. 38-50 ◽  
Author(s):  
B. Degger ◽  
N. Richardson ◽  
C. Collet ◽  
Z. Upton
Keyword(s):  
Growth Factor ◽  
Insulin Like Growth Factor ◽  
Lates Calcarifer ◽  
Factor Ii

Inhibition of insulin like growth factor II autocrine growth of Wilms' tumor by suramin in vitro and in vivo

1996 ◽  
Vol 103 (1) ◽  
pp. 49-56 ◽  
Author(s):  
Timothy S. Vincent ◽  
Debra J. Hazen-Martin ◽  
A.Julian Garvin
Keyword(s):  
Growth Factor ◽  
Wilms Tumor ◽  
Insulin Like Growth Factor ◽  
Autocrine Growth ◽  
Factor Ii

scholarly journals Dual role for transcription factor AP-2 in the regulation of the major fetal promoter P3 of the gene for human insulin-like growth factor II

1999 ◽  
Vol 338 (3) ◽  
pp. 799-806 ◽  
Author(s):  
Luc E. G. RIETVELD ◽  
Annemie M. C. B. KOONEN-REEMST ◽  
John S. SUSSENBACH ◽  
P. Elly HOLTHUIZEN
Keyword(s):  
Growth Factor ◽  
Human Insulin ◽  
Binding Sites ◽  
Mutational Analysis ◽  
Dual Function ◽  
Insulin Like Growth Factor ◽  
Factor Ii ◽  
In Cells

The human insulin-like growth factor II (IGF-II) gene contains four promoters that are differentially active during cell growth and development. Promoter 3 (P3) is the most active promoter in fetal and non-hepatic adult tissues. In addition to its expression during development, P3 is also the major promoter in many tumour tissues and IGF-II-expressing cell lines. Here we show that AP-2 has a dual function in P3 regulation in vivo as well as in vitro. In cells expressing low levels of endogenous AP-2, AP-2 overexpression activates P3, whereas P3 promoter activity is inhibited in cells containing abundant AP-2. Four potential AP-2-binding sites were identified in footprinting studies with recombinant AP-2. One of these AP-2-binding sites is located within the previously identified element P3-4 that contains two adjacent binding sites for IGF-II promoter-binding proteins IPBP3 and IPBP4/5. By applying binding competition assays and mutational analysis it is shown that AP-2 interferes with IPBP3 binding and transactivation in vivo as well as in vitro. Furthermore, AP-2 can bind additional elements in the proximal P3 promoter that also contribute to AP-2-mediated transactivation as shown by transient transfection assays. From these results we conclude that AP-2 is an important regulator in vivo and in vitro of IGF-II P3 activity.

scholarly journals O efeito molecular e estrutural do hormônio tiroideano no esqueleto

2004 ◽  
Vol 48 (1) ◽  
pp. 183-195 ◽  
Author(s):  
Cecília H.A. Gouveia
Keyword(s):  
Growth Factor ◽  
Insulin Like Growth Factor ◽  
Receptores Nucleares

O hormônio tiroideano é essencial para o desenvolvimento, maturação e metabolismo ósseos normais. Durante o desenvolvimento, a deficiência do hormônio tiroideano resulta em atraso na maturação do esqueleto e disgênese das epífises, resultando em redução do crescimento e anormalidades esqueléticas. O hormônio tiroideano também tem efeito no osso do adulto. A tirotoxicose é freqüentemente associada ao aumento do metabolismo ósseo e diminuição da massa óssea. Embora a importância do hormônio tiroideano no desenvolvimento e metabolismo ósseos seja clara, os mecanismos que medeiam os efeitos desse hormônio no tecido ósseo apenas começam a ser desvendados. O hormônio tiroideano pode atuar indiretamente no esqueleto, aumetando a secreção de hormônio do crescimento (GH) e insulin-like growth factor-1 (IGF-1); ou diretamente, modulando genes alvo via receptores nucleares específicos. Não se sabe, entretanto, se os principais efeitos do hormônio tiroideano no osso são resultado de ações diretas ou indiretas. Achados in vitro, tais como a presença de receptores de hormônio tiroideano (TR) e a indução de genes e proteínas em células esqueléticas pelo hormônio tiroideano, evidenciam a importância de ações diretas. Esta revisão tem como meta sumarizar os achados in vivo e in vitro relacionados aos efeitos do hormônio tiroideano no esqueleto.

Temporal changes in the expression of the insulin-like growth factor II gene associated with tissue maturation in the human fetus

Development ◽  
1989 ◽  
Vol 106 (3) ◽  
pp. 543-554 ◽  
Author(s):  
A.L. Brice ◽  
J.E. Cheetham ◽  
V.N. Bolton ◽  
N.C. Hill ◽  
P.N. Schofield
Keyword(s):  
Growth Factor ◽  
Cell Types ◽  
Specific Cell ◽  
Insulin Like Growth Factor ◽  
Vitro Fertilization ◽  
Age Related ◽  
Factor Ii ◽  
Metanephric Blastema

The insulin-like growth factors are broadly distributed in the human conceptus and are thought to play a role in the growth and differentiation of tissues during development. Using in situ hybridization we have shown that a wide variety of specific cell types within tissues express the gene for insulin-like growth factor II at times of development from 18 days to 14 weeks of gestation. Examination of blastocysts produced by in vitro fertilization showed no expression, thus bracketing the time of first accumulation of IGF-II mRNA to between 5 and 18 days postfertilization. The pattern of IGF-II expression shows specific age-related differences in different tissues. In the kidney, for example, expression is found in the cells of the metanephric blastema which is dramatically reduced as the blastema differentiates. The reverse is also seen, and we have noted an increase in expression of IGF-II in the cytotrophoblast layer of the placenta with gestational age. The sites of expression do not correlate with areas of either high mitotic activity or specific types of differentiation, but the observed pattern of expression in the kidney, adrenal glands and liver suggests an explanation for the abnormally high IGF-II mRNA expression in developmental tumours such as Wilms' tumour.

Insulin-like Growth Factor II Induces DNA Synthesis in Fetal Ventricular Myocytes In Vitro

1996 ◽  
Vol 79 (4) ◽  
pp. 716-726 ◽  
Author(s):  
Qingquan Liu ◽  
Huajun Yan ◽  
Nicola J. Dawes ◽  
Giuliano A. Mottino ◽  
Joy S. Frank ◽  
...  
Keyword(s):  
Growth Factor ◽  
Dna Synthesis ◽  
Ventricular Myocytes ◽  
Insulin Like Growth Factor ◽  
Factor Ii

scholarly journals Stimulation of glucose uptake by insulin-like growth factor II in human muscle is not mediated by the insulin-like growth factor II/mannose 6-phosphate receptor

1994 ◽  
Vol 300 (3) ◽  
pp. 781-785 ◽  
Author(s):  
B Burguera ◽  
C W Elton ◽  
J F Caro ◽  
E B Tapscott ◽  
W J Pories ◽  
...  
Keyword(s):  
Growth Factor ◽  
Glucose Uptake ◽  
Glucose Transport ◽  
Dependent Diabetes Mellitus ◽  
Obese Patients ◽  
Insulin Like Growth Factor ◽  
Biopsy Material ◽  
Factor Ii ◽  
Lean Group

Although the growth-promoting effects of insulin-like growth factor II (IGF-II) have been intensively studied, the acute actions of this hormone on glucose metabolism have been less well evaluated, especially in skeletal muscle of humans. We and other groups have shown that IGFs reduce glycaemic levels in humans and stimulate glucose uptake in rat muscle. The purpose of the present study was to evaluate the effect of IGF-II on glucose transport in muscle of normal and obese patients with and without non-insulin-dependent diabetes mellitus (NIDDM), as well as to identify the receptor responsible for this action. 2-Deoxyglucose transport was determined in vitro using a muscle-fibre strip preparation. IGF-II were investigated in biopsy material of rectus abdominus muscle taken from lean and obese patients and obese patients with NIDDM at the time of surgery. In the lean group, IGF-II (100 nM) stimulated glucose transport 2.1-fold, which was slightly less than stimulation by insulin (2.8-fold) at the same concentration. Binding of IGF-II was approx. 25% of that of insulin at 1 nM concentrations of both hormones. Obesity with or without NIDDM significantly reduced IGF-II-stimulated glucose uptake compared with the lean group. In order to explore which receptor mediated the IGF-II effect, we compared glucose uptake induced by IGF-II and two IGF-II analogues: [Leu27]IGF-II, with high affinity for the IGF-II/Man 6-P receptor but markedly reduced affinity for the IGF-I and insulin receptors, and [Arg54,Arg55]IGF-II was similar to that of IGF-II, whereas [Leu27]IGF-II had a very diminished effect. Results show that IGF-II is capable of stimulating muscle glucose uptake in lean but not in obese subjects and this effect seems not to be mediated via an IGF-II/Man 6-P receptor.

Transport of Insulin-Like Growth Factor 1 in Intervertebral Disc: Effect of Binding Interactions and Inhomogeneous Distribution of Binding Proteins in Annulus Fibrosus and Nucleus Pulposus

2010 ◽  
Author(s):  
Francesco Travascio ◽  
Chun Yuh Huang ◽  
Wei Yong Gu
Keyword(s):  
Growth Factor ◽  
Intervertebral Disc ◽  
Disc Degeneration ◽  
Reactive Transport ◽  
Binding Proteins ◽  
Insulin Like Growth Factor ◽  
Igf Binding Proteins ◽  
Binding Interactions

The intervertebral disc (IVD), being the largest avascular structure in human body, receives nourishment from the vascular network present near its periannular surface and at cartilage endplates (CEPs). It is believed that insufficient nutritional supply is a major cause for disc degeneration [1]. Understanding the mechanisms of solute transport in IVD is crucial for elucidating the etiology of disc degeneration, and to develop strategies for tissue repair (in vivo), and tissue engineering (in vitro). Transport in IVD is complex and involves a series of electromechanical, chemical, and biological coupled events. This study focused on the implications of solute-tissue reversible binding reactions on transport phenomena in the disc. A two dimensional (2D) finite element model was developed to predict diffusive-reactive transport in IVD. The numerical model was used to simulate transport of insulin-like growth factor 1 (IGF-1) in IVD, in the presence of binding interactions between IGF-1 and IGF-binding proteins (IGFBP-3) located on the extracellular matrix (ECM) of the disc.

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