mRNA expression patterns of insulin-like growth factor system components in human neuroendocrine tumours

2000 ◽  
Vol 30 (8) ◽  
pp. 729-739 ◽  
Author(s):  
Wulbrand ◽  
Remmert ◽  
Zöfel ◽  
Wied ◽  
Arnold ◽  
...  
Keyword(s):  
Growth Factor ◽  
Mrna Expression ◽  
Neuroendocrine Tumours ◽  
Expression Patterns ◽  
Insulin Like Growth Factor ◽  
System Components ◽  
Factor System

Effects of Maternal Diabetes on Fetal Expression of Insulin-Like Growth Factor and Insulin-Like Growth Factor Binding Protein MRNAs in the Rat

1995 ◽  
Vol 147 (2) ◽  
pp. R5-R8 ◽  
Author(s):  
Randal D. Streck ◽  
Veeraramani S. Rajaratnam ◽  
Renata B. Fishman ◽  
Peggy J. Webb
Keyword(s):  
Growth Factor ◽  
Mrna Expression ◽  
Fetal Growth ◽  
Fetal Liver ◽  
Expression Patterns ◽  
Maternal Diabetes ◽  
Limb Bud ◽  
Insulin Like Growth Factor ◽  
Igf Binding Proteins ◽  
Increased Risk

ABSTRACT Matemal diabetes is associated in humans and rats with an increased risk for fetal growth abnormalities and malformations. Therefore, the effect of maternal diabetes on expression of genes that regulate fetal growth and differentiation is of considerable interest. Developmental growth is regulated in part by the expression and availability of insulin-like growth factors (IGFs). Postnatal expression of a subset of the IGFs and IGF binding proteins (IGFBPs) has been demonstrated to be regulated in response to diabetes and other metabolic conditions. We used in situ hybridization to analyze the effect of maternal diabetes, induced by streptozotocin (STZ) prior to mating, upon prenatal rat IGF and IGFBP mRNA expression. At gestational day (GD) 14, the most striking effect of maternal diabetes on fetal IGF/IGFBP gene expression was a marked increase in the abundance of IGFBP-1 mRNA within the liver primordia of fetuses isolated from diabetic dams compared to age-matched controls. This upregulation cannot be entirely due to the approximately one-half-day delay in fetal development (based on limb bud staging) associated with maternal diabetes, as there was no gross difference in the level of IGFBP-1 mRNA between GD13 and GD14 control fetal livers. In contrast, the fetal mRNA expression patterns of IGF-I, IGF-II and IGFBP-2, -3, -4, -5 and -6 were not grossly altered by maternal diabetes. These data are consistent with the hypothesis that IGFBP-1 produced within the fetal liver and secreted into fetal circulation may play a role in regulating rat fetal growth.

Distribution and mRNA Expression of Insulin-Like Growth Factor System in Pulmonary Lymphangioleiomyomatosis

2001 ◽  
Vol 49 (5) ◽  
pp. 421-433 ◽  
Author(s):  
Julio C. Valencia ◽  
Kazuhiro Matsui ◽  
Carolyn Bondy ◽  
Jian Zhou ◽  
Audrey Rasmussen ◽  
...  
Keyword(s):  
Growth Factor ◽  
Mrna Expression ◽  
Insulin Like Growth Factor ◽  
Pulmonary Lymphangioleiomyomatosis ◽  
Factor System

Expression of insulin-like growth factor system components in colorectal tissue and its relation with serum IGF levels

2009 ◽  
Vol 19 (2) ◽  
pp. 126-135 ◽  
Author(s):  
Alina Vrieling ◽  
Dorien W. Voskuil ◽  
Astrid Bosma ◽  
Donné M. Majoor ◽  
Jaap van Doorn ◽  
...  
Keyword(s):  
Growth Factor ◽  
Insulin Like Growth Factor ◽  
Colorectal Tissue ◽  
System Components ◽  
Factor System

Insulin-like growth factor system components in the periodontium during tooth root resorption and early repair processes in the rat

2006 ◽  
Vol 114 (4) ◽  
pp. 318-327 ◽  
Author(s):  
Werner Götz ◽  
Dominique Kunert ◽  
Dongliang Zhang ◽  
Afshar Kawarizadeh ◽  
Stefan Lossdörfer ◽  
...  
Keyword(s):  
Growth Factor ◽  
Root Resorption ◽  
Tooth Root ◽  
Insulin Like Growth Factor ◽  
Early Repair ◽  
Repair Processes ◽  
System Components ◽  
Factor System

scholarly journals Expression and Secretion of the Insulin-like Growth Factor System Components by Pig Liver Cells

2008 ◽  
Vol 21 (9) ◽  
pp. 1244-1251
Author(s):  
I. Kim ◽  
E. J. Jin ◽  
K. Baik ◽  
C. H. Park ◽  
W. K. Kim ◽  
...  
Keyword(s):  
Growth Factor ◽  
Liver Cells ◽  
Insulin Like Growth Factor ◽  
Pig Liver ◽  
System Components ◽  
Factor System
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