scholarly journals Levels of the IGF system components in malignant lesions of the lungs with preventive effect of 1,3-diethylbenzimidazolium triiodide in the experiment

2020 ◽  
Vol 7 (6) ◽  
pp. 73-81
Author(s):  
E. M. Frantsiyants ◽  
I. V. Kaplieva ◽  
L. K. Trepitaki
2021 ◽  
Vol 39 (15_suppl) ◽  
pp. e15095-e15095
Author(s):  
Lidia K. Trepitaki ◽  
Irina V. Kaplieva ◽  
Elena M. Frantsiyants ◽  
Viktoriya L. Volkova ◽  
Dmitry A. Kharagezov ◽  
...  

e15095 Background: The system of insulin-like growth factors (IGF) is involved in carcinogenesis, since it promotes proliferation and survival of tumor cells. The purpose of the study was an analysis of the dynamics of the IGF system components in the lungs of rats with antitumor effect of 1,3-diethylbenzimidazolium triiodide. Methods: The main group included male (n=27) and female (n=27) white outbred rats with sarcoma 45 inoculated into the subclavian vein (2×106 cells in 0.5 mL saline) but not developed in the lungs due to administration of 1,3-diethylbenzimidazolium triiodide (intragastrically, 0.4 mg/kg once a day according to the regimen: administration for 5 days with a 2-day interval). Control group included males (n=14) and females (n=14) with sarcoma 45 growing in the lungs without treatment. Intact groups included 5 males and 5 females. After 4, 5 and 8 weeks of the experiment animals were decapitated, and levels of IGFI, IGFII, IGFBP1, IGFBP2 and IGFBP3 were measured by ELISA in 10% lung homogenates (CUSABIO BIOTECH Co., Ltd., China). Results: The sarcoma development in the lung was accompanied by the IGFI increase by 2.4-3.0 times in males and by 4.3 times in females, and the opposite IGFII dynamics: an increase in males (by 4.6 times) and decrease in females (by 4.3 times), together with the IGFBP decline. 1,3-diethylbenzimidazolium triiodide upregulated IGFI levels in the lungs of all rats on average by 1.3 times (p<0.05) and normalized IGFII in males, while increasing it in females by 1.6 times (p<0.05), together with higher (compared to controls) IGFBP levels. Conclusions: Preventive antitumor effect of 1.3-diethylbenzimidazolium triiodide is based on the stabilization of the IGF system grossly altered during the malignant process development in the lung.


1996 ◽  
Vol 3 (1) ◽  
pp. 39-46 ◽  
Author(s):  
Go Kimura ◽  
Junko Kasuya ◽  
Stefano Giannini ◽  
Yoko Honda ◽  
Subburaman Mohan ◽  
...  

2006 ◽  
Vol 290 (2) ◽  
pp. E363-E371 ◽  
Author(s):  
Daniela Kiepe ◽  
Sonia Ciarmatori ◽  
Anke Haarmann ◽  
Burkhard Tönshoff

The growth plate is an important target tissue for insulin-like growth factors (IGFs), but little is known about the regulation of the IGF system during the developmental sequence of chondrocytes. We therefore examined the expression profile of IGF system components in proliferating vs. differentiating growth plate chondrocytes by use of two cell culture models of the growth cartilage. In rat growth plate chondrocytes in primary culture, IGF-I expression increased twofold during the process of differentiation. IGF-binding protein-3 (IGFBP-3) expression showed a biphasic pattern of with a twofold increase at the onset of differentiation and a downregulation in late differentiating chondrocytes to 25% of baseline levels; the expression patterns of IGFBP-2, -4 and -6 were not dependent on the developmental stage. In IGF- and IGFBP-3-deficient RCJ3.1C5.18 (RCJ) mesenchymal chondrogenic cells, IGFBP-2 and -6 synthesis declined by 50% during differentiation. IGFBP-5 expression was markedly upregulated during the process of differentiation in both cell culture models. Although IGFBP-5 overexpression did not have an IGF-independent effect on RCJ cell differentiation, it promoted IGF-I-enhanced differentiation of these cells. A potential mechanism for this effect is the specific increase of Akt phosphorylation in IGFBP-5-overexpressing cells in the presence of IGF-I, indicating an increased activity of the phosphatidylinositol (PI) 3-kinase pathway. These data suggest that the developmental stage of the chondrocyte is an important determinant of IGF and IGFBP expression and imply a functional role for IGFBP-5 for upregulating IGF action during chondrocyte differentiation in vivo.


2011 ◽  
Vol 21 (6) ◽  
pp. 343-348 ◽  
Author(s):  
Sridhar Muthusami ◽  
Ilangovan Ramachandran ◽  
Senthilkumar Krishnamoorthy ◽  
Ramajayam Govindan ◽  
Srinivasan Narasimhan

1999 ◽  
pp. 457-496 ◽  
Author(s):  
Subburaman Mohan ◽  
David J. Baylink

2007 ◽  
Vol 377 (1-2) ◽  
pp. 70-78 ◽  
Author(s):  
P. Kanagaraj ◽  
M.R. Vijayababu ◽  
R. Ilangovan ◽  
K. Senthilkumar ◽  
P. Venkataraman ◽  
...  

1998 ◽  
Vol 47 (3) ◽  
pp. 295-302 ◽  
Author(s):  
Adrian V. Lee ◽  
Susan G. Hilsenbeck ◽  
Douglas Yee

1996 ◽  
Vol 16 (2) ◽  
pp. 227-236 ◽  
Author(s):  
W.-H. Lee ◽  
G.-M. Wang ◽  
L. B. Seaman ◽  
S. J. Vannucci

Insulin-like growth factor I (IGF-I) is an anabolic pleiotrophic factor essential for postnatal rat brain development, especially during the first 21 days, the “critical growth period.” Cerebral hypoxic–ischemic insults occurring during the perinatal period can result in neuronal necrosis and permanent brain damage. To understand the regulation of the action of IGF-I in response to such a metabolic insult, we investigated the gene expression of IGF-I, type I IGF receptor, IGF binding protein (IGFBP) 2, and IGFBP5 during the first 72 h after hypoxia–ischemiain the immature rat. At 1 h of recovery, messenger RNA (mRNA) levels of all IGF system components were decreased throughout the hemisphere ipsilateral to the carotid artery ligation. This decrease is more pronounced at 24 h of recovery, especially in areas vulnerable to hypoxic–ischemic injury, such as the thalamus and hippocampus. At 72 h of recovery, although IGFBP2 and type 1 IGF receptor mRNA levels remain suppressed, gene expression of both IGF-I and IGFBP5 was activated in reactive astrocytes. Therefore, during the critical growth period in rats, the transcriptional levels of all IGF system components are extremely sensitive to metabolic perturbations associated with cerebral hypoxia–ischemia. The immediate decrease in IGF-I gene expression may be partially responsible for the impending neuronal death and selective vulnerability of myelinogenesis during the perinatal period.


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